Can God create a boulder that is too big for Him to carry???


If the Lord wants you to do anything as a result of what happened I’m sure He will gently let you know–but not through troubling memories. That doesn’t sound like God. To me…”

I wanted to address this with you right now if I may.  I have heard words like this said many many times to people who suffer with PTSD whether it was inflicted by those intent upon doing sever damage or not. I can appreciate that it is something that is said out of sympathy and kindness.  Often though, it is taken more as invalidation and the person (me in this case) might be left feeling more isolated and unsure of themselves and the world around them.

I believe that we as human beings can be very quick to put things in a category with a name and then never let that thing move, change, or evolve.  It is a difficult thing, change, especially when it seems to be painful.  I am not fond of the pains that come with being awakened to the harsh realities of the fallen world around us; at least not all the time.  Still I have to consider that if I am to grow in my character I have to allow for change in the way that I perceive the world around me and ESPECIALLY about how I see and feel about Deity!

Luke 1:37 says that with God nothing shall be impossible. What does that mean? Is it saying that there are things that even God cannot do?  Is it saying that there are times when God cannot be?  OR is it saying God can do all things because for Him NOTHING is impossible?

In Romans 11 these questions are asked:

“Oh, the depth of the riches of the wisdom andi knowledge of God! How unsearchable his judgments,and his paths beyond tracing out! Who has known the mind of the Lord? Or who has been his counselor? Who has ever given to God, that God should repay them? For from him and through him and for him are all things. To him be the glory forever! Amen.”

This statement is packed with questions that seem to pose a certain idea to yours truly. Who is God that I  can label Him as one thing and He will obey me?  Who knows the Lord’s mind better than the Lord that they SHOULD give HIM counsel?  Ha! how many times have I prayed as such?  Do you recall the ever popular prayer of bargaining?  “Dear God if only you would do XYZ I would do LMNOP…”  As if God needed us to make this deal because His whole plan hinged on us.  WOW!!  God knows all things.  God created all things. According to some interpretations of the Bible God is everywhere all the time.  How could He gain counsel from me?  I am NONE of those things.

I cannot agree that God would not help me out in some way through the troubling memories.  In each one I learn more about why I am the way I am.  How God loves me the way that I am because He understands all that it took to make me this way.  I see His hands in the pieces that are shameful and make me shake.  He is the one that is there in it all, the only one in fact that always has been.  God has Not been a daunting task master intent upon my destruction but rather a loving entity giving me strength that I would have NO way of having on my own. 

Putting God in a box about something because I do not like it or it does not seem God-like to me first of all does me NO good.  It can create a sense of falseness and arrogance in my person.  I might feel that I know better about God than another person, or I might offer comfort in a way that is inaccurate and more hurtful than the original wound.  I have been told my entire life that I am evil.  I have been told that I have awful hurtful intentions towards others.  Many have told me that the mean things that I think happen to people because of the immense amount of evil that resides in me.  Pay attention here, I am not trying to hurt you in any way, I am trying to however, make a point…  You saying that my troubling memories serve no good purpose reinforces that belief in me. 

Of course God would not work with me through those, I AM so very bad, malevolent, heinous, corrupt, unpleasant, destructive, hateful, malicious, nefarious, ugly, wicked, vicious, vile ETC…right? 

God, to me, is a master craftsman.  He can do all things, right?  He can make the impossible, well, possible!  If that is true, He can and dare I say He DOES work in and through each harsh and brutal memory that I have, whispering I value and respect you my child in and through each one.  It is both heart warming, and repulsive to say the least. It is heart warming because I always wanted to be respected and valued.  It has been repulsive because the ones from my past who claimed to value me most caused me more emotional, physical, psychological and spiritual damage – ON PURPOSE – than ones who just used me and past on by.  Yet, even in both of those emotions, I find God there as well.

One can hardly say ‘with God nothing is impossible‘ and then in the next breath declare that He can’t do something.  How can that be?  Deciding not to do something is a far cry from not being able to do something.  Don’t you agree?

Because of all that!!!!  I am trying very diligently to NOT put God in a box.  He can do all things. He is the truth of all things. He is the life of all things. With descriptions and praises like these, can God really be limited by my limited and finite understandings?

Can God created a Boulder that is too big for Him to carry?

I do not know the answer to this question but I am constantly intrigued by the ideas behind it.  This questions challenges our beliefs about God.  It speaks to the compulsive attitudes we compartmentalize about Him in our hearts and minds. It is fun and inquisitive on a sarcastic yet simple forthright way.  What do we really know about God?  There are a lot of assumptions and accusations even but what is it that we know?

I submit to you that God is more that simply mysterious.  He is that He is. God is God and has been God forever in the past direction and will be forever in the future direction and ALL the spaces in between.  Because He Was and IS and always Will Be –  and not just WAS – the hope that I feel for life as I know it and how it can still be seems more possible than all the impossible labels and punctuations that we create for and in the name of God.

I AM Yours…

My Dearest Child,

There will be times in your life that will appear to make no sense  –I AM the way

There will be days that you’ll feel you don’t belong  –I AM calling you as you are to be my child

There will be days that will fill you with Sunshine and Joy  –I AM smiling with you

Some moments will ache in your muscles.  You will feel exhausted and too hot or too cold-I AM aware and not only believe you but I believe IN you

Other times tears will fall and you will need someone you can trust  –I AM here with you

From time to time your heart will want to dance and sing  –I AM the rhythm to the music

I AM your melody

There will be times of darkness and you will be afraid -I understand, reach out!  I AM the Light

When you are hungry and parched consider Me in your search to fill your vast longings  –I AM the Bread of Life  –I AM the Living Water

From Eternity to Eternity I AM THAT I AM

I have always been, I AM now, and I always will be

I do not ‘need’ you to be a perfect robotic replica of human perceived perfection

I want a true and loving relationship with you – right now – Just as you are

I AM the Truth.  I AM Love.  I created you.  I AM on the path with you.  I AM accepting you right now.  I AM here with you and You are not alone.  You are a beautiful mess – My beautiful mess.  I AM constantly thinking of you.  I AM blessing you with your special abilities.  I AM always here for you.  You are wanted.  You are loved.  I AM never going to forget about you.  I AM now, have been and always will be here for you and with you

You are because I AM and I love you!



The reply to a Post (just half of the conversation)

An individual sent me copies of “paintings” of what some believe their form of Deity to look like.  Using these pictures as ‘proof’ of their full concept of God  – this individual demeaned and put down their creators as being Unintelligible and ridiculous….

It appears that you have given this matter a lot of thought and deliberation.  You have done some research and have drawn some conclusions that I have come to as well.  Not all of them are similar but many are, and that is most intriguing!

First and foremost – I do not believe that any religion will save you!  NONE!  The only one who can save you is Jesus Christ.  He alone has the power to do this. No one else, and nothing else will, nor can they.

While philosophical and theological discussions are powerful and inspiring in many ways, they cannot

take the place of the truth.  And what or whom is the truth? Jesus is the “way, the TRUTH, and the life…”

(John 14:6).  You have made many valid points about Christian churches, the ‘Trinity’ concept, the

Nicene Creed.  You are incorrect with your statement of – “All religious organizations from the year 325

thereafter to this day (except one) has added to, or taken from the Nicene Creed, to create their own

version of their particular (Chief Articles of Christian Belief) or creed.”

Unless you have looked at every single one, the inclusion of every religious organization –when you use the word ‘all’ – cannot be considered valid.

Have you set your very own eyes on each of them? Read them line for line? Conversed with the creators or members of each?  Can you even name them all? If not, then that statement is not and cannot be correct.

There is a funny thing about art though – paintings, drawn murals, anything put together by person or persons – only shows the artist’s understanding, perception, and thus are NOT proof of any kind.  Personally I like to think of things in a more intimate and personal manner.  My artistic expression of choice is ‘creative vocabulary’ and I am a vocabulist with my own erudite answers to such criticisms and complaints.  I understand that not all choose my methods, and that is okay.  Just because I put words on a page, and someone likes them and makes a billion copies and hands them out to everyone they can – does NOT prove that I am right, nor does it prove I am wrong.  It is about content and context. Without either, nothing truthful can be maintained, let alone established.

While I do not believe that there are any pictures, drawings, or forms of artistic expression that will give anyone a ‘perfect’ understanding of God – I am actually offended that you call someone else’s concept “Incomprehensible and Unintelligible.”  Wow, that is an incredible statement.  How harsh and cold it seems to me.  I do not agree with you on many things, but I would never hold something that you made up to an audience of people who were seeking in a similar fashion, and criticize it – especially by calling it something as ‘innocent’ as “Unintelligible.”  Can you imagine how a person might feel seeing something they made, or something they hold very dear, being called – out right stupidity?!?!?!   I know it happens, quite a bit, all over the planet in fact.  (This is another point you do not have to agree with on.) But to me – that is very wrong.  You and I both think we are right!  I do not believe that thinking I am right allows me to poke fun at another person’s interpretation of Deity, especially on any kind of public forum.  The fastest way to hurt someone is to call them stupid, or to say that they are unintelligible.  Asking questions is great!  But words are powerful, and because of that power … we (and I totally include myself here) often use our words to put others down, rather than to build them up.  I hate it when I realize I have done this.  I try very honestly to NOT do this on purpose.  I am human, therefore flawed.  I am working on it with God, like many of us are.
The word ‘Trinity’ is not found in the Bible.  However, just because you do not agree, or understand it does not make it incorrect, or impossible to accept and understand. While I do not currently subscribe to the entire concept of ‘Trinity’ there are some who do.  They love this idea and believe in it – as you do in your own concept of GodHood.

Using your resources I looked up ‘Trinity’ in the online Wikipedia.  (Here is the link: )

This is what it states: “The Christian doctrine of the Trinity (from Latin trinitas “triad”, from trinus “threefold”)[1] defines God as three consubstantial persons,[2]expressions, or hypostases:[3] the Father, the Son (Jesus Christ), and the Holy Spirit; “one God in three persons”. The three persons are distinct, yet are one “substance, essence or nature”.[4] In this context, a “nature” is what one is, while a “person” is who one is”

You said in your paper that the concept or idea of the ‘Trinity’ is non-Biblical.  Is it non-Biblical to you because you disregard the verses that this concept is derived from?  Is it non-Biblical to you because you don’t want to think it might possibly hold some water?  Or, is it because you cannot accept the idea that God could defy the laws of physics that He Himself created?  If there is another reason for your idea it was not clearly stated. Just because something does not make sense to YOU, does not mean it cannot make sense to someone else.  I am not saying that you have to believe it.  I am not saying I completely agree with the entire ‘Trinitarian’ concept either.  What I am saying is, that trying to understand, instead of pouncing on something that doesn’t make sense to you, with an open mind can take a person so much further than they would ever hope to get on their own.

Your use of terms (in bold) such as “Real God” and “What the Bible Really Says” seem arrogant and condescending.  The whole world – according to you, for the past 2000 years with scholars, professors, archeologists, PhDs, and the many skilled yet unlearned who studied the Bible every day of their adult lives – has been and is still full of people that do not know the “Real God,” nor do they know “What” the Bible “Really Says?  How sad that perspective is to me.  If that is the case, then why do you go to places like or for any information about religion – specifically, when you already know God with an ‘absolute understanding?’  Perhaps you just want a general knowledge and not each leader’s ideas, huh?  Neither site is run by a religion.  You might think they are accurate and impartial but let me let you in on a little known secret.   Wikipedia is submitted to by regular peeps like you and me.  They seek clarification but accuracy is not their most pressing concern.

You used the following quote in your paper:

If you don’t accept the trinity than you’re a cult!”

That is laughable at best.  I am sure it has been said to you and I agree with you that it is seriously ridiculous, (I hope that is ‘their’ direct quote … the grammar is off which delights me lol).  Does that quote sting you at all? Are you offended at the idea of someone saying that you are in a cult?  Then if any part of that is yes, you can see how words can hurt from that simple incorrect and insensitive statement.

Page three second paragraph – …..   There is so much that is incorrect about that one paragraph. I almost do not know where to begin.  First of all, the ALL Christian churches part is ABSOLUTELY incorrect.  Furthermore, the “all Baptist churches” statement is also FUNDEMENTALLY in error.

Have you attended one lately?  Have you attended any ever?  I do not claim to belong to any religion, but when I do go to church, I often attend a Baptist sect.  There are ZERO pictures of Deity to be found there.  Absolutely NONE!  We sing of God. We talk of God. We read from the Word of God.  We do not hang pictures. Nor do we have any graven images of what we believe God looks like.  One person’s idea of God, accepted by some and mass produced does NOT make it any more valid than the supposed proof of other’s ideas presented in your paper.  Taking a gander online about one thing or another can give you some kind of idea about it but blatant cavalier generalizations about things you have not experienced is not only hurtful and incredibly insensitive, it is in NO way appealing and has great dearth of the ‘logical’ conclusions that are drawn up in this paper.

Top of page five – ………….  Great question! Quite forcefully built but also deceptive at the same time.  You appear to be asking a question that is sincerely inquisitive.  In the same breath you put ‘claim,’ ‘belief,’ ‘disbelief,’ ‘accepted world-wide Christian pictures,’ ‘harmony,’ and causing further conflict you create a sameness between the words ‘faith’ and ‘religion.’  What?  You might as well say this – so you go to church but you don’t believe what they teach, even though they have pictures!?!

Pictures are not proof!

Going to church, no matter what church it is, does not depict who you are. It is not usually all that you think.  Going to church cannot save you and protect you! You are NOT the church you belong to.  Your faith is based on you and your longing for and maintenance of a Godly relationship, PERIOD.

I love that people use their artistic talents to show people the love of God that they feel. While I love that they use these talents to express their extreme passion and faith, it still does not prove that what their perception is in fact – fact.  It is merely an outward expression of their inward beliefs. Faith does not always make complete logical sense.  Faith is fuzzy sometimes and can prompt you to ask questions. Religion dictates what you should and should not do.  God loves us all.  God wants a relationship with each one of us.  Religion will tell you what you must do.  God is always there. He will help you, but will not force you to do everything.  Faith and Religion are NOT the same.  They NEVER have been.  They NEVER will be.

Now to your religion: The one you have “found” that makes you happy.  I appreciate your stand point that your church declares the Father and Son to be separate and distinct.  The LDS church does believe that, and can cherry pick versus in the Bible that can seem to confirm that point of view.  Remember –  “We believe the Bible to be the word of God – as far as it is translated correctly… (Articles of Faith #8)?”  From that idea come many that follow creating a discord between people and God’s Word.  I am not saying that your religion is alone in this type of Tyrannical idea that only OUR ideas are correct about ‘whatever’ because it seems that many many are.

You want to talk about God in completeness, which I celebrate and applaud.  However, you also say you know with an “absolute understanding” who Heavenly Father really is.  I tell you with my own personal experience (I understand my opinion contradicts your own), you do NOT have an absolute understanding.  You have not seen God with your own eyes.  You have not touched Him, to know whether he has a hand or not.  You were not present when the world was created, at least you do not recall it.  Having an ‘absolute understanding’ implies that you know everything there is to know about whatever it is you are talking about.  Admittedly I don’t have that about God; heck, I don’t even have that about myself!  And I don’t know anyone who does.  God is mysterious. Right? That is Biblical.  We can know things. This is true!  However, absolute understanding belongs to God.

Just because a person says, “I am one of his witnesses, and in a coming day I shall feel the nail marks in his hands and in his feet and shall wet his feet with my tears. But I shall not know any better then than I know now that he is God’s Almighty Son, that he is our Savior and Redeemer…”  – does not make it truth.  I am not saying it is or isn’t, just so you know.  Many have told me that this very account was very acclaimed and wide spread.  Bruce McConkie was claiming to have seen Jesus Christ and to know Him.  You believe it. I know because you have told me so.  Grandma W… has this quote on her kitchen wall. She has for as far back as I can remember it.  It is popular.  It is compelling.  It is one person’s account of their perceived understanding and interpersonal relationship with Deity.  Anyone can tear it apart. Many people have.  What good would that do me here and now?  Who am I to tell you that what you are believing in is wrong anyhow?
How could I encourage any positive inspiration in you, if I curse, destroy, belittle and with no class but arrogance on my part, say something as simple as, this quote is “Incomprehensible…according to Impossible to understand or comprehend: Unintelligible.”  And, of course, the quote is “Non-Biblical.”  If I believe that, it is one thing.  If I were to say the above and not think about how you would feel about those ‘innocent’ words, especially knowing that you value and treasure Mr. McConkie’s words – what good would come from that?  Would you be more wounded?  Would Grandma be wounded? Yes, I believe you both would.

You say that you want to know truth. You say that you also know everything there is to know about God.  If you think that you know all there is to know about God, than you don’t have anything else to learn about God.  Is that what you intended the paper to say?

I get that you want to share your faith!  I am so happy that you are being bold about it. I am very proud of you in that respect.  Still, if you already have all you need, and that is how it sounds from your paper, then the document is not only extremely cavalier but also heartbreaking.

Pictures are not proof. I think I have made that pretty clear. 

The Nicene Creed – to me – seems another plot for people of a “controlling mind set” (religion) to manipulate and control others relationships with Deity.  Jesus said, “Come, follow me.”  He did not say, make rules for others to follow!  Having Godly morals and doing ‘good’ to mankind is what He did.  Therefore, I will do my best to do that as well.  I cannot be perfect, and neither can you or anyone else in this life be perfect.

Your ideas, while rough and assuming are also fruitful and thought out in some respects.  I encourage you to keep studying.  Do not limit your focus to only ONE set of resources, if you can.  You have a world-wide network at your fingertips.  All you have to do is reach out.  God is there.  God is here. God is everywhere.  I am both inspired and confused with your paper.  I hope you will continue to search, learn, and grow.

I love you.  Honestly, I am pretty damn sure that I get a lot of my questionings and ways of thinking from my observance of you.  You like to take a concept and break it down to its smallest components and then see if you can put it back together.  I love to do that myself!  You use facts and emotionalism to create the world around you.  The world does function in this manner but with a stronger embellishment on the latter expression.  I do hold emotions in high esteem. With that said however, I cannot put emotions above fact.  I use the emotions that possess me in a sometimes counterproductive way.  Unfortunately, I have used raw emotion to lead me into things that were not worthy of my time.  If emotion, and emotion alone, could lead us to absolute authenticity – then what of learning, seeking answers, and why all the questions that emotions cannot address?

I am also going to continue to search, learn and grow.

Just one more thought.  If a person came to you and said they had all kinds of knowledge; then they began to spin a web of ‘extraordinary’ understandings that fascinated you and made you FEEL good; would you believe them?  Why, or why not?

More Information on Relapsing Polychondritis

all this info was taken from the following at: 

Relapsing Polychondritis is an episodic, inflammatory, and destructive disorder involving primarily cartilage of the ear and nose but also potentially affecting the eyes, tracheobronchial tree, heart valves, kidneys, joints, skin, and blood vessels. Diagnosis is by a combination of clinical, laboratory, imaging, and sometimes biopsy findings. Treatment usually requires prednisone and other immunosuppressants.

Relapsing polychondritis affects men and women equally; onset typically is in middle age. An association with RA, systemic vasculitis, SLE, and other connective tissue disorders suggests an autoimmune etiology.

Symptoms and Signs

Acute pain, erythema, and swelling most commonly affect the pinna cartilage. Nasal cartilage inflammation is the next most common manifestation, followed by arthritis that varies from arthralgias to symmetric or asymmetric nondeforming arthritis involving large and small joints, with a predilection for the costochondral joints and knees. The next most common manifestations, in decreasing order of frequency, are inflammation of the eye (eg, conjunctivitis, scleritis, iritis, keratitis, chorioretinitis); cartilaginous tissue of the larynx, trachea, or bronchi (causing hoarseness, cough, and tenderness over the laryngeal cartilage); internal ear; cardiovascular system (eg, aortic regurgitation, mitral regurgitation, pericarditis, myocarditis, aortic aneurysms, aortitis); kidney; and skin. Bouts of acute inflammation heal over weeks to months, with recurrences over several years.

Advanced disease can lead to destruction of supporting cartilage, causing floppy ears, saddle nose, pectus excavatum, and visual, auditory, and vestibular abnormalities. Tracheal narrowing can lead to dyspnea, pneumonia, or even tracheal collapse. Coexisting systemic vasculitis (leukocytoclastic vasculitis or polyarteritis nodosa), myelodysplastic syndrome, or cancer is possible.


  • Clinical criteria
  • Sometimes biopsy

Diagnosis is established if the patient develops at least 3 of the following:

  • Bilateral chondritis of the external ears
  • Inflammatory polyarthritis
  • Nasal chondritis
  • Ocular inflammation
  • Respiratory tract chondritis
  • Auditory or vestibular dysfunction

Biopsy of involved cartilage, most often the pinna, is helpful if clinical diagnosis is not clear-cut.

Laboratory tests are done. They are not specific but may help exclude other disorders. Synovial fluid analysis reveals mild inflammatory changes that are nonspecific but help rule out an infectious process. Blood tests may show normocytic-normochromic anemia, leukocytosis, elevated ESR or γ-globulin levels, and occasionally positive rheumatoid factor, antinuclear antibodies (ANA), or, in up to 25% of patients, antineutrophil cytoplasmic antibodies (ANCA). Abnormal renal function may indicate an associated glomerulonephritis. A positive c-ANCA test (ANCA that are reactive mainly to proteinase-3) suggests granulomatosis with polyangiitis (previously Wegener granulomatosis), which can cause similar findings (see Granulomatosis with Polyangiitis (GPA)).

The upper and lower airways should be evaluated, including complete spirometric testing and chest CT, when the diagnosis is made.


Mortality rates have decreased with newer therapies. Survival is now 94% after 8 yr, with death typically resulting from collapse of laryngeal and tracheal structures or from cardiovascular complications such as large-vessel aneurysm, cardiac valvular insufficiency, or systemic vasculitis.

(94% ???  That sounds fantastic!  I have seen many older statements that said 48% – 50% after 5 years.)


  • NSAIDs or dapsone

for mild ear disease

  • Corticosteroids
  • Sometimes methotrexate

or other immunosuppressants (eg, cyclosporine

, cyclophosphamide


, anti-TNF drugs)

Mild recurrent ear disease may respond to NSAIDs in anti-inflammatory doses, ordapsone

(50 to 100 mg po once/day). However, most patients are treated withprednisone

30 to 60 mg po once/day, with tapering of the dose as soon as there is a clinical response. Some patients require chronic use. In such patients,methotrexate

7.5 to 20 mg po once/wk can reduce the requirement for corticosteroids. Very severe cases may require other immunosuppressants, such as cyclosporine

, cyclophosphamide

, anti-TNF drugs (eg, infliximab


), or azathioprine

(see Immunomodulatory, cytotoxic, and immunosuppressive drugs). None of these therapies has been tested in controlled trials or has been shown to decrease mortality. If tracheal narrowing causes stridor, a tracheostomy or stent may be needed.

More extensive tracheobronchial collapse may require tracheal reconstruction. Eye disease may sometimes be recalcitrant to treatment, especially when involving the sclera, and has a poor prognosis. All patients should be closely monitored for atherosclerosis given the risk of premature atherosclerosis in systemic vasculitides. Patients on long-term corticosteroid therapy should receive osteoporosis prophylaxis. Prophylaxis for opportunistic infections, such as Pneumocystis jirovecii,should be added if combination immunosuppressive therapy is used.

Endotracheal intubation can be technically difficult because of tracheal involvement and narrowing; also, intratracheal manipulation can lead to life-threatening postanesthetic deterioration by causing further glottal or subglottal inflammation. Thus, endotracheal intubation should be avoided whenever possible (eg, instead using local and regional anesthesia). When endotracheal intubation is unavoidable, preparations should be made for emergency cricothyrotomy.

Key Points

  • Consider relapsing polychondritis if patients develop inflammation of the pinna or nasal cartilage, particularly with symptoms and signs compatible with respiratory tract chondritis or unexplained arthritis, ocular inflammation, or auditory or vestibular dysfunction.
  • Biopsy the affected cartilage if necessary to confirm the diagnosis.
  • Treat mild disease with NSAIDs or dapsone


  • Treat more severe disease with corticosteroids and sometimes methotrexate

or other immunosuppressants.

  • Avoid endotracheal intubation or, if it is unavoidable, prepare for emergency cricothyrotomy.

Last full review/revision June 2013 by Rula A. Hajj-ali, MD

Content last modified October 2013

Saying Goodbye to Maria

Yesterday I found out that a dear mate of mine had passed away. Here is something that you don’t know about me… I use the act of blowing soap bubbles as a sort of symbolic way to give things to God. So, last night a few hours after I found out about my friend, I went outside and blew bubbles as the snow was falling. It was so beautiful. To me very soothing, watching the bubbles dance in the light and hover and eventually fly away. It was so cold, but two of my best mates were out there with me, and that made it all the more meaningful to me. Just before we departed the snow, my mate Sas….. said a prayer. When situations like this occur, I am reminded of all the wonderful people that have been and are still in my life. God is good and my friend is with Him now. Though I will miss her, I am also very happy for her. Sweet dreams Maria!
This is a woman who was so patient and kind with me. Though she didn’t always believe me, she always believed IN me.

I wrote this letter, and took it with me to the clinic yesterday, for them to send to her.

This is what it said…

My Dear Maria,

I have been missing you lady!  From what I know, you are not well enough to come to work AND I cannot even make an appointment for later right now.  This is very concerning for me about you.  I do not know your address or any personal information, and I know that is appropriate, so I HOPE that this letter will get to you.

I am going to go see ‘Mandy’ Something at the family practice portion of the clinic.  She was the one I went to the last time I could not get in to see you.  She was kind and helpful.  I am glad that she is there – but she isn’t you.

I am so glad that you have been there for me, and my others who have very much appreciated you as well.  We all make mistakes, and I am totally included here, and I want you to know that if I have done something that has hurt you in any way – please know that I am sorry.  (Not saying you didn’t wanna come back to work because of me (smiley face) I just really respect you and want you to know that.)  Since we are all prone to make mistakes, and I am not saying that you need to read this, I want you to know that I accept you for who you are!  I forgive us both for mistakes that we may have made.  I know that you do your best and I do as well.  I hope that you can feel me here because you have been of infinite worth to me in the last few years that we have known each other.

I think that you and I are a ton alike.  We are both very sick.  We both cannot do all that we long to do.  I am unable to move a great deal of the time, and even when I can it is very limited.  I want so very badly to be a lot that I am not.  But, I wanna tell you that you are a lot that so many are not.  You love God with your whole heart! I have grown in my walk with the Lord because of our visits.  Your encouragement and love has grown in me a garden of faith and compassion for others like us.  I cannot show it as often as I would like, but YOU do mean a great deal to me.

Thank you for being attentive and listening to my complaints.  Thank you for helping me as you have been able.  Thank you for NEVER shaming me or guilting me in your office.  That is very sacred to me.

Please do not feel obligated to do the Polychondritis thing for/with me.  You got me started and I am thankful for that.  If and when you feel better and can come back, I would love to return to your office.  However, I am going to keep plugging along while I am able until your return – deal?

If you want, my information is included and you can contact me as you would wish.

Email : xxxxxxxxxxxxxxxxx

Phone: xxxxxxxxxxxxxxxxxxxxxxx

Address :



I know this isn’t your standard get well letter.  Then again, I am not your standard patient – and friend.
With all my heart I pray for you.  If you choose to not contact me that will be okay, I am very grateful for the time I did get to spend with you.

I pray that Jesus blesses you abundantly and that you have peace my dear Maria S…!



Not everything in this life makes sense.

The doctor ‘Mandy’ something was very kind, and a best friend of Maria, who was my doctor.  Upon hearing the news, after I cried and stuffs… I pulled the letter out of my purse and asked if this Mandy lady would make sure that Maria’s daughter would get it.  She smiled and said that she would.

So many things going on all the time … is that life?  Are there no breaks then?  Is there ever a moment of peace that is that?  A whole moment of peace?  Or is that more of an after life thought?  Is that why people say Rest In Peace?

I am broken – hearted because Maria is gone.  But I am also very happy for her as well.  She is with God now right?  It doesn’t get any better than that!

I don’t know if I have told you this, but if I have I am gonna tell you again okay?

I had an appointment with Maria this last Friday, so a week ago now.  I saw her around noon thirty.  She was not feeling well.  She had not attended work M-Th that week.  I walked into her office with a smile on my face and she had the best one she could muster on hers as well.  She had wanted to attend the small funeral thingy I had on the 18th of Oct, but had been unable to do so.  I brought her the full program.  I also had, at the funeral, a basket of star shaped pillows that played the song ‘Twinkle twinkle little star’ that guests were requested to take (with a greeting card) and give to someone they loved and whom they knew needed to know that they were loved.  So, I decided to give mine to Maria.  I filled out the card and handed the card and the Yellow star pillow to her last Friday.   She smiled at me.  “God told me to make sure I came to work today,” she said, “When I got here and saw your name on my schedule I knew why.”

The visit was a good one, and she was helping me as she was able.  I remember thinking how wonderful she was and how grateful I was that she listened to God and came to work, in spite of how awful she felt.  I was so happy to see her.  In my struggle to find answers, she was a kind person in a world of hurtful strangers.  I am most honored to have shared the same space with her.

Yesterday when I found out that she had passed I immediately recognized God’s hand in all of that.  Coincidence is man’s way of keeping God anonymous … I heard that somewhere and really agree.  But, God isn’t anonymous…and neither are His works.

I appreciate, love, and am so grateful for Maria.

Sweet dreams Maria!  God be with you till we meet again!

Relapsing Polychondritis

All information taken from and online source : 

Relapsing polychondritis (RP) is a severe, episodic, and progressive inflammatory condition involving cartilaginous structures, predominantly those of the ears, nose, and laryngotracheobronchial tree. Other affected structures may include the eyes, cardiovascular system, peripheral joints, skin, middle and inner ear, and central nervous system.

The array of possible presenting symptoms and the episodic nature of relapsing polychondritis may result in a significant delay in diagnosis. In addition, no laboratory findings are specific for relapsing polychondritis. A laboratory evaluation commensurate with the spectrum of reported symptoms is indicated to ascertain the presence of complicating conditions. The mainstay of treatment is systemic corticosteroid therapy.


The etiology of this rare disease is unknown; however, the pathogenesis is autoimmune. The evidence for an autoimmune etiology includes pathological findings of infiltrating T cells, the presence of antigen-antibody complexes in affected cartilage, cellular and humoral responses against collagen type II and other collagen antigens, and the observation that immunosuppressive regimens most often suppress the disease.[4]

Humoral response

The specificity of autoimmune injury to cartilaginous tissues has led investigators to test the hypothesis that a cartilage-specific autoantibody is central to the pathogenesis of relapsing polychondritis. Various studies find circulating antibodies to cartilage-specific collagen types II, IX, and XI to be present in 30%-70% of patients with relapsing polychondritis. Researchers have found that antibodies to type II collagen are present during acute relapsing polychondritis episodes and that the levels correlate with the severity of the episode.[5]

Treatment with prednisone is associated with a decrease in antibody titers. Antibodies to collagen types I, II, and III are believed to result from cartilage destruction; it has been proposed that antibodies are formed as a primary event in relapsing polychondritis.[5] However, anticollagen type II antibodies are not specific to relapsing polychondritis; they have been identified in other arthritides such asrheumatoid arthritis (RA). The epitope specificity of the antibodies in relapsing polychondritis differs from those in RA, suggesting different mechanisms for formation and pathophysiologic roles.

Autoantibodies to minor cartilage-specific collagens (ie, types IX and XI) have been described. They are more likely to be found in association with antibodies to type II collagen in patients with relapsing polychondritis. Furthermore, levels of antibodies to matrilin 1, an extracellular matrix protein predominantly expressed in tracheal cartilage, were significantly higher in patients with relapsing polychondritis, especially in those with respiratory symptoms, than in patients with Wegener granulomatosissystemic lupus erythematosus, or RA and in healthy controls.[6]

Most patients with relapsing polychondritis had high titers of antifetal cartilage antibodies during the early acute phase. The antifetal cartilage antibodies were found in 6 of 9 patients and only 4 (1.5%) of 260 patients with RA, exclusively in long-standing disease.[7] A report of relapsing polychondritis in the newborn of a mother with relapsing polychondritis suggests that antibodies crossing the placenta are necessary and sufficient to elicit the entire clinical syndrome.

Using proteomic surveillance to identify ubiquitous cellular proteins in patients with relapsing polychondritis, researchers identified 5 proteins that may be autoantigens. These include (1) tubulin-alpha ubiquitous/6, which, as a family, are main components in microtubules; (2) vimentin, an intermediate filament protein; (3) alpha-enolase; (4) calreticulin, a Ca2+ –binding chaperon indispensable for cardiac development; and (5) colligin-1/2. All but tubulin-alpha have been described as autoantigens in other autoimmune diseases (eg, RA, mixed connective-tissue diseaseBehçet disease). Although autoantibodies to tubulin-alpha have been reported in other autoimmune conditions, immunoglobulin G (IgG) antibodies to tubulin-alpha chains are rarely reported and may have diagnostic value in persons with relapsing polychondritis.[8]

Cellular response

Although an inflammatory infiltrate of lymphocytes and neutrophils is the dominant histopathologic feature of relapsing polychondritis, little attention has been paid to the possible role of cellular immune responses in this condition. The association of relapsing polychondritis with HLA-DR4 also suggests an autoimmune pathogenesis. Individuals with HLA-DR4 were found to have a relative risk of 2 for developing relapsing polychondritis. The studies suggest the role of genetic factors in determining risk for developing relapsing polychondritis.

An elegant double-transgenic mouse model provides further evidence that HLA associations are important in the development of relapsing polychondritis. The model demonstrated that more than one HLA class II molecule might be required for expression of susceptibility. The model suggests an important role for cell-mediated immune responses and provides a means for acquiring a detailed understanding of its pathogenesis.

Natural killer T (NKT) cells, lymphocytes discrete from other T, B, and natural killer cells, come in two varieties: CD4+ and CD4/CD8. Antigen-presenting cells present antigen to the NKT cells via the major histocompatibility complex–like molecule CD1d. NKT cells are decreased in number and function in several other autoimmune diseases, including multiple sclerosis, RA, systemic lupus erythematosus, systemic sclerosis, and type 1 diabetes mellitus.

Researchers have quantified CD4/CD8 and CD4+ V-alpha+ V-beta11+ NKT cells and found them decreased in patients with active or quiescent relapsing polychondritis compared with healthy controls. Analysis of the secreted cytokine profile and of binding of alpha-galactosylceramide–loaded CD1d to NKT cells suggests that CD4+ NKT cells play an important role in T1-helper responsiveness in patients with relapsing polychondritis.[9]

Serum levels of 17 cytokines from 22 patients with relapsing polychondritis experiencing a clinical flare were compared with those in age-matched controls. Three of the cytokines, interleukin 8, macrophage inflammatory protein 1-alpha, and monocyte chemoattractant protein-1, were found to be significantly elevated in patients with relapsing polychondritis. All 3 chemokines are proinflammatory and result in accumulation and activation of neutrophils, eosinophils, and monocytes/macrophages.[10]

Additionally, a group of researchers found T cells directed against collagen type II in one patient. A T-cell clone was identified and was found to be specific for a certain region of the collagen type II peptide. This research indicates that a T-cell response to collagen type II may play a role.[11]

Animal models

Mouse and rat models have been helpful in elucidating the autoimmune origin of relapsing polychondritis. Immunization of rats with native bovine type II collagen resulted in bilateral auricular chondritis, with histologic findings similar to the findings of human relapsing polychondritis in 12 of 88 (14%) rats. In addition, 8 of 12 rats developed arthritis. Severe auricular chondritis was accompanied by immunofluorescence positive for IgG and C3 in affected cartilage and by circulating IgG that was reactive against native bovine type II collagen.

Immunization of a different strain of rats with native chick type II collagen was associated with auricular chondritis, in addition to the intended collagen-induced arthritis. Biopsy studies showed that the few auricular lesions contained IgG and C3. Antibodies to native type II collagen were found in the sera of rats that developed auricular chondritis and in rats with collagen-induced arthritis.[12]

Although most data implicate cartilage collagens as the immunogens in relapsing polychondritis, immunization of rats with matrilin 1, a noncollagenous cartilage matrix protein, is associated with development of a clinical syndrome resembling relapsing polychondritis. The syndrome differed significantly from the collagen immunization disease model in that the trachea, nasal cartilages, and kidneys primarily were affected, and the joints and auricles were spared. Matrilin 1 is found in highest levels in the tracheal cartilage and in the nasal septum, likely explaining the observed clinical differences. Matrilin 1 is also found in adult auricular cartilage and costochondral cartilage and is absent in articular cartilage. The presence of both humoral and cellular responses to matrilin 1 has been detected in a patient with significant involvement of the auricular, nasal, and tracheobronchial cartilage and with little arthritis.[13]

The same investigators demonstrated a crucial role for B cells and C5 in the induction of relapsing polychondritis–like symptoms. Additionally, pathogenicity of matrilin 1–specific antibodies in their matrilin 1–induced relapsing polychondritis mouse model was recently recognized. The authors note that further investigation is needed into the role of B cells, complement, and cell-mediated immunity to better understand this complex disease.[13]

Recently, transgenic mice that expressed HLA-DQ6a8b developed spontaneous polychondritis in middle age. This condition is characterized by auricular and nasal chondritis with polyarthritis. As opposed to mice with collagen type II–induced polychondritis, mice with spontaneous polychondritis do not show the overwhelming collagen type II immune response and may serve as a better animal model of relapsing polychondritis.[14]

Other autoimmune disorders

The hypothesis of an autoimmune etiology for relapsing polychondritis is also supported by the high prevalence of other autoimmune disorders found in patients with relapsing polychondritis. McAdam et al reported that 25%-35% of patients with relapsing polychondritis had a concurrent autoimmune disease.[15]

Table. Autoimmune Conditions Reported in Patients With Relapsing Polychondritis(Open Table in a new window)

Disease Patients With Condition/Total Patients References
Systemic vasculitis 3 (5%) of 62 Zeuner et al[16]
11 (10%) of 112 Michet et al[17]
8 (12%) of 66 Trentham and Le[18]
28 (18%) of 159 McAdam et al[15]
50 (13%) of 399 Total
Cutaneous leukocytoclastic vasculitis 2 (33%) of 6 Priori et al[19]
6 (5%) of 112 Michet et al[17]
8 (7%) of 118 Total
Thyroid disease 8 (5%) of 159 McAdam et al[15]
10 (15%) of 66 Trentham and Le[18]
2 (33%) of 6 Priori et al[19]
4 (4%) of 112 Michet et al[17]
2 (3%) of 62 Zeuner et al[16]
26 (6%) of 405 Total
Rheumatoid arthritis* 8 (5%) of 159 McAdam et al[15]
3 (2%) of 180 Piette et al[20]
8 (7%) of 112 Michet et al[17]
7 (11%) of 62 Zeuner et al[16]
26 (5%) of 513 Total
Systemic lupus erythematosus† 2 (1%) of 159 McAdam et al[15]
9 (5%) of 180 Piette et al[20]
1 (17%) of 6 Priori et al[19]
6 (5%) of 112 Michet et al[17]
3 (5%) of 62 Zeuner et al[16]
21 (4%) of 519 Total
Sjögren syndrome (possible) 5 (3%) of 159 McAdam et al[15]
5 (5%) of 111 Piette et al[20]
10 (4%) of 270 Total
Ulcerative colitis 3 (2%) of 159 McAdam et al[15]
2 (3%) of 62 Zeuner et al[16]
5 (2%) of 221 Total
Crohn disease 2 (1%) of 180 Piette et al[20]
1 (2%) 62 Zeuner et al[16]
1 (100%) of 1 Haigh et al[21]
4 (2%) of 243 Total
Mixed connective-tissue disease 5 (3%) of 180 Piette et al[20]
2 (2%) of 112 Michet et al[17]
7 (2%) of 292 Total
Takayasu arteritis 3 (2%) of 180 Piette et al[20]
Mesenteric panniculitis 3 (2%) of 180 Piette et al[20]
Spondyloarthropathy 2 (1%) of 180 Piette et al[20]
3 (3%) of 112 Michet et al[17]
2 (3%) of 62 Zeuner et al[16]
7 (2%) of 354 Total
Diabetes mellitus 1 (2%) of 62 Zeuner et al[16]
3 (2%) of 159 McAdam et al[15]
4 (2%) of 221 Total
Reactive arthritis/psoriatic arthritis 2 (1%) of 159 McAdam et al[15]
1 (< 1%) of 112 Michet et al[17]
3 (1%) of 271 Total
Systemic sclerosis 2 (1%) of 159 McAdam et al[15]
Raynaud syndrome 2 (1%) of 159 McAdam et al[15]
Glomerulonephritis 2 (1%) of 159 McAdam et al[15]
Dysgammaglobulinemia 2 (1%)of 159 McAdam et al[15]
Pernicious anemia 1 (1%) of 159 McAdam et al[15]
Behçet disease* 1 (< 1%) of 112 Michet et al[17]
Psoriasis 2 (1%) of 180 Piette et al[20]
Lichen planus 2 (1%) of 180 Piette et al[20]
Primary biliary cirrhosis 1 (< 1%) of 112 Michet et al[17]
*Individual patients may carry more than one autoimmune diagnosis.

†Reported as 13 (20%) of 66 prevalence by Trentham and Le without division by disease

In addition, several reports have linked relapsing polychondritis with internal malignancy. It is thought to be paraneoplastic in these cases. The underlying malignancy is most often hematological in nature, but solid tumors have also been described.[22]



United States

In clinical reports and reviews, relapsing polychondritis is reported to be a rare disease. The annual incidence in Rochester, Minnesota, was noted to be 3.5 cases per million population.[23]


The 5-year survival rate associated with relapsing polychondritis has been reported to be 66-74% (45% if relapsing polychondritis occurs with systemic vasculitis), with a 10-year survival rate of 55%. In another report, a survival rate of 94% at 8 years has been reported.[18] However, these data may represent relapsing polychondritis in patients with less severe disease than patients studied in earlier reports.

The most frequent causes of death associated with relapsing polychondritis include infection secondary to corticosteroid treatment or respiratory compromise (10%-50% of deaths result from airway complications), systemic vasculitis, and malignancy unrelated to relapsing polychondritis.

Although the life expectancy in all patients with relapsing polychondritis is decreased compared with age- and sex-matched healthy individuals, patients with renal involvement have a significantly lower age-adjusted life expectancy. Of those with renal disease, uremia is the third most frequent cause of death.

Complications of relapsing polychondritis such as saddle-nose deformity (see Media File 9), systemic vasculitis, laryngotracheobronchial stricture, arthritis, and anemia in patients younger than 51 years portend a poorer prognosis than in age-matched patients with relapsing polychondritis without complications. Among patients older than 51 years, only anemia is associated with a poorer prognosis. Renal involvement is a poor prognostic factor at all ages.

Saddle-nose deformity. Courtesy of the University of Washington, Division of Dermatology.

Complications of relapsing polychondritis include vertigo, tinnitus, voice hoarseness, joint deformity, epiglottitis, scleritis, conjunctivitis, iritis, need for permanent tracheotomy (severe cases), severe pulmonary infection, blindness, frail chest wall, respiratory failure, aortic regurgitationmitral regurgitation, aortic dissection, and glomerulonephritis-associated renal failure.


Relapsing polychondritis is most common in whites. Although relapsing polychondritis has been found in persons of all races, little data are available for nonwhite persons.


Reviews from the 1970s and 1980s found that relapsing polychondritis has no sexual predilection. However, reviews in 1998 and 2002 suggested a slight female predominance.[24, 18] Saddle-nose deformity and subglottic stricture are more common in females.


Relapsing polychondritis may occur at any age; however, the disease usually has an onset during the fifth decade of life. No relationship exists between age of onset and sex.


The array of possible presenting symptoms and the episodic nature of relapsing polychondritis (RP) may result in a significant delay in diagnosis. In a review of 66 patients, the elapsed time from patient presentation for medical care for a related symptom to diagnosis was reported to be 2.9 years.[18] In fact, one third of patients with diagnosed relapsing polychondritis see 5 or more physicians before the correct diagnosis is made.

The affected systems and symptoms reported in patients with relapsing polychondritis before and after diagnosis include the following:

  • General – Intermittent fever, weight loss, and skin rash (see Physical)
  • Audiovestibular – Sudden ear pain (unilateral or bilateral), inability to sleep on affected side, floppy ear, suddenly diminished hearing, tinnitus (occasional or persistent), otitis media, ear drainage, vertigo (with or without nausea and vomiting), and unsteadiness (See the image below.)Floppy ear. Courtesy of the University of Washington, Division of Dermatology.
  • Musculoskeletal – Polyarthritis or monoarthritis, myalgias, back pain, rib pain, sternal pain, calf pain or claudication, and migratory or generalized arthralgias
  • Respiratory – Dyspnea, wheezing, cough, exercise intolerance, hoarseness, and recurrent infection
  • Gastrointestinal – Dysphagia
  • Nasal – Feeling of fullness across nasal bridge, saddle-shaped nose, mild epistaxis, and painful, red, and swollen nose
  • Ocular – Decreased visual acuity, conjunctivitis, episcleritis, scleritis, history of ocular inflammation, diplopia, and eyelid swelling
  • Cardiovascular – Chest pain, abdominal pain, history of pericarditis, abnormal heart rate or rhythm, syncope, and history of subacute myocardial infarction (found on ECG)
  • Central nervous system – Headache, ataxia, confusion, cranial nerve palsy, confusion, psychiatric signs, focal weakness/sensation changes, dementia, and seizures


Diagnostic criteria for relapsing polychondritis first were proposed by McAdam et al and have been modified several times. Perform biopsy only if clinical criteria are in question.

McAdam et al criteria (3 of 6 clinical features necessary for diagnosis)

  • Bilateral auricular chondritis
  • Nonerosive seronegative inflammatory polyarthritis
  • Nasal chondritis
  • Ocular inflammation
  • Respiratory tract chondritis
  • Audiovestibular damage

Damiani and Levine criteria (1 of 3 conditions necessary for diagnosis)

  • Three McAdam et al criteria
  • One McAdam et al criterion plus positive histology results
  • Two McAdam et al criteria plus therapeutic response to corticosteroid or dapsone therapy

Michet et al criteria (1 of 2 conditions necessary for diagnosis)

  • Proven inflammation in 2 of 3 of the auricular, nasal, or laryngotracheal cartilages
  • Proven inflammation in 1 of 3 of the auricular, nasal, or laryngotracheal cartilages plus 2 other signs including ocular inflammation, vestibular dysfunction, seronegative inflammatory arthritis, and hearing loss

Signs and symptoms of relapsing polychondritis include the following:

  • Auricular chondritis
    • Of patients with relapsing polychondritis, 85%-95% develop auricular chondritis.
    • Unilateral or bilateral auricular pain, swelling, and redness develop suddenly but spare the lobules. See the image below.Auricular edema and erythema sparing the lobule. Courtesy of Gregory J. Raugi, MD, PhD.
    • The pain and redness usually resolve within 2-4 weeks but may recur.
    • The ear cartilage softens and collapses forward. The external auditory canal can collapse after 1 or more episodes. See the images below.Forward listing ear. Courtesy of the University of Washington, Division of Dermatology.Bilateral inflammation and structural collapse of the auricles in a patient found to have aortic dissection. Courtesy of the University of Washington, Division of Dermatology.
    • Nodularity of the auricle may develop.
    • Calcification occurs in 40% of patients.
  • Nonerosive seronegative inflammatory polyarthritis
    • A seronegative nonnodular arthritis develops in 52%-85% of patients. The acute onset of an inflamed joint may mimic a crystal arthropathy.
    • Most commonly, the arthritis is asymmetric, oligoarticular or polyarticular, nondeforming, and nonerosive. One case of arthritis mutilans has been reported.[25]
    • The ankles, elbow, wrists, proximal interphalangeal joints, metacarpophalangeal joints, and metatarsophalangeal joints are often involved, although any joint may be affected.
    • The costochondral, sternoclavicular, and sternomanubrial joints may be involved.
    • The forefeet are usually spared.
    • Effusions may accompany arthritis and may be noninflammatory or mildly inflammatory.
  • Nasal chondritis
    • Nasal chondritis occurs in 48%-72% of patients with relapsing polychondritis.
    • The nasal chondritis is acute and painful and accompanied by a feeling of fullness over the nasal bridge.
    • Mild epistaxismay be present.
    • A saddle-nose deformity may develop in longstanding disease. See the image below.Saddle-nose deformity. Courtesy of the University of Washington, Division of Dermatology.
  • Ocular inflammation
    • Collagen types II, IX, and XI are found in the cornea and sclera. Autoantibodies to these collagens, which are found in patients with relapsing polychondritis, may be responsible for direct harm to the eyes.
    • Of patients with relapsing polychondritis, 50%-65% develop ocular sequelae related to episodic inflammation of the uveal tract, conjunctivae, sclerae, and/or corneas.
    • The most common conditions are episcleritis (39%) and scleritis (14%). See the image below.Unilateral episcleritis. Courtesy of Gregory J. Raugi, MD, PhD.
    • Eyelid edema, iritis, and retinopathy are found in 9% of patients, and 5% of patients have ocular muscle paresis or optic neuritis.
    • Peripheral ulcerative keratitisis found in 4% of patients and has been associated with perforation, endophthalmitis, and bilateral enucleation.
    • Papilledema, visual field defects, ptosis, lid retraction, proptosis, and cataracts may also be found on examination.
  • Respiratory tract chondritis
    • Respiratory tract involvement affects 40%-56% of patients with relapsing polychondritis and may involve any portion of the respiratory tree, including the distal bronchi.
    • Tenderness to palpation may occur over the anterior trachea or thyroid cartilage.
    • Chondritis weakens the tracheal cartilage rings, resulting in wheezing, dyspnea, cough, and hoarseness.
    • The upper airways can eventually become stenosed and are replaced by collapsible fibrotic tissue. Airways superior to the thoracic inlet collapse upon inspiration, and airways below the thoracic inlet collapse upon expiration; therefore, both inspiratory stridor and expiratory wheezing may be noted on auscultation.
    • Inflammation and swelling of the glottis, larynx, and subglottic tissues may require tracheostomy.
    • Acute inflammation of the distal airways can lead to obstruction and recurrent pneumonia.
  • Audiovestibular damage
    • Audiovestibular derangements are experienced by 46%-50% of patients, usually those with concomitant auricular chondritis.
    • Sudden loss of hearing is usually permanent, while tinnitus, nausea, vomiting, nystagmus, and vertigo may subside. In some patients, hearing loss is attributed to vasculitic damage to the eighth cranial nerve.
  • Cardiovascular disease
    • Relapsing polychondritis has been reported to affect the cardiovascular system in 24% of patients.
    • Aortic and mitral valve regurgitation, aortic aneurysm, aortitis, aortic thrombosis, pericarditis, first- to third-degree heart block, andmyocardial infarction, at times mediated through ostial stenosis of a coronary artery or arteries, have been reported.
    • Relapsing polychondritis aortitis exhibits inflammation in the media, resulting in loss of glycosaminoglycans and elastic tissue.
      • Any region of the aorta and more than one region simultaneously may be affected. In descending order of frequency, they include the ascending aorta, aortic ring, descending thoracic portion, and abdominal aorta, potentially existing silently rupture and death.
      • The most common clinical presentations include aortic arch syndrome, abdominal aortic aneurysm, and aortic regurgitation.
      • The clinical presentation of aortic regurgitation (resulting from ascending aorta involvement) may include left ventricular failure. Aortic regurgitation may result from damage to the aortic cusps or from annular dilatation due to destruction of supporting tissues.
    • Skin disease
      • Skin lesions are found in 17%-39% of patients with relapsing polychondritis.
      • Specific lesions are limited to erythema and edema overlying the inflamed cartilaginous structures. See the image below.Severe auricular edema and inflammation. Courtesy of the University of Washington, Division of Dermatology.
      • Various nonspecific skin lesions have been reported.
        • Aphthous ulcersare the most common.
        • Limb nodules, purpura, papules, sterile pustules, superficial phlebitis, livedo reticularis, limb ulceration, and distal necrosis have been reported.
        • Rarer findings include Sweet syndromeurticarial vasculitis, andKaposi sarcoma.
        • Some findings likely represent the skin manifestations of the many conditions associated with relapsing polychondritis rather than specific manifestations of relapsing polychondritis itself.
      • Cutaneous vasculitis: The prevalence of biopsy-proven cutaneous (small vessel) leukocytoclastic vasculitis is approximately 10%, while the prevalence of systemic (including skin) medium-to-large vessel vasculitis ranges from 11%-56%. It may appear as in its typical form of palpable purpura or as hemorrhagic bullae, typically on the lower extremities or other dependent areas.
      • Erythema elevatum diutinum: This has been described in 2 patients with relapsing polychondritis.[26, 27]
      • Cutaneous polyarteritis nodosa: A patient with relapsing polychondritis presented with relapsing painful red nodules from 1-3 cm in size, occurring on the entire skin and accompanied by arthralgias and myalgias.
      • Other cutaneous lesions reported in patients with relapsing polychondritis and vasculitis included the following:
        • Palpable purpura
        • Acute febrile neutrophilic dermatosis (Sweet syndrome)
        • Subcutaneous inflammatory nodules resembling erythema nodosum
        • Localized ulcerating neutrophilic conditions resembling pustules, furuncles, abscesses, and ulcerating abscesses
      • Panniculitis: This is characterized by 5- to 10-cm tender erythematous nodules showing septal and lobular inflammation.[28]
      • Other skin conditions: Isolated case reports of other cutaneous manifestations of relapsing polychondritis include the following:
        • Hyperpigmentation
        • Pustular psoriasis
        • Macular purpura of the palms, soles, lower limbs, and buttocks
        • Erythematous papular plaques of the face, upper and lower extremities, and thorax
        • Alopecia universalis
        • Actinic granulomas
        • Urticaria
        • Angioedema
        • Livedo reticularis
        • Erythema multiforme
      • Mouth and genital ulcers with inflamed cartilage (MAGIC syndrome): MAGIC syndrome is characterized by an overlap of relapsing polychondritis with Behçet disease. Firestein et al proposed this condition in 1985 in a report of 5 patients.[29] The two types of MAGIC syndrome are as follows:[30]
        • The more common type begins with the oral and genital ulcers of Behçet disease.
        • The second, less common, type is the polychondritis type, in which genital ulcers or erythema nodosum follows the initial presentation of oral ulcers and polychondritis.
      • Central nervous system
        • CNS manifestations of relapsing polychondritis are rare and can vary.
        • It is believed that vasculitis of the small and/or medium sized arteries is the underlying etiology.[31] Neurologic symptoms may present before other more frequent manifestations of relapsing polychondritis.
        • Patients may present with seizures, memory loss, delusions, limb weakness, paresthesias or gait disturbances, or other cerebellar symptoms.
        • Cranial nerve damage is common in relapsing polychondritis-associated CNS vasculitis and most often affects the second cranial nerve, followed less commonly by the sixth, seventh, and eighth cranial nerves.
        • Limbic encephalitis has been reported associated with relapsing polychondritis.[32, 33]
        • Aseptic meningitishas been reported infrequently in relapsing polychondritis.[34]
        • Clinical neurologic assessment is an important aspect of the physical examination of patients with relapsing polychondritis.
      • Renal
        • From 1943-1980, 129 patients with relapsing polychondritis were seen at the Mayo Clinic, of whom 29 (22%) had evidence of glomerulonephritis based on a diagnostic renal biopsy or the presence of microhematuria and proteinuria.[35]
        • Patients with renal damage are older and more likely to have extrarenal vasculitis and arthritis.
        • A proposed mechanism in the pathogenesis of renal involvement in relapsing polychondritis derives from the deposition of immune complexes leading to glomerular damage.[35]
        • Pathological biopsy findings include segmental necrotizing glomerulonephritis with or without crescents, interstitial lymphocytic infiltrates, interstitial fibrosis, active tubulitis, and glomerulosclerosis.
        • The response to treatment varies from stabilization of renal function to renal failure.
      • Other conditions
        • Relapsing polychondritis has been seen in patients with underlyingmyelodysplastic syndromeand, less often, lymphoma. These cases may be paraneoplastic in nature.
        • Acute mastitis may be found in relapsing polychondritis.[21]
        • Thromboembolism has been reported.


The cause of relapsing polychondritis is not known. Familial clustering has not been observed. Susceptibility for developing relapsing polychondritis is increased slightly by the HLA-DR4 haplotype.

Three intriguing case reports suggest that hormonal influences may be important in relapsing polychondritis. Two men have developed relapsing polychondritis after receiving injections of luteinizing hormone-releasing hormone, and a woman with arthritis mutilans had a sudden exacerbation of her condition and new onset of atrophy of the auricular cartilage, nasal septum, weight loss, and deafness after receiving an injection of chorionic gonadotropin.[36]

Differential Diagnoses

Laboratory Studies

No laboratory findings are specific for relapsing polychondritis (RP). Anemia, if present, is typically normochromic and normocytic and is associated with a poor prognosis. Nonspecific indicators of inflammation (eg, elevated erythrocyte sedimentation rate, elevated levels of C-reactive protein) are often present. Mild leukocytosis may be detected.

Because relapsing polychondritis is associated with many multisystemic diseases, a laboratory evaluation commensurate with the spectrum of reported symptoms is indicated to ascertain the presence of complicating conditions.

Use antinuclear antibody reflexive panel, rheumatoid factor, and antiphospholipid antibodies (if history of thrombosis is found) to evaluate for other autoimmune connective-tissue diseases.

For a vasculitis workup, perform a CBC count with differential; metabolic panel; creatinine, liver transaminase, and serum alkaline phosphatase studies; urinalysis dipstick and microscopic evaluation of sediment; cryoglobulins; viral hepatitis panel; antinuclear antibody (ANA); and antineutrophil cytoplasmic antibody (ANCA) tests.

Use the purified protein derivative test to evaluate for exposure to tuberculosis. (Tuberculosis is often overlooked as an infectious cause of perichondritis.)

Use serologic tests for syphilis if it is suspected, including rapid plasma reagent or VDRL testing. Saddle-nose deformity is a clinical manifestation of congenital syphilis and can go undiagnosed into adulthood; however, it can also be a consequence of gumma formation in adulthood.

Cultures may be indicated, depending on the clinical presentation, as follows:

  • Sputum cultures for bacteria and acid-fast bacilli may be needed in patients with respiratory symptoms.
  • Bacterial, acid-fast bacilli, and fungal cultures may be appropriate for cartilage biopsy samples, especially from the respiratory tree.
  • Blood cultures may be useful in the assessment of febrile episodes that are combined with nausea, vertigo, and/or muscle weakness.
  • Bacterial and viral cultures of the cerebrospinal fluid may be indicated to exclude meningitis or to help exclude aseptic meningitis or CNS vasculitis.

Imaging Results

Chest radiography (posteroanterior [PA] and lateral views)

Tracheal stenosis may be observed on plain radiographs. See the image below.

Tracheal stenosis on chest x-ray film. Courtesy of Julie E. Takasugi, MD.

Calcification of cartilaginous structures supports the diagnosis of relapsing polychondritis.

Coexisting systemic vasculitis may be suggested by the presence of pulmonary parenchymal infiltrates.

Spiral CT scanning (without contrast)

Spiral CT scanning (without contrast), from the superior trachea to the lower lobe bronchi, is advised in patients with relapsing polychondritis and respiratory symptoms.

Spiral CT scanning is a noninvasive test that readily identifies tracheal and bronchial thickening, stenosis, and calcification. Smooth anterior and lateral wall thickening with sparing of the posterior wall of the trachea and mainstem bronchi is virtually pathognomonic for relapsing polychondritis.

High-resolution CT scanning can reveal air trapping and diffuse or focal thickening of the airways. Expiratory CT scanning can be used to evaluate for air trapping and malacia of the airways. A series of 18 patients with relapsing polychondritis and pulmonary symptoms revealed that 94% had airway malacia and air trapping on dynamic expiratory CT scans.[37] The authors suggest that this modality should be used in all patients with relapsing polychondritis to allow for early detection of airway compromise. However, they did not provide the duration of disease in the study population, nor did they correlate the findings with those of pulmonary function tests. The benefit of dynamic expiratory CT scanning is unproven but may provide more information in difficult cases.

CT scanning results correlate well with pulmonary function tests, identifying obstructive patterns. CT scanning is not only safer but is also more sensitive and specific than bronchoscopy.


Yamashita et al reported on the use of of fluorodeoxyglucose (FDG)-PET/CT for the diagnosis of relapsing polychondritis and evaluation of disease activity. According to the authors, FDG-PET/CT is a potentially powerful tool for the early diagnosis of RPC, especially in patients without easily biopsied organ involvement, and facilitates evaluation of disease extent and disease activity during treatment. Typical FDG accumulation was noted in the following sites in the 13 patients studied[38] :

  • Tracheobronchial tree (nine patients)
  • Costal cartilage (five)
  • Joints (five)
  • Larynx (four)
  • Nasal cavity/paranasal sinuses (three)
  • Auricles (three)
  • Lymph nodes (three)
  • Aorta (one)


MRI has been a useful adjunct in the clinical diagnosis of relapsing polychondritis. MRI is better able to distinguish between edema, fibrosis, and inflammation than is CT scanning.

T1-weighted images, T2-weighted images, and T1-weighted images with gadolinium contrast provide characterization of relapsing polychondritis-related changes in cartilaginous tissues.

MRI also reveals thickening of the thoracic aorta before dilatation occurs.

MRI may be useful for monitoring the effects of treatment.

Posteroanterior and lateral dye contrast pharyngotracheogram

PA and lateral dye contrast pharyngotracheogram may be helpful if tracheal narrowing or edema is suggested.

Both PA and lateral views are required to avoid underestimating the severity of stenosis or swelling.


Scintigraphy may prove helpful for identifying potential sites for biopsy to aid the histologic diagnosis when the clinical diagnosis is in doubt (ie, because of unfulfilled diagnostic criteria).

Technetium-99m methylene diphosphonate bone scintigraphy has been used in the evaluation of chest pain, allowing identification of possible sites for biopsy in costochondral tissues.

Gallium-67 citrate scintigraphy has also been found to show increased uptake in affected areas.

Other Tests

Pulmonary function testing (PFT) with flow-volume loops is strongly recommended in patients who present with respiratory symptoms, since PFT may assist in the differential diagnoses and provide information about severity of the disease. This may also be used to monitor patients’ disease activity. PFT in patients with relapsing polychondritis who have respiratory involvement demonstrates a nonreversible obstructive pattern with collapse and stenosis of the airways. The decrease in forced expiratory volume in 1 second correlates with the degree of dyspnea.

Perform ECG to assess patients with relapsing polychondritis who demonstrate signs of vasculitis. Also, perform ECG to monitor these patients, since they may incur silent ischemia if vasculitis has developed.

An echocardiogram may be needed to assess aortic root dilatation and degree of aortic regurgitation.


Intubation may be dangerous and futile.

Tracheostomy is usually the best method for providing an airway in patients with relapsing polychondritis in acute respiratory distress (because of the high likelihood of tracheal or bronchial stenosis or edema).

Biopsy of the cartilage is a potential source of infection and cosmetic damage. Perform biopsy on cartilage only if histopathological data are required to meet the diagnostic criteria for relapsing polychondritis.

Biopsy of skin lesions (nonadjacent to cartilage) may provide useful adjunctive information.

Histologic Findings

Biopsy of cartilage in patients with relapsing polychondritis demonstrates chondrolysis, chondritis, and perichondritis. The cartilage loses its basophilia, probably by release of sulfated proteoglycans from the matrix, and the chondrocytes are decreased in number and may appear pyknotic. Early relapsing polychondritis is characterized by a mixed inflammatory infiltrate of lymphocytes, neutrophils, and plasma cells in the perichondrium. As the cartilage degenerates, mononuclear cells and macrophages infiltrate the matrix. The cartilage matrix is eventually destroyed and replaced by fibrous connective tissue. Despite the presence of clinical erythema, overlying skin is normal.

Distant lesions with the clinical appearance of vasculitis have histologic features consistent with the clinical syndrome, including leukocytoclastic or granulomatous vascular injury.


No controlled trials of therapy for relapsing polychondritis (RP) have been published. The goal of treatment is to abate current symptoms and to preserve the integrity of cartilaginous structures.

The mainstay of treatment is systemic corticosteroid therapy. Prednisone (20-60 mg/d) is administered in the acute phase and is tapered to 5-25 mg/d for maintenance. Severe flares may require 80-100 mg/d. Most patients require a low daily dose of prednisone for maintenance; however, intermittent administration of high doses during only flares of the condition is successful in rare cases. McAdam et al found that continuous prednisone decreased the severity, frequency, and duration of relapses.[15] See the images below.

Same patient as in Image 5 after 4-6 weeks of steroid treatment. Note resolution of auricular inflammation with nodularity and forward listing of the ears. Courtesy of the University of Washington, Division of Dermatology.Close-up view of same patient as in Image 6. Forward flopping of ear with nodularity after steroid treatment. Courtesy of the University of Washington, Division of Dermatology.

Other medications reported to control symptoms and, perhaps, progression of the disease, include dapsone (25-200 mg/d), azathioprine, methotrexate (MTX; 7.5-22.5 mg/wk), cyclophosphamide, and cyclosporin A. MTX has been administered beginning at 7.5 mg/wk, increasing up to 22.5 mg/wk in conjunction with steroid administration and has been found to significantly decrease corticosteroid requirements while controlling symptoms.

Case reports have described successful treatment with anti–tumor necrosis factor-alpha inhibitors infliximab, etanercept, and adalimumab. Anakinra, an interleukin 1 receptor antagonist; leflunomide, which inhibits pyrimidine synthesis; and rituximab, an anti-CD20 chimeric antibody, have also shown benefit.[39, 40, 41, 42, 43]

Oral administration of nonsteroidal anti-inflammatory drugs (NSAIDs) has not been effective.

Medical care must include assessment for and treatment of other confounding or concurrent autoimmune disorders.

Surgical Care

Surgeries encountered in the care of patients with relapsing polychondritis may include tracheostomy, permanent tracheotomy placement, tracheal stent placement, aortic aneurysm repair, cardiac valve replacement, and saddle-nose deformity repair. The benefits of any proposed surgery must be weighed adequately against the patient’s risk for infection, especially in the event of acute relapse, since patients are at an increased risk of infection whether or not they are using corticosteroids.

Additionally, patients with relapsing polychondritis and tracheal disease may be at particular risk regarding complications resulting from tracheal intubation and extubation.


Relapsing polychondritis is a complex condition that requires a team approach for patient care.

Dermatologists or specialists in infectious diseases are often involved early in the course of the disease to evaluate the patient for infectious causes of cellulitis or perichondritis.

Rheumatologists usually become the primary care provider and should be involved early in patient care.

Ophthalmologists should also be involved early to diagnose, monitor, and treat the potentially devastating ocular complications.

Cardiologists, neurologists, nephrologists, and otolaryngologists may be asked to manage other aspects of relapsing polychondritis.

Plastic surgeons can aid in nasal reconstruction if saddle-nose deformity is present.

Medication Summary

Prednisone is the drug of choice for relapsing polychondritis (RP) and is used in acute flares and for long-term suppression of inflammation. Continuous treatment with prednisone decreases severity, duration, and frequency of relapses.

In patients who require higher maintenance doses of prednisone, methotrexate (MTX) is often administered as an adjuvant treatment. MTX is used with prednisone to reduce the overall steroid requirement for disease control; however, some patients may eventually be maintained with MTX alone. Dapsone has been beneficial in some patients with mild relapsing polychondritis, although more current clinical experience has found dapsone to be less useful.


Class Summary

These agents are the mainstay of therapy. They have anti-inflammatory properties and cause profound and varied metabolic effects. In addition, these agents modify the body’s immune response to diverse stimuli.

View full drug information

Prednisone (Deltasone, Orasone, Meticorten)

McAdam et al found that continuous use of prednisone decreased severity, frequency, and duration of relapses. Some patients may use reduced prednisone doses or remain steroid free with use of MTX.

For the acute phase, administer 20-60 mg/d and taper to 5-25 mg/d for maintenance. Severe flares may require 80-100 mg/d. Most patients require low daily dose for maintenance; however, rarely, some patients can be treated successfully by intermittent administration of high doses during flares of the condition. In acute airway obstruction, IV pulse steroids are necessary.

Disease-modifying antirheumatic agents

Class Summary

These agents inhibit cell growth and proliferation.

View full drug information

Methotrexate (Folex, Rheumatrex)

Unknown mechanism of action in treatment of inflammatory reactions; may affect immune function. Ameliorates symptoms of inflammation (eg, pain, swelling, stiffness).

Effective steroid-sparing treatment for relapsing polychondritis. Adjust dose gradually to attain satisfactory response.

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Anakinra (Kineret)

Recombinant interleukin 1 receptor antagonist expressed from Escherichia coli.Natural interleukin 1 receptor antagonist produced by macrophages/activated monocytes blocking effects of interleukin 1.

Monoclonal antibodies – Antitumor necrosis factor-alpha inhibitors

Class Summary

These agents inhibit action of TNF-alpha, an inflammatory cytokine implicated for its contribution to rheumatic disease and cancer cachexia. Use described only in case reports.

View full drug information

Infliximab (Remicade)

Chimeric human-murine IgG1-kappa monoclonal antibody that binds to TNF-alpha. Binds both soluble and transmembrane forms and inhibits its binding to its receptors. Cells with transmembrane TNF-alpha bound to infliximab appear to be lysed with complement.

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Etanercept (Enbrel)

Soluble, dimeric recombinant TNF receptor fused to the Fc fragment of human IgG1. This binds to TNF and inhibits its activities.

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Adalimumab (HUMIRA)

Recombinant fully-human IgG1 anti-tumor necrosis factor monoclonal antibody. It binds to TNF-alpha and reduces it ability to effect its biological activities.

Anti-CD20 antigen on B lymphocytes

Class Summary

CD20 is a B-lymphocyte antigen that regulates cell cycle initiation. Use described in one case report.

View full drug information

Rituximab (Rituxan)

Murine/Human chimeric anti-CD20 monoclonal antibody. CD20 is expressed early in pre-B cell development. Binding induces complement-dependent B-cell cytotoxicity along with antibody-dependent cellular toxicity.

Interleukin-1 receptor antagonists

Class Summary

These agents have anti-inflammatory characteristics.

View full drug information

Leflunomide (Arava)

Isoxazole immunomodulatory agent with anti-inflammatory characteristics. Mechanism of action is through the inhibition of dihydroorotate dehydrogenase, which leads to a decrease in proliferative activity.

Although not entirely elucidated, it is thought to inhibit de novo pyrimidine synthesis. It inhibits proliferation of immune cells.


Complications of relapsing polychondritis (RP) include vertigo, tinnitus, voice hoarseness, joint deformity, epiglottitis, scleritis, conjunctivitis, iritis, need for permanent tracheotomy (severe cases), severe pulmonary infection, blindness, frail chest wall, respiratory failure, aortic regurgitation, mitral regurgitation, aortic dissection, and glomerulonephritis-associated renal failure.


In earlier studies, the 5-year survival rate associated with relapsing polychondritis was reported to be 66%-74% (45% if relapsing polychondritis occurs with systemic vasculitis), with a 10-year survival rate of 55%. More recently, Trentham and Le found a survival rate of 94% at 8 years.[18] However, these data may represent relapsing polychondritis in patients with less severe disease than patients studied in earlier reports.

The most common causes of relapsing polychondritis–related death include infection secondary to corticosteroid treatment or respiratory compromise (10-50% of deaths result from airway complications), systemic vasculitis, and malignancy unrelated to relapsing polychondritis.

Complications of relapsing polychondritis such as saddle-nose deformity, systemic vasculitis, laryngotracheobronchial stricture, arthritis, and anemia in patients younger than 51 years portend a poorer prognosis than in age-matched patients with relapsing polychondritis without complications. Among patients older than 51 years, only anemia is associated with a poorer prognosis. Renal involvement is a poor prognostic factor at all ages.

Being Better…

If you don’t understand where I am coming from, that is okay!

You don’t have to.

You are right about my public stance on your religion.  But, let me be a little less vague for you right now. I do not believe ANY religion will save ANY one.  If you are of the opinion that I post anything flippantly then you are wrong.  I think about everything I post.  I am not trying to offend people.  I am trying to create conversation.  My aim is to talk to someone, anyone, who can have a conversation with me.  I want to learn about their perspectives.  I want to ask them intriguing questions.  I want to hear how they came to the conclusions they came to.

Why do you think I talk to you?

Why do I ask you the questions that I ask you?

I am not trying to convert you to my way of thinking! Nor, am I trying to change who you are!  I love you for the you that I know.  If I were in Rome, I might be more public about my disliking of the Catholic church.  My circumstances are such that I know the ins and outs of the your church.  Just because I post an article that is not pleasing to you does not mean that I am against you.  We do not have to agree on everything to be friends.  You can be angry at me and that is fine.  I can be angry with you, and that is also fine.  Not ideal, but eh, life isn’t ideal all the time right?

You said that you liked smart people, but you call yourself dumb.  You said that you love the your faith, and yet you are not ‘active.’  You want to be around people and still you push them away.  These contradictions are compelling and confusing – and perhaps this makes me really strange, but I just want to ask you more questions, and understand you better.  I Love that we are different!  And I love that we are very much alike.  So, it is okay with me that you are angry at me.  Go ahead and be that way.  It does not make me hate you.  I don’t think I could ever hate you.

You may think that I believe everything I read.  I don’t.  You might think I believe if I found it on the internet then it must be true. I don’t.  You can forget what I have said and say that I have not told you specifically anything pertaining to why I dislike your church.  Not true, but you can.  You have not asked specific questions.  Instead, you have a cheeky insinuation  – a veiled insult – in your vague sincerity.

  • So you have studied solely stuff against my church because of what happened to you regarding this church and the people you know in it so that makes it all true not just an opinion? And studying that stuff makes it true? –

Studying and learning about whatever it is does not make it true.  Painting a picture of what you believe does not make it true.  Following someone’s advice because you believe in the person, does not make it good advice.  I Never said that any of this made anything truth.

  • I didn’t just read about it and dismiss it or believe it based on my limited knowledge

You are assuming that my knowledge is limited in this. You think, and correct me if I am wrong here, that I just read stuff from some random person and believe it without testing it out, without seeing how it applies, without experiencing it for myself RIGHT?

The things that I know nothing about, and only have academic knowledge about, while fascinating to me, are not things that I am passionate about.  Why do you think I post so emphatically about your church?  You think I do not have experiential knowledge as well as academic?  What is it that you are so mad at here?  What specifics do you want?

I have never kissed anyone on purpose I have only speculative perception on that one.  However, if you think that I am going to go around kissing everyone to get the experience that many others have – that is gross and a huge “HELL NO!” from me.  I could whore myself out to get ‘real-life’ experience but what good would that do anyone?  On that subject, you would be correct in thinking that my knowledge there is limited.

You might also be wondering if I am trying to get back, in some way, at people who didn’t help me when I needed help, huh?  Also not true. I want more than anything to help them, especially them!

What do you want from me?

If I call ya – you don’t answer nor do you usually call me back. If I text you. You don’t answer.  I email you, you don’t read them.  When you do, we don’t talk about it very much.  You don’t ask me specifics.  You say that if I want you to know I will tell you.  That sucks, by the way.  I denounce it with a great big AHHHHHHHHHHH!!!!  If you wanna know, then ask it. I do not tell you the bulk of things because I do not want to break you!  You are the only one who can tell me what you can handle and what you cannot handle.  I CANNOT decide that for you, and I won’t!  It might surprise you but I care and I have nothing to hide.  I am open about my fears, my excitements, my curiosities, and now a more recent development, my anger.  What more do you want?

I have not lied to you.  When I said that I loved you, I meant it.  Sorry if I have been overbearing.  You told me that some have a difficult time with you because you are intense.  When I agreed with you about that, it may have been confirming some fear that you have had.  You did not question me about it though.  I have thought about it a few times since then.  I was giving you a compliment there, and I am pretty sure you did not take it in that manner.  I too am intense.  Read anything I write, all of them have a level of intensity that is a bit above the norm.  I am ill much of the time now, and so I spend what energy I can being and doing things on purpose.  Doing things in this way require passion and YES some level of intensity.

I have never really had a guy in my life that was like you.  This is my first time trusting a dude like I trust you… and I am fucking it up I know all the time, but I am not gonna quit or give up – unless you ask me to.  The only way I know that I am fucking up and can do better, is if you help me out there.  The excuse that you are ‘just a guy’ doesn’t hold shit!  That would be like me saying another flippant thing just to avoid whatever the truth is… come on man! You are brilliant!  You are sweet, kind, honest and passionate about a lot of things…. We can do better each of us… I want to!

Do you?


This might sound petty, but I woke up with this seemingly insignificant memory.  I hope you don’t mind if I share it with you.

One Friday afternoon I went over to a friend’s house to play.  Her family was much better off financially than mine was.  Though they never said these actual words, my respective parental figures despised them.  This particular afternoon my friend’s mother came home from work early, and brought home some super yummy stuff for dinner.  Salad with all kinds of yummy and healthy toppings!  She asked me if I could stay for dinner, so I called home and asked them if I could.  They were so petty and rude to me on the phone.  I knew that meant when I got home, I was gonna get it.  I asked them what we were gonna have for dinner and they said something like this – Oh I don’t know, probably just some reheated yellow death or something.  (yellow death was our verbiage for Mac n’ cheese.)

Then they went on to tell me how they were grateful for having it, and how ungrateful I was for thinking that people liked me, or wanted me around.  They said that, if anything, they felt sorry for me.  They saw how fat I was and got me salad so I would not eat all of the food at our house, so that someone else might get something to fill their tummies as well.  Then they told me that I had to stay there and eat the salad and hung up the phone.

I was crying when I got off the phone.  But, I didn’t want to have to say why, because I knew that would cause more problems… so I slid my wrist hard against a sharp corner, and scratched it a bit.  Then blamed that for my tears.

The dinner was fantastic!  My friend and her mom were kind, and could speak freely…wo, it was awesome!

Let me take a break in this story for a sec and tell you this.  I loved pizza.  Pizza was my favorite food of all time!  Pineapple and green olives (i know it’s weird) was my absolute most cherished and treasured choice! “They” were very aware of this fact.

When I got home, there were no dishes in the sink. (very rare, since I was the one who usually had to clean up the kitchen etc)  There was a pile of napkins from a pizza store on the table, and one in the middle of the floor right in front of the outside door.  I bent down to pick it up, on it was a bit of sauce, a small piece of pineapple, and two finely cut green olive pieces.  For them to spend money out of the goodness of their heart was rare.  I was broken hearted over this.  I feel so dumb for still being sad about it.

I went outside to toss all the napkins and there were no pizza boxes.  I searched the whole house, yard, and vehicles.

No boxes.  In my head, that meant that they went out of their way, to acquire the napkins and put the stuff they KNEW I loved on it, and left it right where i would find it.  The rest of the night they were grinning at me from ear to ear teasing me and passive aggressively shoving it in my face that I didn’t ‘get to eat their special dinner.’

They did it to teach me a lesson of some sort.

I did learn something – it wasn’t that they are good and I am bad like they wanted.

I learned that some people will push you down simply because they can.  There is no age limit.  This is not limited by race, sex or creed.  There are people who profess to love you who will cut you every chance they get.  I did and still do feel sad about this but their actions, right or wrong, do not make ME bad.

So I gotta pray for them and not because someone said to either!  I know with the passion that they used against me, if they were for God, that same passion could be turned into a fine tool of goodness.  So, I will hope and pray for that.  It does not make this memory any less valid by not taking on some act of revenge, at least not to me.  It is distressing and one of the ‘lighter’ ones I must say.

Some say that we cannot know the sweet without tasting the sour.  Some say that everything we do is a choice.  I am not quite sure where my opinion lies on both of them but while I can I will choose, for them, to pray.