[aside]I dont mind posting the names of 5 MDs, none of whom were helpful. Dr Wones, Dr. Zubritsky, Dr. Carter, and Dr. S…(from the middle east) cant remember his name, and the pathologist Dr. Mutasim.  None knew anything about this disease, nor were helpful in any way, in fact Dr. S was downright derogatory, showing complete ignorance about how great the impact of environmental stimuli can be on diseases in general…that is pretty much an old-school mentality, maybe some “updated” information would benefit his overall knowledge of diseases. One sent me a link to a website about lichen planus which only had the most superficial information, totally useless. I guess he thought he was being helpful.

BTW i think that i have had the tendency for lichen planus for many years so what caused the explosion of lesions is really what I want to know.

Several kinds of hypersensitivity have been described (more will likely be found). TYPES I to IV.

TYPE I -Immediate hypersensitivity happens fast. CD4 T (thymic lymphocyt) cells are involved in adaptive immunity (to pathogens), autoimmunity, asthma, allergic and tumor immunity. Naive CD4 T cells may differentiate into one of several lineages of thymocyte helper cells, (Th1, Th2, Th17, iTreg – about which I know nothing). After the first exposure to the allergen, the CD4 T cells are “sensitized” and immediately effect a response by releasing antibodies (immunoglobulin E (IgE))  which signal mast cells and basophils (with high affinity IgE receptors on their cell membranes and loaded to the hilt with storage granules) to dump out vasoactive amines, e.g. histamine. These chemicals then affect surrounding cells, mainly causing blood vessel dilation and muscle contraction, and cause the inflammation by increasing the permeability of the capillaries to white blood cells and some proteins (thus redness swelling and itching).  Histamine (one of the vasoactive amines) is a cute little molecule (right)(thankUwikipedia). Basophils (left) and eosinophils (center) are cute too (I vectorized two transmission electron micrographs here).

Delayed hypersensitivity is just that, delayed onset. Appearing several hours, days or continuing to appear a week or so after contact with the antigen and depending upon the dose of the antigen. For example poison ivy appearance (at least in my case) comes up between 2 days and a week after exposure, sometimes showing the secondary contact point of the original molecules of urushiol being where two skin surfaces meet..the original spot depositing a lesser amount of urushiol at the point of contact.  While i have never read about it, I do believe there can be systemic poison ivy, for instance when the neighbor weed-wacks their yard full of poison ivy and the droplets of urushiol are aerosolized and breathed.  Would be fun to search that route of exposure (in the literature, not as a test subject).

Delayed hypersensitivity is not antibody dependent, but is a cell-mediated response.

I am going to document what I am thinking about while keeping my hands off the itchy places (not so LOL) to try to figure out what environmental+immune conjunction caused this to surface in my otherwise really healthy 74 year old body.

I don’t know if it will help anyone else in the search for cause, but hopefully it will, and it will allow me do write a history of my own experience (noting everthing I can remember and blaming no one and no thing or even being disparaging..well except maybe a little to the MDs that we depend upon to help us through diseases..and who (in my case) did “not much”. Ha Ha.

I am also going to encourage anyone out there to write a similar history, and though I don’t take comments on this website because so many unscrupulous individuals want to spam and skim and link for their own advantage instead of participating in meaningful discussion. My email can be discovered from the very first entry on this blog, way back when!!, and from one of those websites you can contact me if you want to contribute a long history. My goal is to treat this exactly like a manuscript, and submit it at some point to a scientific journal.

Starting at the beginning (not the beginning of my life obviously, that was 1943) but of contact dermatitis which happened to the best of my recollection in 1968 or 1969, a new time resident of cincinnati, and during a frisby throwing game in burnet woods.  If you are from cincinnati you know burnet woods is a primitive wooded area, small, more a park with a small lake and lots and lots of poison ivy.  I didn’t really know what poison ivy looked like, but in my leather sandals (imported) apparently I ground some poison ivy oil and got a really bad case of it from that afternoon.  I mention it because of the inflammatory process of the poison ivy itself, but back then, leather, and imported leather was tanned with some pretty harsh chemicals, including chromium.  Every time (which was probably one or two more times) I wore the sandals i re-got poison ivy.  Chromium is the key word. Urushiol is the next key word as it is the oil in poison ivy that causes the allergic dermatitis. HERE is a lay website for some important information. A host of things can cause allergic dermatitis; food, cosmetics, metals (i could never wear stainless, nickel plated or silver earrings) and it also can be caused by paints and mortars and cement and grout.

That the exposure on my feet was to 1) several unknown tanning compounds, 2)as well as the urushiol (which causes a T-lymphocyte response), what appears to me to be a really good combination for an adjuvant effect, causing an senhanced response.

I did get poison ivy pretty seriously in 1975, but to my knowledge there was no other environmental exposure at that time. (except possibly, chromium in silk screen paint which i used a lot of (and probably still have some in my basement… SKRINK brand)..greens and blues.  Direct contact of Cr(VI) compounds with intact skin can induce chromium dermatitis or sensitization. and a government document on chromium toxicity.
So chromium has been a part of my life for a long time, though maybe not in a good way.

Fast forward many years, to “fun with polymer clay” when in the 1980s i used lots of FIMO, and likely all colors, though I cannot distinctly remember which colors i used most, but very definitely there was blue, and likely green.  I used enough of that early FIMO to produce a contact dermatitis in the palms of my hands, little bumps, not terribly itchy that i can remember, but enough to make me “wake up” and know that polymer clay in that formulation was a contact allergen for me.  And fast forward another 30 years and it is back to polymer clay again, not too careful this trip around, but no contact dermatitis on my hands (the clay does stick to hands…. especially with some pigments,  black clay and red polymer clay are particularly noticeable, but I don’t doubt for a second that they all stick.

The take home message is that we do get exposures…to many things…. not all of which our bodies treat as benign.