This short research article is a worthwhile read because it implicates mast cells in nearly all autoimmune diseases of the skin and mucosa. I believe my MC is the same disease as my skin rash, just in a different location. Of course now I know I need to protect my lungs from being the next target of the attack. I understand there is great risk of interstitial lung disease if I don't get treatment.
That said, can anyone glean anything from this article that might suggest next steps for me? Remind me, where can I find a mast-cell expert doctor in the DC area? Are they usually immonologists, rhuematologists, or something else? I'll check the Mastocytosis organization website.
Would mast-cell stabilizing creams and antihistamines be enough to slow or stop this process or do I need more heavy-duty systemic treatments aimed at the mast cells? What would those be?
Here is an excerpt from the article. Seems Tex was right all along...
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2946445/
Now I'm wondering whether the rash of DM is/should be considered a form of Cuteneous Mastocytosis?New Roles for Mast Cells in Autoimmunity
Mast cells, which do not usually circulate in the blood but acquire their phenotype in the tissues where they reside, are central mediators of a wide variety of stimuli. Shrestha and colleagues (10) are the first to directly implicatemast cells in the pathogenesis of human DM skin disease, although mast cells have been reported as a prominent infiltrating cell of the skin lesions of dogs with DM (19). Increased numbers of mast cells have been reported in polymyositis patients in the muscle tissue, particularlyin areas of necrosis and regeneration (20)and as part of the interstitial inflammatory infiltrate (21), although an increased number of mast cells was not found to be present in juvenile DM muscle biopsies (10).
Over the past decade an expanded role for mast cells has emerged, not only as the cell critical in the response to allergens, but as a primary cell for host defense and initiation of innate immune responses in tissues located at the interface between the host and the environment, especially the skin, mucosa, gastrointestinal and respiratory tracts. Mast cells are not only activated by the high affinity IgE receptor, but also by Fc gamma receptors, complement receptors and toll-like receptors after interaction with bacterial products and viral RNA, and even by physical stimuli including ultraviolet B irradiation (22;23). Notably, ultraviolet B irradiation and viruses have been implicated as some of the possible environmental risk factors for DM (6;24). Activated mast cells secrete a number of pro-inflammatory mediators including type I interferons, TNF-α, IL-6, and IL-1β and result in the influx of TH2 T lymphocytes and dendritic cells, all of which are thought to be critical factors in the pathogenesis of DM (22;23;25). Mast cells then may be an early key initiator of the pathogenic sequence of events in DM, at least in the skin tissue.
Mast cells are emerging as a critical player inmediating a number of systemic and organ-specific autoimmune diseases. In a K/BxN mouse model of rheumatoid arthritis, knock out of mast cells by two different pathways (deficiency of stem cell factor and of c-kit, a mast cell differentiation factor) leads to abrogation of disease, whereas engraftment of mast cells restores joint inflammation (26). Agents that inhibit mast cell degranulation, such as salbutamol, slow the progression of collagen-induced arthritis (27). In the MRL/lpr mouse model of lupus, a dense mast cell infiltrate is present in the dermis of the affected skin lesions in animals older than 4 months of age; and, this correlates with decreased histamine methyltransferase activity and prolonged activation of histamine in the affected skin tissue (28). Mast cells are also increased in the affected skin of patients with chronic cutaneous lupus (28). Activated mast cells have also been reported in the skin of patients with systemic sclerosis, and mast-cell targeted therapies improve the skin disease of the tight-skin mouse model of scleroderma (22). Mast cell deficient mice either do not develop disease, as in bullous pemphigoid, or have less severe and delayed disease, as in the experimental autoimmune encephalomyelitis model of multiple sclerosis (22;27). Mast cells likely play a role in the pathogenesis of a number of other autoimmune disorders, including Graves’ disease, systemic vasculitis, insulin-dependent diabetes, Sjogren’s syndrome, Guillain-Barre syndrome and pemphigus vulgaris, based on the findings of increased mast cell numbers in the affected tissues and/or an improvement in disease with mast cell-targeted therapies (22).
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3196299/Cutaneous mastocytosis is the proliferation of mast cells in the skin without any evidence of involvement of other organs. Symptoms can be only cutaneous or only systemic, depending if there is local or generalized release of mediators from mast cells. Mast cells can infiltrate multiple organs, including skin, spleen, bone marrow, liver, and lymph nodes, with the skin being the most frequent target.
Cutaneous mastocytosis is associated with local and systemic symptoms, including cutaneous flushing; blisters; dyspnea; rash; exacerbation of asthma; hypotension; gastrointestinal disorders, such as gastroesophageal reflux; ulcers; and diarrhea. These symptoms result from mast cell degranulation with the release of several mediators, histamine being the most significant of all mediators, which can cause both local and systemic reactions.
Most cases of cutaneous mastocytosis start in childhood. TMEP is a rare form, occurring more often in adults than children. The age of manifestation has an important value for prognosis. Most pediatric patients with cutaneous mastocytosis show improvement in symptoms over time, with 50 percent showing resolution of symptoms in adolescence and only 10 to 15 percent persisting in adulthood.
In pediatric patients, unlike in adults, it is believed that a transitory deregulation of growth factors occurs. In adults, a c-kit proto-oncogene mutation is observed, which entails a mast cell hyperplasia. The c-kit encodes the KIT proto-oncogene, a tyrosine kinase, which is the mast cell's growth factor receptor. This particular mutation, however, was not found in pediatric patients or familial mastocytosis. Although the c-kit mutations are not found in all patients with cutaneous mastocytosis, proto-oncogene alterations may indicate a more aggressive behavior of the mastocytosis.
Cutaneous mastocytosis may appear in four clinical variants: urticaria pigmentosa, isolated mastocytoma, cutaneous diffuse or erythrodermic mastocytosis, and telangiectasia macularis eruptiva perstans. The occurrence of systemic symptoms may indicate the presence of associated hematological diseases or even a systemic mastocytosis condition. Signs of systemic involvement include hepatosplenomegaly, lymphadenopathy, and bone alterations.
I'm going to see if my dermatologist can still ask for staining and a mast cell count on my skin biopsy. I doubt he'll agree, but I'll try.
). I am trying to propose that ADM is in fact a novel form of cutaneous mastocytosis, and I believe I can achieve remission by stabilizing the mast cells involved. 
Of course, I believe that there is a rebound effect in mast cell numbers when a corticosteroid is discontinued (that's why I believe that a very long dosage tapering process of budesonide seems to work much better than the traditional faster taper), but that doesn't mean that the treatment can't work as claimed.