One or more deep, undermined ulcers known as pyoderma gangrenosum may develop on the lower extremities of patients with inflammatory bowel disease and several other types of systemic illness. These ulcers are generally filled with healthy granulation tissue and are surprisingly free of pus and crust. The undermined margin of skin around the ulcer is usually deeply violaceous. A variety of bacterial organisms colonize these ulcers, but treatment with ordinary antibiotic agents does not bring about clinical improvement. The pathogenesis of the ulcers is not known. The ulcers of pyoderma gangrenosum do not respond to topical therapy but often resolve if the associated inflammatory bowel disease can be successfully treated. Systemic administration of steroids results in direct improvement of the cutaneous ulcers as well as in improvement of the gastrointestinal disease. The oral administration of dapsone may enhance the effect of steroids. Oral administration of cyclosporine and multiple other therapies have also been suggested.Ulcers are occasionally seen in patients with rheumatoid arthritis. Such ulcers are particularly likely to occur in those patients who have markedly elevated titers of rheumatoid factor. This observation suggests that circulating immune complexes may play a role in the pathogenesis. Unfortunately, the response of these ulcers even to high-dose steroids is not as good as that obtained in patients with inflammatory bowel disease.
Patients with myeloma, especially when the paraprotein is immunoglobulin A in type, may also develop cutaneous ulcers that simulate the lesions of pyoderma gangrenosum. 
These patients often have scattered purpuric and pustular lesions also.
A small number of patients have been reported with a variant of pyoderma gangrenosum in which hemorrhagic bullae precede the breakdown and ulceration of the skin. Most of these patients have leukemia, or preleukemia, of the myelocytic type.
Ulcers resulting from vasculitic processes may be found in patients with nodular vasculitis (erythema induratum), polyarteritis nodosa, giant cell arteritis, and Wegener’s granulomatosis. Ulcers resulting from vascular occlusion may develop in patients with arteriosclerosis, hypertension, and diabetes. Ulcers resulting from traumatic damage are sometimes seen in patients with neuropathic complications of diabetes or leprosy.
Patients with advanced mycosis fungoides and other forms of peripheral T-cell lymphoma often develop deep ulcers of the skin as a result of destructive infiltration with malignant T-cell lymphocytes. The presence of such ulcers signals the terminal phase of the disease.
Several deep fungal diseases are associated with cutaneous ulceration. In the United States the most common fungal infections responsible for ulcer formation are sporotrichosis, coccidioidomycosis, histoplasmosis, and North American blastomycosis. The diagnosis is best confirmed by culture, but organisms are also sometimes visible in biopsies taken from the edge of the ulcers. The cutaneous lesions of deep fungal infection are particularly likely to be found in patients who are immunocompromised.
Several of the atypical mycobacterial infections also result in cutaneous ulcers. The most common of these infections is that resulting from Mycobacterium marinum. This infection is acquired by those who swim in infected swimming pools or who work with infected aquariums.
Rarely, systemic atypical mycobacterial infections result in ulceration from disseminated disease. This is particularly likely to occur in immunocompromised persons.
Tags:bacterial organisms, granulation tissue, inflammatory bowel disease, Lesions, pyoderma gangrenosum, rheumatoid arthritis, rheumatoid factor, Systemic Disease, systemic illness ulcers
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