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Results for “Pyoderma Gangrenosum”

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At least 1,009 records · Page 56Linked to original sources
PubMed1977

[Immune deficiences during pyoderma gangrenosum associated with a polycythemia vera].

A deficiency in cellular immunity was demonstrated in a patient suffering from polycythaemia rubra vera in the myelofibrosis stage. Intradermal reactions to classical antigens (candidine, trichophytine, streptokinase, streptodornase, tuberculine) were negative, as was the di-nitrofluorobenzene test. However, the T lymphocyte count was normal. There was no disturbance in humoral immunity. Phagocytosis was normal but leucocyte migration, studied in vitro, was nil. The possibility of an intrinsic abnormality in the polynuclear neutrophil is evoked.

Adrenal Cortex Hormones↗
PubMed1976

Cryoimmunoglobulin IgGk with microtubular ultrastructure associated with pyoderma gangrenosum.

Recurrent gangrenous leg ulcers were associated with a monoclonal IgGk cryoglobulinaemia, though without overt myeloma. Cryoprecipitation of the serum in vitro gave a reversible gel with microtubular structure, built from the monomer and with a high degree of order. The same structure was found distending the superficial vessels of the ulcer biopsy, as well as extravascularly. There was no vasculitis, and luminal obstruction appeared responsible for the ulceration. Microtubular structures occur in nature among diverse proteins and viruses. The protein studied here is similar to a reported instance of myeloma cryo-IgGk.

Blood Vessels↗
PubMed1975

"Streaking leukocyte factor," arthritis, and pyoderma gangrenosum.

A 14-year-old boy with a 12-year history of episodes of sterile pyarthrosis and cutaneous inflammation and ulceration was found to possess a serum factor which enhanced the random migration of leukocytes in vitro. The serum factor was isolated by Sephadex G-200 gel filtration and found to have a molecular weight of approximately 160,000. This partially purified principle enhanced the random migration of purified normal human neutrophils or mononuclear leukocytes by up to 200% without influencing chemotaxis. Trauma or other stimuli may lead to an accumulation of this serum factor in some tissues of the patient with resultant excessive leukocyte influx and heightened local activity of the leukocytes in the inflammatory exudate.

Adolescent↗
PubMed1990

[Long-term follow-up of pyoderma gangrenosum (PG) associated with aortitis syndrome (AOS)].

It is known that PG is often associated with AOS. However, there have been no reports on long term follow-up of PG associated with AOS. We experienced a case of a 16 year old female who suffered from PG and AOS. The onset of both diseases occurred at the same time. On admission, many pustules and ulcers were found on the extremities. There was no finding of vasculitis in histopathological examinations. Development of skin lesions of PG coincided with the progress of AOS. But, AOS was progressive even when the patient was free of skin eruptions. It was concluded that the activity of PG was not always parallel to that of AOS.

Adolescent↗
PubMed1980

Pyoderma gangrenosum: clinical and laboratory findings in 15 patients with special reference to polyarthritis.

Fifteen consecutive patients with PG have been studied during the period 1971-78. Systemic disease was found in 13 of the patients and preceded the skin disease in 10 patients by 1-25 years. Only two patients had ulcerative colitis. One patient had paroxysmal nocturnal hemoglobinuria and three patients had an IgA myeloma. Eight patients had polyarthritis; this was classical seropositive rheumatoid arthritis in two patients, and a seronegative inflammatory polyarthritis in six patients. Four patients had an unusual progressive erosive seronegative polyarthritis without evidence of granulomatous bowel disease, psoriasis, genital, urinary tract or eye disease. In three of these four patients the arthritis preceded the PG. Synovial fluid analysis showed depressed complement levels and in one patient deposits of immunoglobulins and complement were demonstrated in the synovial membrane. The course of the arthritis was progressive with development of disabling joint deformities and erosive destruction of joints, despite treatment with penicillamine, corticosteroids and nonsteroidal anti-inflammatory drugs. One other patient had severe degenerative joint disease and chondrocalcinosis in association with a seronegative inflammatory polyarthritis, and another patient had ulcerative proctitis and severe degenerative joint disease secondary to chronic seronegative inflammatory polyarthritis. None of the patients had colitic arthritis, but in view of the association between PG and ulcerative colitis, some patients previously reported with PG and joint disease may have been suffering from the arthritis of ulcerative colitis. PG developed at the site of skin trauma in six patients. The natural history of the skin disease ran one of two courses: an acute, progressive course in which the ulcers rapidly enlarged until arrested by treatment; and a chronic course in which the lesions extended slowly and which after a period of weeks began to show signs of spontaneous healing. In only the patients with ulcerative colitis was there any correlation between the activity of the associated disease and the onset and progression of the skin disease. Serum complement levels were normal and no circulating cryoprecipitable immune complexes were found. Skin histology showed no evidence of vasculitis and direct immunofluorescence examination of involved skin was negative for IgG, IgM, IgA and C3. No consistent abnormality of cell-mediated immunity or neutrophil function was found and no significantly increased prevalence of any HLA antigen type was noted. Twelve patients have been treated with systemic corticosteroids. Six of these patients developed serious steroid complications and four patients have died, all from complications of steroid therapy.

Adolescent↗