We failed to find a record ofintra-abdominal granuloma annulare lesions, and this case apyars to be the first of visceral granuloma annulare. The relation -tveen diabetes mellitus and generalised granuloma annulare has been a subject of speculation for years but remains unclear. Haim et al reported 13 patients with generalised granuloma annulare, three of whom had overt mild non-insulin dependent diabetes and seven others carbohydrate intolerance after provocative oral prednisolone.3 Other studies, however, have not confirmed this observation. A more recent report has suggested an association between granuloma annulare and insulin dependent diabetes.4 The relation between diabetes and granuloma annulare is made more complex by the histological appearance of necrobiosis lipoidica diabeticorum, granuloma annulare, and rheumatoid nodules. Each ofthese conditions includes collagen necrobiosis, and all three variants have been seen in a patient who had insulin dependent diabetes and a sister with rheumatoid arthritis.5 The histological similarities among these conditions are so great that they may share the same or a very similar pathogenesis. Immune complex deposition seems the most probable common pathway.Finally, in our patient there appeared to be a relation between diabetic control and the granuloma annulare. Poor diabetic control was associated with an exacerbation of the lesion, which in turn resulted in excessive working of the ileostomy, which was evident whatever the cause of his poor diabetic control. Biopsy sections of the skin and mesenteric nodes showed several discrete foci of connective tissue necrosis in the dermis and subcutaneous fat. The zones of necrosis were surrounded by histiocytes showing well marked palisading (figure). The histiocyte reaction was not strikingly tuberculoid. There were no giant cells, and no evidence of arteritis was detected. The cell mediated immune response was evaluated in vivo in 29 patients.twith clinically severe haemophilia by means of the dinitrochlorobenzene skin test. All patients had a response below the median normal value, and in 19.the response was on or below the lower limit of the normal range. There was no difference in skin response between patients positive and negative for the human immunodeficiency virus (HIV; formerly known as human T cell lymphotropic virus Im or lymphadenopathy associated virus). In tbe whole group, and in seronegative patients (n= 17), there was aan inverse relation between exposure to clotting factor and skin response. In seropositive patients (n= 12) no such association was apparent.This study shows that clotting factor concentrate impairs the cell mediated immune response to a new antigen in the absence of infection with HIV.

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SF and serum JIA samples can impair bone growth at the growth plate. In synovial fluid, the effect is variable but resistant to treatment with IL-1beta, IL-6 and TNF-alpha specific antibodies and IGF-1, suggesting that other factors in this biological fluid may also have an effect on longitudinal growth through IGF-1-independent mechanisms.

IL-18 is highly expressed in muscle tissue in the context of inflammatory myopathies and based on its plausible effector functions could provide a novel therapeutic target in future.

The density and microanatomical location of CD4 and CD8 lymphocytes and of monocytes/macrophages at the site of a tuberculin test were measured in 13 patients with sarcoidosis, and the results were compared with those seen in a group of healthy controls. The cellular infiltrate was significantly reduced in the sarcoid subjects compared with the controls for all cell phenotypes studied; the ratio of CD4 positive:CD8 positive lymphocytes was significantly increased in the sarcoid group. Clinically negative reactions showed substantial numbers of infiltrating mononuclear cells, although not as great as in clinically apparent reactions.A clinically negative tuberculin reaction does not necessarily imply anergy to the test substance and should not be termed "negative".