The prevalence of cutaneous fungal infection was studied in 72 patients who had undergone renal transplantation and compared with a group of age and sex matched controls. Samples were obtained from toe nails, toe webs, and the upper back; clinically suspicious lesions from other areas were also examined. A total of 576 sites were sampled (288 in each group). Pathogenic fungi were identified from 44 sites (15%) in the renal transplant (RT) group compared with 26 sites (9%) in the control group, (P less than 0.05). However, site-specific differences were less marked; no difference was found between the RT group and controls when the results from the toe nails and toe webs were analysed separately. Trichophyton mentagrophytes was the most common species isolated from both groups. Colonization of the back with Pityrosporum yeasts was significantly more common in the RT group, but few patients in either group had tinea versicolor. 'Mixed infections', with more than one species of fungus isolated in an individual, were only found in the RT group. We also examined the relationship between the presence of fungal infection and the presence or absence of cutaneous malignancy in the renal transplant group. No increase in the prevalence of fungal colonization was found in those patients who had developed cutaneous malignancy compared with those who had not.
Patients from a renal transplantation unit with an unusually high incidence of polycythaemia were divided into polycythaemic and control groups. The rate of rise of haemoglobin concentration was not significantly different in the two groups. The polycythaemic group received a significantly lower dose of azathioprine (p < 0.005) and included more patients with polycystic disease than the control group (p < 0.05). An effect of azathioprine on bone marrow function was suggested by the polycythaemic group also having a higher mean white cell count (p < 0.02). Azathioprine dosage correlated negatively with post-transplantation polycythaemia regardless of the original cause of renal failure.
These results support the theory that many cases of Ogilvie's syndrome are the result of excessive large bowel parasympathetic suppression rather than sympathetic overactivity.
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