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To study associations of bullous pemphigoid (BP) with internal diseases, we conducted a retrospective case control study assessing the frequency of selected diseases - diabetes mellitus, neurological diseases, malignant tumors, benign prostate hyperplasia, hypertension and ischemic heart disease in patients with BP. 89 patients with BP, whose data were retrieved from the register of the Centre of bullous diseases from the period of 1991-2006, were matched with 89 controls of the same age and gender, recruited from patients treated for other skin diseases. The frequency of internal diseases at the time of the onset of BP was evaluated by unconditional logistic regression adjusted for age and gender and maximum likelihood test for contingency tables. Neurological disease was found in 42.7% of the patients and in 19.1% of controls. This difference was statistically significant (p value = 0.001). Moreover, regression analysis has shown that patients with neurological disease in the age group >or= 80 years have significantly higher risk of pemphigoid than patients without neurological disease (odds ratio 10.55; 95% confidence interval 2.68 to 41.49). Most frequent were cerebral stroke in men and dementia in women. For other diseases and other age groups, no statistically significant influence was found.

The proportion of T lymphocyte populations was assessed using monoclonal antibodies (OKT3, OKT4, OKT8) and spontaneous E-rosette tests with SRBC (for total and active TE cells) in 36 patients with cutaneous leishmaniasis subdivided according to the clinical variety. The T cell profile was normal in patients with simple cutaneous leishmaniasis of early ulcerative type whereas active TE cells and OKT4 positive cells were reduced in some cases of late ulcerative type. A significant reduction of active TE cells and of OKT4 positive cells (helper/inducer phenotype) and increase of OKT8 positive cells (suppressor/cytotoxic phenotype) was observed in peripheral blood of all patients with persistent active lesions and leishmaniasis recidivans. In patients with highly ulcerated persistent lesions a low proportion of active TE cells was also demonstrated in cellular extracts from dermal tissue. The results support the data obtained in experimental leishmaniasis that lack of helper/inducer cells and generation of suppressor T cells may be responsible for the development of chronic leishmaniasis.