Sebaceous adenomas in an MYH associated polyposis patient of Indian (Gujarati) origin.

MYH associated polyposis is an autosomal recessive polyposis syndrome with a high risk of large bowel cancer, caused by mutations in the DNA repair gene MYH. Founder mutations have been described in different ethnic groups. Muir Torre Syndrome is the association of internal malignancies with sebaceous gland tumours; Lynch Syndrome/Hereditary Non Polyposis Cancer is the best known cause. There has been a previous report of sebaceous gland tumours in an Italian patient with MYH associated polyposis. We describe a man of Indian (Gujarati) descent who has MYH associated polyposis and multiple sebaceous adenomas of the skin.

Juvenile sarcoidosis after BCG vaccination.

We report the case of a 2-year-old boy with juvenile sarcoidosis, in whom the cutaneous lesions first arose at the site of and soon after a BCG vaccination. Juvenile sarcoidosis is rare, and the pattern of clinical features is distinct from the adult form of sarcoidosis, possibly related to immunologic development. The cause of sarcoidosis is unknown, although there is much interest in the possibility of mycobacterial species operating as antigenic stimuli to initiate the disease. This case suggests that the Mycobacterium bovis present in the BGC vaccination may have been etiologically important in the development of sarcoidosis.

Retroviruses and psoriasis.

Psoriasis occurs with at least undiminished frequency in HIV infected individuals. The behaviour of psoriasis in HIV disease is of interest, both in terms of pathogenesis and therapy, because of the background of profound immunodysregulation. It is paradoxical that, while drugs that target T lymphocytes are effective in psoriasis, the condition should be exacerbated by HIV infection. Antiretroviral therapy may improve psoriasis in tandem with improvement in the overall clinical and virological condition of the patient. The aetiopathogenesis of psoriasis is unknown but genetic and environmental factors are thought to be involved. There are controversial issues regarding the immunological basis of psoriasis and the role of CD4+ versus CD8+ T lymphocytes. Current opinion favours an autoimmune basis for psoriasis, although the precipitating activating signal(s) within psoriatic plaques remains unknown. The immunodysregulation resulting from HIV infection may trigger psoriasis in those genetically predisposed by the Cw*0602 allele. Since CD8+ T cells recognize antigen in the context of class I molecules, the identification of a human leucocyte antigen class I association in HIV-associated psoriasis strengthens the argument for an important role for CD8+ T lymphocytes in the immunopathogenesis of psoriasis. HLA-Cw*0602 could act as a cross-reactive target for cytotoxic T lymphocytes responding to processed peptides from microorganisms. Human retrovirus-5 is a recently described, partially characterized retrovirus and has been implicated in the pathogenesis of psoriatic arthropathy but not psoriasis.