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Biomedical subjects

T Cainelli

Publications and source records attributed to T Cainelli.

At least 73 records · Page 4Linked to original sources
PubMed1990

Antiphospholipid antibodies and necrotizing purpura.

A 30-year-old woman with recurrent necrotizing purpura on the legs which did not fit, to our knowledge, within any distinctive pathological entity, is described. Laboratory investigations disclosed a mild thrombocytopenia and antiphospholipid antibodies, i.e. lupus anticoagulant and anticardiolipin. Cutaneous lesions may be an early marker of the antiphospholipid antibody syndrome.

Adult↗
PubMed1990

[Vulvar pruriginous squamous papillomatosis].

Pruritic vulvar squamous papillomatosis (PVSP) is a recently described clinical entity whose aetiologic agent has been reported to be the human papilloma virus. We have seen 9 patients with PVSP. We believe that our clinical and histological data, along with the results of the in situ hybridizations stress out the evidence of a viral aetiology in the PVSP.

Adult↗
PubMed1989

[Von Willebrand factor multimers in systemic scleroderma].

In scleroderma endothelial cell damage plays an early and pivotal role in the pathogenesis of sclerotic lesions. In our study we determined whether or not plasma from 11 consecutive patients with scleroderma contained a subset of larger than normal (supranormal) multimers of von Willebrand factor which are potent inducers of platelet aggregation and adhesion. Supranormal multimers were found in all patients, but in none of the normal controls. Supranormal multimers may contribute to the pathogenesis of systemic sclerosis by inducing platelet aggregation and enhancing adhesion to subendothelium.

Adult↗
PubMed1988

HLA-DR and DQ antigens in lichen planus.

A study on HLA-DR and DQ typing in 40 patients with lichen planus (26 males and 14 females) and in 92 normal blood donors of both sexes was performed. Twenty-seven patients had cutaneous lesions, 11 cutaneous and mucosal involvement and 2 patients had oral erosive lesions. Serological typing revealed a highly significant increase of HLA-DR 1 antigen in the patient group. No difference has been observed on the prevalence of DR1 antigen among the different clinical status of the disease.

Adult↗