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Biomedical subjects

C W Fink

Publications and source records attributed to C W Fink.

At least 55 records · Page 3Linked to original sources
PubMed1979

Different HLA-D associations in adult and juvenile rheumatoid arthritis.

HLA-D typing was performed in 126 patients with juvenile rheumatoid arthritis. HLA-DW4, the antigen found in previous studies to characterize adult rheumatoid arthritis, had a significantly lower frequency in children with arthritis than in normal controls (P less than 0.04). By contrast, in children the antigens HLA-DW7 (P less than 0.03) and HLA-DW8 (P less than 0.01) were increased compared to controls. The antigen TMo, detected with homozygous typing cells from a child with juvenile rheumatoid arthritis, was found to be related to the cross-reactive specificities HLA-DW7 and DW11. 46% of the patients with persistent pauciarticular arthritis of childhood typed for the antigen TMo, compared to only 1% of normal controls. Thus the relative risk for persistent pauciarticular arthritis in relation to the presence of TMo was 67.7 (P less than 0.0001). These results provide evidence of fundamental differences between adult rheumatoid arthritis and arthritis of childhood. The latter group appears to include a population distinguishable clinically and characterized in these studies by the HLA-D determinant TMo.

Adult↗
PubMed1976

Polyarteritis in children.

Polyarteritis was diagnosed in three girls, 9 to 10 years old, by kidney and skin biopsies. They were treated with a combination of prednisone (1.5 to 2 mg/kg) and cyclophosphamide (2 mg/kg) for up to 12 months. The illness was severe in all three, complicated by hypertension, seizures, pulmonary infiltrates, renal failure, or hallucinations. All three patients are alive and well with no or minimal residual symptoms two to three years after therapy was discontinued. The treatment with corticosteroids or with a combination of steroids and immunosuppressive drugs seems to improve the prognosis of polyarteritis considerably.

Child↗
PubMed1972

Lymphotoxin formation by lymphocytes and muscle in polymyositis.

Muscle pieces from 11 patients with dermatomyositis or polymyositis were incubated with autologous peripheral blood lymphocytes and the supernates examined for the production of lymphotoxin, a mediator of delayed hypersensitivity, using human fetal muscle monolayers as the target cell. In the case of all 10 active patients, production of lymphotoxin was demonstrated. This mediator was also demonstrated when muscle alone was incubated from two patients with extensive cellular infiltration. Lymphotoxic activity was not found in supernates obtained by incubation of muscle from nine control subjects with their autologous peripheral blood lymphocytes. Addition of methyl prednisolone to active cultures inhibited the action of lymphotoxin on the muscle monolayers. Lymphotoxin was not demonstrated when breast tumor tissue from a patient with dermatomyositis was incubated with autologous lymphocytes. The lymphotoxic agent in the active supernates had similar chromatographic properties to those of a sample of purified lymphotoxin. These findings suggest that muscle injury in polymyositis is a result of a cellular immune response to an antigen present in involved muscle tissue.

Adolescent↗