PubMed Health⌕ Search

Biomedical subjects

C M Asplin

Publications and source records attributed to C M Asplin.

43 records · Page 3Linked to original sources
PubMed1976

Necrotizing vasculitis: a circulating immune complex producing inflammatory skin lesions.

A patient with acute necrotizing vasculitis is described in whom tests for circulating immune complexes were negative. The patient's serum injected intradermally produced lesions which closely resembled those occurring spontaneously. When the serum was fractionated, the skin-reactive fraction was found to be associated with IgG, but was of a higher molecular weight than normal IgG. Immunofluorescent studies showed that lesions induced by this active fraction contained IgG and complement in the epidermal basement membrane zone and within the small dermal vessels. We conclude that an immune complex of relatively low molecular weight is present in the active fractions, and capable of initiating the lesions of acute necrotizing vasculitis.

Antigen-Antibody Complex↗
PubMed1976

Evidence for circulating immune complexes in erythema nodosum and early sarcoidosis.

Twenty-two patients were investigated during acute attacks of erythema nodosum with a series of tests for circulating immune complexes. Nineteen had bilateral hilar lymphadenopathy and were considered to have sarcoidosis. Evidence of circulating immune complexes was found in 18, out of 22 patients (including 15 out of the 19 cases of sarcoidosis). The most frequent abnormality was the detection of elevated levels of C3 breakdown products (C3i), which were found in 14 out of 18 tests. The test results returned gradually to normal as symptoms subsided in 20-40 days, but 2 patients still showed abnormalities at 40 days despite the disappearance of symptoms. It is concluded that free immune complexes appear in the circulation during the early stages of acute sarcoidosis and gradually disappear as symptoms subside.

Antigen-Antibody Complex↗
PubMedDate not supplied

Insulin, pancreatic polypeptide, and glucagon antibodies in insulin-dependent diabetes mellitus.

To assess the possible value of the use of high-purity pork insulin (HPPI) in the United States, the serum insulin (I), pancreatic polypeptide (PP), glucagon (G), and somatostatin (SRIF) antibody binding characteristics have been determined in 90 conventional insulin-treated diabetic subjects and related to their degree of metabolic control, as assessed by glycosylated hemoglobin (HbA1) concentration. All diabetic subjects had antibodies to insulin, but there was no relationship between any of the antibody binding characteristics and HbA1 level: 47% possessed PP antibodies; mean +/- SEM HbA1 in these patients was 14.5 +/- 0.3%, identical to those without PP antibodies (14.5 +/- 0.4%); 10% had G binding antibodies with HbA1 levels of 14.6 +/- 0.8%, similar to those without G antibodies. No subject possessed SRIF antibodies. This lack of correlation between antibody characteristics and metabolic control makes it unlikely that, in the majority of patients, treatment with a less immunogenic insulin (HPPI) versus conventional insulin will result in improved diabetic control.

Adult↗
PubMedDate not supplied

Antibodies to viruses and to pancreatic islets in nondiabetic and insulin-dependent diabetic patients.

Autoimmunity is frequently involved in the pathogenesis of insulin-dependent diabetes, and viral infections have been implicated in some cases. We have investigated the possibility that islet cells and viruses share antigenic determinants with the result that antiviral antibodies would cross-react with islet cells. Antibody titers to Coxsackie B2, B3, B4, and B5, Influenza A and B, and mumps viruses were compared with islet cell antibody (ICA) titers in newly diagnosed insulin-dependent diabetic patients and in some diabetic patients followed prospectively for 1 yr postdiagnosis. Nondiabetic patients, with culture-proven Coxsackie B4 infections and large rises in Coxsackie B4 antibody titers, were evaluated for islet cell antibodies. No relationship between ICA and viral antibody titers was found either in diabetic or nondiabetic patients. We conclude that it is unlikely that islet cells and the viruses tested share antigenic determinants and other mechanisms relating viral infection and autoimmunity in insulin-dependent diabetes must be sought.

Antibodies, Viral↗