Biomedical subjects

S B Moore

Publications and source records attributed to S B Moore.

At least 127 records · Page 7Linked to original sources

PubMed1984

Immune thrombocytopenias: tests for platelet antibodies.

In a study of 49 consecutive patients for whom a test for platelet antibodies had been ordered, tests were performed for both cell-bound and serum platelet antibodies. In cases of autoimmune thrombocytopenia (ITP), the test result for cell-bound antibody was more likely to be positive than was the test result for serum antibody. In three patients with ITP who were taking systemic corticosteroids, however, the result of the CBPAT was negative. A similar phenomenon occurred in a patient with SLE. The result of the SPAT correlated best with the presence of alloantibodies formed during pregnancy or after blood transfusion.

Adrenal Cortex Hormones↗

PubMed1984

Anti-type II collagen antibodies in rheumatoid arthritis. The influence of HLA phenotype.

Antibodies to native chick and bovine Type II collagen were measured by radio immunoassay, in 83 rheumatoid arthritis (RA) patients and 14 normal controls. Anti-chick Type II collagen and anti-bovine Type II collagen antibodies were found in 48% and 43% of RA patients, respectively. A strong correlation of antibodies to chick and antibodies to bovine collagen was described, suggesting cross-reactivity between different collagen species. There was an association between the presence of anti-native Type II collagen antibody and the expression of HLA-DR2. It is suggested that the production of anti-collagen antibody may be under genetic control in RA, but not associated with the major genetic marker of disease susceptibility, HLA-DR4.

Animals↗

PubMed1984

Transfusion-induced alloimmunization in patients awaiting renal allografts.

Lymphocytotoxic antibodies can be induced by the immunologic stimulus of pregnancy, blood transfusion, or tissue allograft. The presence of such antibodies can delay or prevent renal transplantation. However, a history of prior transfusion exposure has been strongly associated with excellent renal allograft survival. The problem of ensuring this 'transfusion effect' while minimizing the risk of alloimmunization is real for patients awaiting renal allografts. We examined the influence of pregnancy, allograft rejection, and transfusions on the levels of lymphocytotoxic antibodies in the sera of patients awaiting renal transplantation. The results indicate that transfusions alone have a minimal effect on alloimmunization in men and in nulliparous women. The influence of transfusions alone was seen in 77% of men and 86% of women showing less than 10% panel reactivity. Deliberate transfusion policies for patients awaiting renal allografts should be designed to minimize transfusion exposure to parous patients or those who have previously rejected a renal graft.

Antilymphocyte Serum↗

PubMed1983

Management of transfusion in the massively bleeding patient.

Adequate and safe transfusion support of massively bleeding patients requires a thorough understanding of the complications of hemorrhagic shock, a well-developed system of identifying patients and blood samples, and a clearly delineated communication system between clinicians and blood bank. The support plan must also be designed to minimize the predictable complications by active intervention with blood and component therapy.

Blood Coagulation Disorders↗

PubMed1983

HLA and nasopharyngeal carcinoma in North American Caucasoids.

In Chinese, nasopharyngeal carcinoma (NPC) has been associated with HLA alleles. Twenty-four Caucasoids with NPC were HLA typed (24 AB, 16 DR). No associations were found in comparisons with normal healthy controls.

HLA Antigens↗

PubMed1983

Transfusion-related acute lung injury associated with passive transfer of antileukocyte antibodies.

Acute lung injury (ALI) is an infrequently recognized complication of transfusion therapy. Although the role of passive transfer of leukoagglutinating antibodies has been acknowledged, there is little documentation of the relationship of these antibodies in transfused blood to the human leukocyte antigen (HLA) phenotype of the recipient. Recently, we observed 5 cases of transfusion-related ALI, and in all cases leukoagglutinating and lymphocytotoxic antibodies were found in serums of the transfused blood products. In 3 cases, the antibodies corresponded to the HLA antigens of the recipient. Multiparous blood donors whose plasma contains these antibodies represent a potential transfusion hazard. It is recommended that blood component usage from donors implicated in these reactions be restricted to frozen or washed red blood cells. The incidence of leukoagglutinin-associated ALI may be more frequent than previously appreciated. Current concepts of the mechanism of microvascular pulmonary injury are discussed in relation to these cases.

Acute Disease↗

PubMed1983

The syndrome of gastric argyrophil carcinoid tumors and nonantral gastric atrophy.

Records of the 30 cases of gastric carcinoid at the Mayo Clinic showed that the gastric mucosa was normal, hyperplastic, or atrophic (nonantral) in 12, 2, or 16 patients, respectively. In the atrophic group, the tumors were in the gastric body and fundus; small, polypoid, and multicentric; and associated with fundal argyrophil cell hyperplasia. In immunocytochemical studies, minor tumor cell populations stained positively for 5-hydroxytryptamine, gastrin, and somatostatin in 1 case and for 5-hydroxytryptamine in 3 others. Metastasis occurred in 3 patients. Twelve patients had pernicious anemia. Parietal cell or intrinsic factor antibodies or both were present in all 12 patients tested. Each of the 7 patients with an intact antrum had massive hypergastrinemia. No common HLA-A, -B, or -DR antigen pattern was detected among the 10 patients tested. The results suggest that nonantral gastric atrophy predisposes to gastric carcinoid as well as to gastric carcinoma.

Adult↗

PubMed1983

Immunologic, clinical, and pathologic aspects of human graft-versus-host disease.

The three necessary factors in the development of graft-versus-host disease are the histoincompatibility of the host and the effector cells of this process, the immunoincompetence of the host, and the capability of effector cells to proliferate and attack host tissues protractedly in vivo. The disease may affect the alimentary tract, liver, bronchopulmonary tree, bone marrow, reticuloendothelial system, vascular endothelial cells, or epidermis. Graft-versus-host disease is potentially reversible or controllable if prompt, aggressive therapy is instituted. The recommended treatment is a combination of methotrexate, high-dose prednisone, and antithymocyte globulin.

Aged↗

PubMed1983

Hemochromatosis: genetic or alcohol-induced?

To evaluate the roles of alcohol and genetic factors in hepatic iron overload, we studied prospectively 61 patients selected solely on the basis of increased stainable hepatic iron (grade 3 or 4). Independent comparisons were made between alcoholic (n = 20) and nonalcoholic (n = 41) patients, and between patients wih affected relatives (n = 25) and those without (n = 36). For the entire group, the mean value for mobilizable iron was 19.6 g and the prevalence of HLA-A3 was 69.6%, both findings compatible with genetic hemochromatosis. Subgroups were no different in clinical features (diabetes, pigmentation, cardiomyopathy, hypogonadism, or arthropaty), histologic findings (fat, inflammation, fibrosis), indexes of iron metabolism (serum iron, transferrin saturation, chelatable iron, and mobilizable iron stores), or frequency of HLA-A3 and HLA-B7. The only exception was that mean hepatic iron concentration was lower in alcoholic patients than in nonalcoholic patients (17,344 vs. 28,553 micrograms/g dry wt, p less than 0.001). Similarity between subgroups in almost all parameters examined is consistent with the hypothesis that heavy deposition of hepatic iron, as observed in our patients, is an indication of genetic hemochromatosis, regardless of alcohol consumption or the findings of affected relatives. The lower concentrations of hepatic iron in alcoholic patients, despite equal body stores in both groups, suggest that alcohol may alter the distribution of storage iron in genetic hemochromatosis.

Adult↗

PubMed1983

Linkage evidence for genetic heterogeneity among kinships with hereditary motor and sensory neuropathy, type I.

Previous reports have shown linkage of hereditary motor and sensory neuropathy, type I (HMSN I), a dominantly inherited hypertrophic neuropathy, to the locus for the Duffy blood group on the long arm of chromosome 1. Two kinships that were extensively studied and reported almost 20 years ago and used to show heterogeneity among kinships with peroneal muscular atrophy and to characterize HMSN I were investigated for linkage to various blood erythrocyte and lymphocyte (HLA) antigens. Strong evidence against linkage to the Duffy blood group locus was found for one kinship, whereas suggestive evidence for linkage was found for the other. These data imply that HMSN I is heterogeneous--that is, caused by different genetic mechanisms. The HMSN I that is not linked to the Duffy locus might be identified as HMSN IA, and the HMSN I that is linked to the Duffy locus might be designated as HMSN IB. HMSN IA was not linked to other blood types or HLA antigens. In addition, no evidence for linkage to blood types and HLA was found for spastic paraplegia with peroneal muscular atrophy and sensory loss (HMSN V).

Adolescent↗

PubMed1983