PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “DEFICIENCY DISEASES”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 55 records · Page 3Linked to original sources
PubMed1977

Immunoglobulin deficiency diseases of the intestine.

Marshak has emphasized the role of the gastrointestinal tract as a major immunologic organ and described the radiologic findings of immunoglobulin deficiency diseases of the small intestine. According to his classification the radiologic findings include multiple nodular defects, edema and increased secretions associated with Giardiasis, a sprue-like pattern, and thickened folds. In this report, the role of the intestine in the immune response is briefly reviewed and several of the radiologic features of immune deficiency diseases and those of benign nodular lymphoid hyperplasia are illustrated.

Adolescent↗
PubMed1977

Schizophrenia as a prostaglandin deficiency disease.

Evidence that schizophrenia may be a prostaglandin deficiency disease comes from three main sources: (1) all effective antischizophrenic drugs stimulate prolactin secretion and prolactin is a potent stimulator of prostaglandin synthesis; (2) schizophrenics are resistant to pain and inflammation and are free of rheumatoid arthritis and there is increasing evidence that prostaglandins play important roles in pain, inflammation, and rheumatoid arthritis; (3) high doses of drugs recently shown to be prostaglandin antagonists cause schizophrenia-like syndromes. The hypothesis is not necessarily inconsistent with current transmitter theories of schizophrenia since prostaglandins modify transmitter secretion and action. It does indicate radically new approaches to investigation, treatment, and drug design not suggested by the transmitter concepts.

Antipsychotic Agents↗
PubMedDate not supplied

[Effectiveness of a water iodination system for preventing iodine deficiency diseases in Central Africa].

Iodine deficiency disorders are major problems in most developing countries. According to WHO more than one billion people worldwide are at risk for iodine deficiency. However, prophylaxis programs based on the distribution of iodized salt have been unsuccessful in developing countries for socioeconomic reasons. We tested the efficacy of iodination of water with sodium iodide incorporated into silicone matrices (Rhône-Poulenc-Rorer-Doma). Nine such matrices were placed into each of the 198 wells supplying more than 90% of the 85,037 inhabitants of the Nana-Grebizi prefecture (figure 1). Efficacy was evaluated by following classical markers of iodine deficiency in representative samples of the population (figure 2): goiter size was measured immediately before (T = 0, n = 3,090) and twelve months after (T = 12, n = 2,645) installation of the matrices; and urinary iodine concentrations were assayed at T = 0 (n = 319), 6 (n = 304) and 12 (n = 261). The prevalence of goiter was 60.9% (visible goiter 10.7%, cretinism 0.7%) and the median urinary iodine concentration was 2.1 (95% confidence interval 2.0-2.3) micrograms/dl. Thus the population suffered from severe iodine deficiency. All villages were severely affected, despite inter-village variations (tables 1 and 2, figure 4). Twelve months after iodination of wells, the overall prevalence of goiter fell to 44.5% (p < 0.0001, table 1 and figure 3) and that of visible goiter to 2.5% (p < 0.0001). With the exception of one village (Bokanzi) the prevalence of goiter decreased by 18.6 to 56.3% (table 1).(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1982

Evidence of normal functional levels of activated protein C inhibitor in combined Factor V/VIII deficiency disease.

Human activated protein C (APC) is a plasma serine protease that possesses amidolytic and anticoagulant activity. The rate at which the amidolytic and anticoagulant activity of APC was neutralized in normal plasma was essentially identical to that observed in plasma obtained from four individuals with combined Factor V/VIII deficiency disease. Incubation of radioiodinated APC with either normal human plasma or the combined Factor V/VIII-deficient plasmas resulted in the formation of a stable complex (Mr = 96,000) of the enzyme and a plasma protein as determined by sodium dodecyl sulfate-polyacrylamide gel electrophoresis. Pretreatment of the radiolabeled APC with diisopropyl fluorophosphate prevented the formation of the enzyme-protein complex. On the basis of its ability to form a complex with radiolabeled APC, the APC-binding protein was purified to homogeneity from normal human plasma by ammonium sulfate fractionation, heparin-agarose chromatography, and QAE-Sephadex A-50 chromatography. The APC-binding protein (Mr = 54,000) is a glycoprotein, and possesses an amino-terminal sequence of Gly-Arg-Thr-Cys-Pro-Lys-Pro-Asp. The amino-terminal sequence of the APC-binding protein exhibited considerable homology with bovine colostrum inhibitor and pancreatic trypsin inhibitor, but no apparent sequence homology with the plasma serine protease inhibitors. Affinity-purified antibody against APC-binding protein immunoprecipitated a complex of radiolabeled APC and native APC-binding protein from normal human plasma. Complex formation was virtually eliminated in plasma immunodepleted of the APC-binding protein. Quantitative electroimmunoassay indicated essentially equal levels of APC-binding protein antigen in normal plasma compared with plasma from four patients with combined Factor V/VIII deficiency disease.

Blood Proteins↗
PubMed1986

Pathogens in children with severe combined immune deficiency disease or AIDS.

We evaluated the frequency and severity of illnesses caused by various microbial pathogens in 15 children with severe combined immune deficiency disease (SCID) and 8 with acquired immune deficiency syndrome (AIDS). There were 35 viral, 23 bacterial, 19 mycotic and 13 parasitic infections. Nineteen of the 23 patients died of infection; Pneumocystis carinii pneumonia, giant-cell pneumonia due to paramyxoviruses and various disseminated viral infections were responsible for most deaths in both groups. The emerging role of paramyxoviruses was illustrated by the fact that they were responsible for giant-cell pneumonia in seven patients. Viral enteric infections were frequent in both groups. The variety of infectious microorganisms and the severity of resulting illnesses in the patients with AIDS were similar to those in the patients with SCID.

Acquired Immunodeficiency Syndrome↗