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Results for “Immunologic Deficiency Syndromes”

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At least 793 records · Page 44Linked to original sources
PubMed1981

Nonspecific alpha-naphthyl acetate esterase activity of T-lymphocytes: study in healthy newborns and children, in immune deficiencies and juvenile rheumatoid arthritis.

The aim of this study was to compare the E rosette-forming cells and nonspecific alpha naphthyl esterase (ANAE)-positive lymphocyte values in normal and pathologic situations. In newborns, the ANAE-positive lymphocytes represented less than 60% of the E rosette population. During the first year of life, E rosette-forming cells (E-RFC) reached normal values as soon as one month whereas only three-fourths of the T cells exhibited an ANAE-positive staining. In adult T cell populations, nearly 90% were ANAE-positive. Our observations of immune deficiencies suggested that the relative proportions of E-RFC and ANAE-positive lymphocytes were generally comparable to normal values. However, in the majority of the patients with very low or absent E-RFC (severe combined immune deficiencies, Di George syndrome, and congenital rubella), some ANAE-positive lymphocytes could be detected. Our immunologic survey shows that the ANAE-positive lymphocytes were in a normal range 2 years after a bone marrow transplantation in severe combined immune deficiencies patients. One child who exhibited a normal amount of E-RFC and whose lymphocytes failed to respond in vitro to mitogens had practically no ANAE-positive lymphocytes. An elevated amount of ANAE-positive cells in juvenile rheumatoid arthritis may reflect an augmentation of the T helper functions which permanently stimulated in vivo immunoglobulin production.

Adolescent↗
PubMed1989

Pneumocystis carinii pneumonia in HIV-positive and HIV-negative patients. An epidemiological, clinical and histopathological study of 18 patients.

Pulmonary histopathological and clinical changes associated with Pneumocystis carinii pneumonia (PCP) were found to be less severe in 10 HIV-positive patients (group A) with acquired immunodeficiency syndrome (AIDS) than in 8 patients (group B) with other immune deficiencies. Lung biopsies from group A showed minimal thickening of the alveolar walls from oedema and slight mononuclear cell infiltration, while in group B alveolar wall thickening was more prominent with distinct mononuclear cell infiltration and evidence of diffuse alveolar damage and interstitial fibrosis. Infection with P. carinii cysts was heavy in 60%, moderate in 30% and mild in 10% in group A patients v. heavy in 0%, moderate in 14% and mild in 86% in group B patients. These findings appear to suggest that AIDS/PCP presents with a heavy parasite load but only minimal histopathological changes that are reversible and that atypical change as observed in PCP in other immune deficiencies are caused by previous or concomitant insults other than pneumocystosis. Milder propagation of P. carinii in HIV-negative patients may be because there is a lack of undamaged type I pneumocytes to which trophozoites probably need to be attached at a certain developmental stage.

Acquired Immunodeficiency Syndrome↗
PubMed1981

Multiple congenital anomalies, thymic dysplasia, severe congenital heart disease, and oligosyndactyly with a deletion of the short arm of chromosome 5.

A female infant was born at term with congenital anomalies and a deletion of the short arm of chromosome 5. The anomalies included thymic dysplasia and lymphocyte-depleted nodes of the type seen in combined immune deficiency; atrial and ventricular septal defects, pulmonary valve atresia, and anomalous pulmonary-bronchial communication through the lungs; and shortness of forearms with syndactyly of fingers. A review indicates that the association of cardiac lesions, thymic dysplasia, oligosyndactyly and deletion of chromosome 5p is unique.

Abnormalities, Multiple↗
PubMed1979

Evidence for defective immunoregulation in the syndrome of familial candidiasis endocrinopathy.

We studied three children with candidiasis endocrinopathy syndrome, together with their parents and five siblings, to explore the possibility that defective immunoregulation allows autoimmune phenomena to be involved in the pathogenesis of this syndrome. Inheritance of the syndrome appeared to be autosomal recessive. Immunologic abnormalities in this family included hypergammaglobulinemia, selective IgA deficiency, anergy, autoimmune endocrinopathies and active chronic hepatitis. Defective suppressor T-cell function was noted in the two surviving children with clinically apparent disease and in a clinically normal sibling. Analysis of the immunologic abnormalities in the family suggests that defective immunoregulation rather than disordered effector mechanisms may explain the large number of immunologic defects noted. These defects, in turn, may result in the clinical manifestation of the syndrome.

Adolescent↗
PubMed1983

Immunodeficiency.

Explore the source record for details and available documents.

Acquired Immunodeficiency Syndrome↗
PubMed1985

[Opportunistic Toxoplasma gondii infections].

In children with cellular immune deficiency, toxoplasmosis may result in severe infection, chiefly because of cerebral impairment presenting as meningo-encephalitis or as a pseudo-tumoral syndrome. Allogenic bone marrow transplantation or AIDS are high risk situations. Most often it is a reviviscence of former foci toxoplasma cysts. Diagnosis is difficult because serology is not contributive. Isolation of trophozoites in the cerebrospinal fluid is rare. CAT scan and sometimes cerebral biopsy allow unquestionable diagnosis. Early treatment (pyrimethamine, sulfadiazine, spiramycine) may lead to complete recovery.

Acquired Immunodeficiency Syndrome↗
PubMed1982

Malabsorption syndrome, coccidiosis, combined immune deficiency, and fulminant lymphoproliferative disease.

Coccidia were found in a patient suffering from malabsorption syndrome. In addition, immunologic investigation showed combined humoral and cellular immunodeficiency. Treatment with metronidazole induced the disappearance of coccidia from the stool and clinical remission. Six months later, the patient was seen with acute lymphoproliferative disease and died thereafter. The possible relationship between malabsorption, immunodeficiency, coccidiosis, metronidazole, and malignancy is reviewed.

Adult↗
PubMed1988

[Induction of immunologic deficiency by benzene and its correction by administration of anabol].

Cellular immunity and activity of enzymes of xenobiotic metabolism have been investigated. It has been shown that administration of benzene induces a stable immune deficiency syndrome characterized by a decrease in the quantity if antibody-forming cells, T-killers and T-suppressors. The activity of enzymes (cytochrome P-450 and cytochrome C reductase) was also inhibited. It has been shown that anabol can stimulate the parameters of cellular immunity and enzyme activity. Benzene intoxication was demonstrated to be a model of immune deficiency syndrome similar to the clinical pattern. Anabol was shown to be an effective immunomodulator.

Adjuvants, Immunologic↗