Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0021051 (immunodeficiency)
 71,517 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The presence and concentration of haemoglobin in saliva of anti-human immunodeficiency virus (HIV) positive subjects, anti-HIV-negative subjects at high risk of infection, and healthy controls were studied. One hundred eighty-eight subjects were anti-HIV-positive intravenous drug abusers (IVDA), 22 were anti-HIV-positive homosexual men, 23 were anti-HIV-positive heterosexual contacts, 132 were anti-HIV-negative IVDA, 35 were anti-HIV-negative homosexual men, and 154 were healthy controls. Two milliliters of saliva was collected in the morning before brushing teeth, and the presence and the concentration of haemoglobin were determined. Based on hemoglobin, the data show that the anti-HIV-positive IVDA have the highest tendency to bleeding. The difference between this group with respect to anti-HIV-negative IVDA (P < 0.05) and compared with healthy controls (P < 0.01) is statistically significant. This is also true of anti-HIV-positive heterosexual contacts with respect to healthy controls (P < 0.01). Our data show that all at-risk groups, both anti-HIV positive and anti-HIV negative, have higher haemoglobin concentration than the control group; this difference reaches statistical significance only between anti-HIV-positive IVDA and controls (P < 0.01). The concentration of haemoglobin is significantly higher in subjects with CD4+ lymphocytes < 200/mm3 compared to subjects with CD4+ lymphocytes > 200/mm3 (P < 0.01), in subjects with AIDS-related complex (ARC)/AIDS compared to asymptomatic/PGL subjects (P < 0.01), and in subjects with stomatitis compared to subjects without stomatitis (P < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Blood in saliva of patients with acquired immunodeficiency syndrome: possible implication in sexual transmission of the disease. 830 18

Seven of eight rhesus monkeys (RM) coinfected with simian immunodeficiency virus (SIV) and Mycobacterium leprae harboured acid-fast bacilli (AFB) at sites of dermal inoculation and/or at disseminated sites at times of humane sacrifice (up to 270 days post-M. leprae inoculation) due to SIV-induced debilitation or, in one long term survivor's case, to date over 3 years post-M. leprae inoculation. Detectable AFB were cleared in biopsies of inoculation sites of RM inoculated with M. leprae alone after 63 days postinoculation; these sites have, so far, remained AFB-negative, thereafter. Compared to animals infected with M. leprae alone, RM coinfected with SIV plus M. leprae showed: 1, completely suppressed serum antibody responses to M. leprae-specific PGL-I antigen, but strong anti-SIV Gp120 antibody responses; 2, impaired sensitization of blood mononuclear cells (MNC) to in vitro recognition of M. leprae-specific antigens in blastogenic stimulation assays; 3, impaired in vitro responses of blood MNC to nonspecific (ConA) blastogenic stimuli; and 4, early post-M. leprae inoculation, there was a significant incremental diminution of percentages of blood CD4+CD29+ T-cells in addition to the existing SIV-induced diminished percentages of CD4+CD29+ T-cells. The results indicate that humoral and cellular immune responses to M. leprae antigens are compromised in M. leprae-inoculated RM previously infected with SIV. These results provide an immunologic basis for the demonstration of enhanced M. leprae persistence or leprosy susceptibility in SIV-M. leprae coinfected RM.
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PMID:Impaired responses to Mycobacterium leprae antigens in rhesus monkeys experimentally inoculated with simian immunodeficiency virus and M. leprae. 962 93

A total of 46 Rhesus monkeys (RM) was inoculated with Mycobacterium leprae (ML) and followed clinically and immunologically for extended periods. Twenty-one (45.7%) of the RM developed leprosy spanning the known leprosy spectrum, with six of 21 (28.6%) having disease in the borderline lepromatous to lepromatous area of the spectrum. RM with paucibacillary forms of leprosy produced predominantly IgG anti-phenolic glycolipid (PGL-I) antibodies and positive lepromin skin test and/or in vitro blastogenesis responses; IgM anti-PGL-I predominated in animals with BB-LL leprosy and correlated with negative immune responses to lepromin. IgG anti-PGL-I antibodies persisted in a number of RM for several years without histopathological evidence of leprosy, suggesting possible persisting subclinical infection. The data show that RM are a valuable model for the study of leprosy. Eleven of the 46 RM were inoculated with ML from sources infected with simian immunodeficiency virus (SIV), the monkey counterpart to the human immunodeficiency virus (HIV). The possible effect of SIV on the clinical outcome of ML infection could not be determined due to insufficient numbers of animals to yield statistically significant results.
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PMID:Experimental leprosy in rhesus monkeys: transmission, susceptibility, clinical and immunological findings. 980 79

Our understanding of hereditary cancer syndromes in children, adolescents, and young adults continues to grow. In addition, we now recognize the wide variation in tumor spectrum found within each specific cancer predisposition syndrome including the risk for hematologic malignancies. An increased understanding of the genetic mutations, biologic consequences, tumor risk, and clinical management of these syndromes will improve patient outcome. In this article, we illustrate the diversity of molecular mechanisms by which these disorders develop in both children and adults with a focus on Li-Fraumeni syndrome, hereditary paraganglioma syndrome, DICER1 syndrome, and multiple endocrine neoplasia syndrome. This is followed by a detailed discussion of adult-onset tumors that can occur in the pediatric population including basal cell carcinoma, colorectal cancer, medullary thyroid cancer, and adrenal cortical carcinoma, and the underlying hereditary cancer syndromes that these tumors could indicate. Finally, the topic of leukemia predisposition syndromes is explored with a specific focus on the different categories of syndromes associated with leukemia risk (genetic instability/DNA repair syndromes, cell cycle/differentiation, bone marrow failure syndromes, telomere maintenance, immunodeficiency syndromes, and transcription factors/pure familial leukemia syndromes). Throughout this article, special attention is made to clinical recognition of these syndromes, genetic testing, and management with early tumor surveillance and screening.
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PMID:Predisposition to pediatric and hematologic cancers: a moving target. 2485 36

Castleman disease (CD) was first described and most commonly occurs in the form of classic hyaline-vascular-type CD with hyperenhancing localized (unicentric) nonneoplastic lymphadenopathy. CD may affect any body region including unusual locations for isolated lymph node enlargement. This makes CD a great mimicker of more common benign and malignant masses in the neck, chest, abdomen, and pelvis. CD masses commonly raise the suspicion of lymphoma, paraganglioma, neuroendocrine tumor, metastatic adenopathy, solid parenchymal tumors, and infectious or inflammatory diseases. The less common plasma cell-type CD, mixed CD, and human herpes virus-8-associated CD (HHV8-CD) are more prone to lead to generalized (multicentric) adenopathy without the typical nodal hyperenhancement and are associated with B symptoms and hematologic and immunologic manifestations. The generalized forms of CD have a worse prognosis, which can approach that of malignancies. CD has multiple known associations with neoplasms, skin diseases, blood dyscrasias, and immunodeficiency, which include certain forms of lymphoma; paraneoplastic pemphigus; polyneuropathy, organomegaly, endocrinopathy, M protein, and skin changes syndrome; and plasma cell dyscrasias. Cytokine overproduction (IL-6) is an important pathogenetic factor in the development of CD. The treatment is accordingly variable, from curative or diagnostic resection of a solitary lesion to systemic chemotherapy or anti-IL-6 therapy.
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PMID:The great mimickers: Castleman disease. 2492 66


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