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)

Over a 2-year period, thyroid function was studied in 102 patients infected with the human immunodeficiency virus (HIV) and in 102 age- and sex-matched controls with various infectious diseases. Biochemical abnormalities were observed in 1-20% of the patients, depending on thyroid indices, but thyroid disease (hypothyroidism) was diagnosed in only 1. Compared to controls, patients, especially those with the acquired immunodeficiency syndrome (AIDS), had a significant increase in serum thyroxine-binding globulin, a lower T3 and free thyroxine index, and a higher frequency of thyroglobulin antibodies.
Thyroid 1991
PMID:Biochemical thyroid profile in patients infected with the human immunodeficiency virus. 182 60

The pathogenesis of human autoimmune diseases, including Graves' disease, remains to be elucidated. Recently, Ciampolillo et al. proposed that human immunodeficiency virus type 1 (HIV-1)-related retroviruses were involved in Graves' disease. Using Southern blot analysis, they found specific integration of exogenous sequences homologous to HIV-1 gag region in genome DNA of thyrocytes and peripheral blood lymphocytes (PBL) of patients with Graves' disease. In order to test their hypothesis, we examined the presence or the absence of HIV-1 gag-related sequences in Japanese Graves' patients using the polymerase chain reaction (PCR) in addition to Southern blotting. Sets of primer pairs used in PCR were designed to cover the whole span of the HIV-1 gag region. Hybridization was performed in both relaxed and stringent conditions. Our results showed that neither Southern blot hybridization nor PCR gave positive signals in any of the samples examined from Graves' patients. This suggests that HIV-1 or its closely associated viruses are unlikely to be involved in the pathogenesis of Graves' disease in Japan.
Thyroid 1991
PMID:Lack of evidence for the presence of human immunodeficiency virus type 1-related sequences in patients with Graves' disease. 184 30

A 49-yr-old homosexual man with acquired immunodeficiency syndrome presented with a left-sided neck mass. He was found to have a firm goiter. He was clinically euthyroid, but had laboratory evidence of primary hypothyroidism. Radioactive iodine scan of the thyroid showed homogeneous uptake over an enlarged right lobe and absence of uptake over the left lobe. Two fine needle aspiration biopsies of the thyroid revealed the presence of Pneumocystis carinii (P. carinii) organisms on the Gomori's methenamine silver strain. After courses of iv and oral therapy with trimethoprim-sulfamethoxazole, a third fine needle aspiration biopsy failed to reveal any organisms. A repeated radioactive iodine scan of the thyroid showed return of uptake over the left lobe. Thyroid function tests normalized with levothyroxine, and the goiter decreased in size. To our knowledge, this is the first report of hypothyroidism associated with P. carinii infection of the thyroid. P. carinii infection should be considered in the differential diagnosis of human immunodeficiency virus infected individuals presenting with cold thyroid nodules. Fine needle aspiration biopsy is a valuable tool in assessing these patients.
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PMID:Pneumocystis carinii infection of the thyroid in a hypothyroid patient with AIDS: diagnosis by fine needle aspiration biopsy. 199 26

Thyroid hormone (T3) receptor (T3R) regulates the human immunodeficiency virus type 1 (HIV-1) long terminal repeat (LTR) by binding to and activating thyroid hormone response elements (TREs) embedded within the viral NF-kappa B and Sp1 motifs. The TREs within the NF-kappa B sites are necessary for activation by T3 in the absence of Tat, while those in the Sp1 motifs function as TREs only when Tat is expressed, suggesting that Tat and T3R interact in the cell. Transactivation of the HIV-1 LTR by T3R alpha and several receptor mutants revealed that the 50-amino-acid N-terminal A/B region of T3R alpha, known to interact with the basal transcription factor TFIIB, is critical for activation of both Tat-dependent and Tat-independent responsive sequences of the LTR. A single amino acid change in the highly conserved tau 1 region in the ligand-binding domain of T3R alpha eliminates Tat-independent but not Tat-dependent activation of the HIV-1 LTR by T3. Ro 5-3335 [7-chloro-5-(2-pyrryl)-3H-1,4-benzodiazepin-2(H)-one], which inhibits Tat-mediated transactivation of HIV-1, also inhibits the functional interaction between Tat and T3R alpha. Binding studies with glutathione-S-transferase fusion proteins and Western (immunoblot) analysis indicate that T3R alpha interacts with Tat through amino acids within the DNA-binding domain of T3R alpha. Mutational analysis revealed that amino acid residues in the basic and C-terminal regions of Tat are required for the binding of Tat to T3R alpha, while the N terminus of Tat is not required. These studies provide functional and physical evidence that stimulation of the HIV-1 LTR by T3 involves an interaction between T3R alpha and Tat. Our results also suggest a model in which multiple domains of T3R alpha interact with Tat and other factors to form transcriptionally important complexes.
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PMID:Interactions of thyroid hormone receptor with the human immunodeficiency virus type 1 (HIV-1) long terminal repeat and the HIV-1 Tat transactivator. 760 79

Thyroid dysfunction has been reported following single dose and fractionated radiation in the context of bone marrow transplantation (BMT). Limited data are available regarding this complication following hyperfractionated radiation. We undertook a retrospective analysis of thyroid function in 150 patients who received BMT at our institution, and who were alive and disease-free for at least 1 year after transplant. There were 100 pediatric patients and 50 adult patients, with a median follow-up of 6.2 years for the whole group. These patients had acute (n = 91) or chronic leukemias (n = 36), severe aplastic anemia (n = 18) or immunodeficiency disorders (n = 5). The majority of the patients received radiation-based cytoreductive regimens including 129 patients who received hyperfractionated total body irradiation (TBI) to a total dose of 1375 cGy or 1500 cGy and 10 patients who received total lymphoid irradiation (TLI) to a total dose of 600 cGy. Twenty two patients of the cohort of 150 patients (14.7%) and 21 of the 139 patients (15.1%) who received hyperfractionated radiation were found to have developed hypothyroidism, 11-88 months after transplant (median 49 months). Eight patients had received 1375 cGy and 12 patients 1500 cGy TBI, while one patient was treated with 600 cGy TLI and one patient was treated with chemotherapy only (busulfan and cyclophosphamide). Three patients had primary thyroid failure with an elevated TSH and a low T4 index, while 19 patients had compensated hypothyroidism with an elevated TSH but a normal T4 index. Six of eight patients with untreated compensated hypothyroidism recovered spontaneously.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Thyroid dysfunction following bone marrow transplantation using hyperfractionated radiation. 774 58

Human immunodeficiency virus (HIV) infection is associated with altered levels of glutathione (GSH) in cells and extracellular fluids. GSH is essential for lymphocyte proliferation and inhibits HIV replication. Therefore, determination of GSH and glutathione disulfide (GSSG) levels could be useful as indicators of the progression of the disease. Thyroid hormone levels are altered in acquired immuno-deficiency syndrome (AIDS), such that thyroid hormone might be a useful prognostic indicator of the severity of AIDS. Pneumocystis carinii pneumonia (PCP) is a debilitating disease of the lung that can accompany HIV infection. The effects of pulmonary infections were assessed in AIDS patients on thyroid hormone, GSH, GSSG levels and other parameters. Two groups of AIDS patients were selected, a group with PCP and a control group with other respiratory diseases. GSH was evaluated in plasma, pulmonary lavage fluid, pulmonary biopsy tissue and buccal cells. Levels of GSSG in pulmonary lavage fluid were higher in PCP patients than in controls, which suggests that PCP patients suffer from oxygen radical toxicity in their lungs. PCP patients may have altered plasma GSH utilization such that damaged lung tissue may become less efficient at using plasma GSH. Patients with PCP may have altered CD4 cell functions such that thyroid hormone levels do not correlate with CD4 cell counts. Patients with AIDS and secondary infections of the lung were found to have altered GSH redox states, probably indicative of physiologic adaptation to AIDS.
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PMID:Pneumocystis carinii pneumonia in HIV infected patients: effects of the diseases on glutathione and glutathione disulfide. 818 48

Thyroid function was evaluated in 119 human immunodeficiency virus (HIV) infected patients at different stages of infection, compared with euthyroid normal subjects and hepatitis C virus infected blood donors as control groups. The low T3 state, well documented in severe nonthyroidal illnesses, was not found in these HIV infected patients. They showed lower FT4 levels and higher TSH and TBG values than euthyroid normal controls. These findings suggested a thyroid hypofunction becoming more evident with the progression of the infection as also supported by the presence of antithyroid autoantibodies mainly found in the symptomatic stages of the infection.
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PMID:Thyroid hypofunction related with the progression of human immunodeficiency virus infection. 837 Sep 15

Thyroid function and regulation were studied in 14 consecutive male outpatients with asymptomatic human immunodeficiency virus (HIV) infection (CDC II/III, n = 8) or AIDS (CDC IV, n = 6) who were free of concomitant infections and hepatic dysfunction, and in eight healthy, age- and weight-matched male controls. Blood was sampled every 10 minutes over 24 hours for measurement of thyrotropin (TSH). Thereafter, thyroid hormones and TSH responsiveness to thyrotropin-releasing hormone (TRH) were measured. Triiodothyronine (T3) and thyroxine (T4) did not differ between HIV-infected patients and controls, but HIV patients had lower thyroid hormone-binding index ([THBI] HIV patients, 1.01 +/- 0.02; controls, 1.11 +/- 0.03; P < .02), free thyroxine (FT4) index (94 +/- 3 v 110 +/- 4, P < .01), FT4 (11.8 +/- 0.4 v 14.3 +/- 0.4 pmol/L, P < .01), and reverse triiodothyronine (rT3) values (0.18 +/- 0.01 v 0.26 +/- 0.02 nmol/L, P < .001) and higher thyroxine-binding globulin ([TBG] 20 +/- 1 v 16 +/- 1 mg/L, P < .02) values. Mean 24-hour TSH levels were increased in HIV patients (2.39 +/- 0.33 v 1.44 +/- 0.16 mU/L, P < .05), associated with increased mean TSH pulse amplitude and TSH responsiveness to TRH. No differences were observed between asymptomatic HIV-seropositive and AIDS patients. In conclusion, there is a hypothyroid-like regulation of the pituitary-thyroid axis in stable HIV infection, which differs distinctly from the euthyroid sick syndrome in non-HIV-nonthyroidal illnesses.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hypothyroid-like regulation of the pituitary-thyroid axis in stable human immunodeficiency virus infection. 849 9

Clinical, biochemical and immunological evidence suggests that thyroid hormones would be helpful in human immunodeficiency virus disease either by itself or as an adjuvant to present-day therapies. During prolonged non-thyroidal illnesses such as human immunodeficiency virus disease, thyroid function tests could be misleading or difficult to interpret. Human immunodeficiency virus disease could mask a hypothyroid state which might be intracellular. Thyroid hormones are the only consistent natural stimulator of both the primary lymphoid tissue (thymus and bone marrow) and secondary lymphoid tissue (circulating lymphocytes, spleen and lymph nodes). There is abundant historical precedent for using thyroid hormone as a safe pharmacological agent against human immunodeficiency virus disease.
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PMID:Thyroid hormone therapy in patients infected with human immunodeficiency virus: a clinical approach to treatment. 889 24

We analyzed the kinetics of CD4 cells, human immunodeficiency virus (HIV) viral load, and autoantibodies in acquired immune deficiency syndrome patients with Graves' disease (GD) after immune restoration on highly active antiretroviral therapy (HAART; retrospective study). Five patients (median age, 41 yr) were diagnosed with GD after 20 (range, 14-22) months on HAART on the basis of clinical and biological hyperthyroidism, diffuse hyperfixation of thyroid scan, and the presence of anti-TSH receptor (anti-TSHR) antibodies (Ab). GD was diagnosed several months after the plasma HIV ribonucleic acid load became undetectable, when the CD4+ cell count had risen from 14 (range, 0-62) to 340 (range, 163-460) x 10(6) cells/L. Antithyroid peroxidase (anti-TPO) and anti-TSHRAb appeared 14 (range, 9-18) and 14 (range, 11-20) months after starting HAART and 12 (range, 6-15) and 11 (range, 9-17) months after the increase in CD4+ cells. In 3 patients, TPOAb preceded TSHRAb by 3-10 months. No other autoantibodies were detected. Thyroid antibodies were absent in a group of 55 HIV-1-positive patients with comparable response to HAART and no symptoms of hyperthyroidism (cross-sectional study). Thyroid-specific autoimmunity can occur upon immune restoration with HAART. Our observations suggest a relationship between thymus-dependent immune reconstitution after immunosuppression and autoimmunity and may provide insight into the pathophysiology of GD.
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PMID:Sequential occurrence of thyroid autoantibodies and Graves' disease after immune restoration in severely immunocompromised human immunodeficiency virus-1-infected patients. 1109 63


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