Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Psoriasis is a disorder of abnormal keratinocyte proliferation mediated by T lymphocytes. Initiation of psoriasis is associated with an influx and activation of CD4 T lymphocytes into the dermis and epidermis, and resolution with an influx and activation of CD8 T lymphocytes within the epidermis. As a result of these observations it was postulated that cyclosporin (CsA) should prove to be an effective treatment for psoriasis. A total of 82 patients with psoriasis have been treated with CsA. Thirty patients with moderate disease were treated for periods up to 12 weeks, and comprised a short-term study. Two groups have been treated with long-term CsA. A group of 18 patients have been treated for greater than 1 year but less than 3 years, (mean 2.1) and a group of 10 patients for 4.0-5.5 (mean 5) years. A total of 15% of patients can be maintained on less than or equal to 2 mg/kg/day; 55% on 3 mg/kg/day, 80% on 4 mg/kg/day, and 92% on 5 mg/kg/day. Hypertension occurred in 17% of patients in the short-term study, 29% in the 2.1-year group and 44% in 5-year group. Blood pressure returned to normal in all hypertensive patients when CsA was discontinued for 1 month. Nephrotoxicity was assessed by serum creatinine levels and glomerular filtration rate (GFR) and renal biopsy in the 5-year group. In the short-term group there was no significant rise in the serum creatinine.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Psoriasis: immunopathology and long-term treatment with cyclosporin. 150 22

Increases in physical fitness are often associated with improvements in certain chronic diseases, such as hypertension and coronary heart disease. Recent evidence has shown that exercise also influences the neuroendocrine and immune systems, resulting in a potential to benefit those with chronic immunodeficiency diseases. Therefore, exercise may prove to have a profound impact on the management of the acquired immunodeficiency syndrome (AIDS). Our current work includes the investigation of the immunologic and stress-attenuating effects of an aerobic exercise training program for individuals at risk for AIDS. Upon completion of training, the subjects showed a significant increase in helper/inducer (CD4) cells and the inducer subset (CD45RA+CD4+) which activate suppressor/cytotoxic (CD8) cells. These increases, which average about 50 cells per cubic millimeter, are comparable to those observed in some studies of the AIDS drug comparable to those observed in some studies of the AIDS drug azidothymidine (AZT), but without the accompanying side effects. Also, individuals undergoing aerobic training reported no increases in anxiety and depression in response to notification of a positive HIV-1 serologic status. These findings taken together indicate that an aerobic exercise training program may enhance certain critical components of cellular immunity as well as acting as a buffer for the detrimental mood changes that typically accompany stress, thus providing a timely, promising behavioral approach to helping HIV-1-infected individuals.
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PMID:Aerobic exercise training in an AIDS risk group. 168 Jan 8

Magnetic resonance (MR) scans were performed as part of a prospective neuropsychological study within the Multicenter AIDS Cohort Study. Fifty HIV-1-seronegative men, 85 HIV-1-seropositive men without constitutional symptoms, and 14 with symptomatic HIV disease underwent MR imaging using a uniform protocol. Scans were rated by neuroradiologists blinded to all clinical details except age. The majority of MR scans were normal in all of the clinical groups and no covert mass lesions or diffuse white matter abnormalities were identified. Focal hyperintensities in the white matter were observed in 24% of the HIV-1 seronegatives, 26% of HIV-1 asymptomatic seropositives (CDC II/III), and 17% of those with ARC/AIDS. No significant associations were noted between the white matter hyperintensities and HIV-1 serostatus, neurological abnormalities, CD4 count, alcohol or drug use, hypertension, or smoking. In one individual classified with early HIV-1 dementia, MR demonstrated several hyperintensities in the deep parietal white matter, but at autopsy no microscopic abnormalities corresponding to the MR findings were identified. Our studies imply that focal white matter hyperintensities identified on MR are not specific for HIV-1 infection and are probably incidental and of no clinical significance.
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PMID:Incidental white matter hyperintensities on magnetic resonance imaging in HIV-1 infection. Multicenter AIDS Cohort Study. 240 15

In order to test whether circumvention of clinical resistance can be obtained in common solid tumours by targeting different drug resistance mechanisms, a phase I clinical and immunological study was designed. The purpose of the study was to determine the dose of cyclosporin A (CsA), in combination with doxorubicin (DOX) and ifosfamide (IFX), needed to achieve steady-state whole-blood levels of 2000 ng ml-1 and the associated toxicity of this combination. Treatment consisted of CsA 5 mg kg-1 as a 2 h loading infusion, followed by a CsA 3 day continuous infusion (c.i.) (days 1-3) at doses that were escalated from 10 to 18 mg kg-1 day-1. Chemotherapy consisted of DOX 55 mg m-2 by i.v. 24 h c.i. (day 2) and IFX 2 g m-2 i.v. over 1 h on days 1 and 3. Treatments were repeated every 4 weeks. Eighteen patients with previously treated resistant solid tumours received 39 cycles. Mean steady-state CsA levels > or = 2000 ng ml-1 were reached at 5 mg kg-1 loading dose followed by a 3 day c.i. of 16 mg kg-1 day-1 or greater. Haematological toxicity was greater than expected for the same chemotherapy alone. One patient died of intracranial haemorrhage due to severe thrombopenia. Other observed toxicities were: asymptomatic hyperbilirubinaemia (46% cycles), mild nephrotoxicity (20% cycles), hypomagnesaemia (72% cycles), mild increase in body weight (100% cycles), hypertension (15% cycles) and headache (15% cycles). Overall the toxicity was acceptable and manageable. No alterations in absolute lymphocyte number, the lymphocyte subsets studied (CD3, CD4, CD8, CD19) or CD4/CD8 ratio were observed in patients receiving more than one treatment cycle, although there were significant and non-uniform variations in the values of the different lymphocyte subsets studied when pre- and post-treatment values were compared. There was also a significant increase in the CD4/CD8 ratio. Tumour regressions were observed in two patients (epidermoid carcinoma of the cervix and Ewing's sarcoma). The CsA dose recommended for phase II trials is a 5 mg kg-1 loading dose followed by a 3-day c.i. of 16 mg kg-1 day-1 simultaneously with DOX and IFX at the doses administered in this study.
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PMID:Cyclosporin A and doxorubicin-ifosfamide in resistant solid tumours: a phase I and an immunological study. 757 85

Human anti-CD4 IgG antibodies from 3 HIV-1-infected patients were affinity purified and shown to inhibit HIV-1 binding and infection of HBP-T cells. Lymphocytes from patient A, whose anti-CD4 inhibited HIV-1 binding by 68% and infection by 72%, were cultured and transformed with EBV. A human monoclonal antiidiotype antibody against anti-HIV-1 gp120 (2B) was produced, which inhibited infection of HBP-T cells by 68% at 1 microgram/ml. Mice were immunized with 2B to determine whether this anti-CD4 could be an internal image antiidiotype against anti-HIV-1 gp 120 (Ab1). Two mice produced antisera reactive with rgp120 on ELISA, whereas immunization with normal IgG produced minimal reactivity compared to unreactive normal mouse sera. However, immunoblot competition studies in which affinity-purified anti-HIV-1 gp120 (Ab1) bound to the gp120 band on nitrocellulose strips in the presence of 2B demonstrated enhancement of signal (i.e., binding of Ab2 to Ab1), rather than inhibition of Ab1 binding. Thus 2B is not an internal image of the paratope of anti-HIV-1 gp120 but yet it is capable of inducing an antibody against rgp120. This indicates that the anti-CD4 (Ab2) does bind to the binding site of Ab1, but not as a complete internal image. These data indicate the production of a human monoclonal antiidiotype antibody that inhibits binding of HIV-1 to CD4 and induces the production of antibody against HIV-1 gp120, without being an internal image antiidiotype (Ab2 beta).
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PMID:Production of a human anti-CD4 monoclonal antibody with antiidiotype to anti-HIV type 1 glycoprotein 120. 763 65

Pregnancy is associated with modifications in the maternal immune system that may be involved in the absence of rejection of the fetoplacental graft characterized by the presence of paternal antigens. This active and specific tolerance towards the fetoplacental unit seems to be compromised in pregnancy-induced hypertension (PIH). To evaluate whether the immunological state in patients with PIH is altered with respect to normal pregnant women we studied 15 patients with PIH, 15 uncomplicated pregnant and 10 healthy nonpregnant women using monoclonal antibodies directed to specific lymphocyte antigen determinants, cytokines (TNF) and soluble molecules (sIL-2R, sCD8). The percentage of CD4 lymphocytes and of natural killer (NK) cells was significantly higher in PIH patients compared to controls (CD4: 42.9 +/- 10.5 vs. 32.7 +/- 12.5%; p < 0.05; NK: 14.7 +/- 6.3 vs. 8.3 +/- 3.4%; p < 0.01). However, these values did not differ when compared to normotensive nonpregnant controls (CD4: 53.1 +/- 5.9%; NK: 17.2 +/- 7.1%). In addition, the soluble IL-2 receptor (sIL-2R) was higher in PIH patients when compared to control patients (725.5 +/- 194.2 vs. 482.5 +/- 187.2 U/ml; p < 0.01). The immune response observed in normal pregnancies responsible for the tolerance towards the fetoplacental unit seems to be altered in PIH patients as suggested by higher levels of CD4 and NK cells, and sIL-2R. This may lead to a chronic rejection syndrome and be involved in the pathophysiology of PIH.
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PMID:Cell-mediated immunity imbalance in pregnancy-induced hypertension. 785 7

The case of a renal transplant recipient with a known history of iv drug abuse but unknown human immunodeficiency virus (HIV) status who presents after having a stable renal allograft function for 4 yr, with acute/subacute advanced renal failure, nephrotic syndrome, and hypertension, as well as clinical and histologic findings of thrombotic microangiopathy, is reported. He was subsequently found to have a positive serology for HIV-1 with a low CD4 count but no clinical manifestations of the acquired immunodeficiency syndrome. He was treated conservatively with zidovudine (AZT). The patient never regained graft function and was ultimately discharged from the hospital on maintenance dialytic therapy. This is, to our knowledge, the first report of thrombotic microangiopathy in an HIV-1-infected patient presenting late in the course as acute/subacute renal allograft failure.
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PMID:Late renal allograft failure secondary to thrombotic microangiopathy-human immunodeficiency virus nephropathy. 801 72

The main pathologic findings in 23 patients with acquired immunodeficiency syndrome (AIDS) and Chagas' disease are reviewed; five are from our own experience and 18 from the literature. The presence of Trypanosoma cruzi parasites and/or T. cruzi antibodies in blood and cerebrospinal fluid was recorded and computerized tomograms of the brain were evaluated. Twenty (87%) of the 23 subjects developed severe, multifocal or diffuse meningoencephalitis with necrosis and hemorrhage associated with numerous tissue parasites. The second most severely affected site was the heart. Seven (30.4%) of the 23 cases had myocarditis on pathologic examination. It was acute in four patients, chronic in two, and simultaneously acute and chronic in one. Acute myocarditis and meningoencephalitis are interpreted as being caused by relapses of chronic T. cruzi infections. An AIDS permissive role is suggested for these conditions since immunologic defense against T. cruzi is mediated mainly by T lymphocytes, whose CD4 subpopulation is depleted in patients with this disease. Consequently, AIDS is a factor that may favor the reactivation of T. cruzi infections. The lesions reported in the association of Chagas' disease with AIDS were compared with those reported from patients without AIDS having fatal, acute, vector-transmitted infections, contaminated blood transfusions, or accidental exposures in the laboratory. For the latter three, meningoencephalitis is uncommon. Only immunosuppressed cases of Chagas' disease have been described as having a pseudotumoral presentation that shows expanding lesions with a mass effect in the cranial cavity that causes intracranial hypertension and simulates neoplasms (tumors such as gliomas, lymphomas, metastases, etc.).
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PMID:Pathology of patients with Chagas' disease and acquired immunodeficiency syndrome. 814 85

Incidence, type and clinical significance of cardiac involvement in advanced HIV infection was determined in 32 patients (30 men, two women; mean age 34.2 [21-52] years; mean CD4-cell number 52.2 [0-192]/microliters) over a period of 31 months. Any cardiac involvement was assessed diagnostically by one- and two-dimensional and Doppler echocardiography, complemented by other examinations and results of treatment. 14 patients (43.8%) had abnormal cardiac findings, presumably AIDS-associated. This included left ventricular pump dysfunction of various degrees of severity (n = 11), left ventricular dilatation (n = 2), pericardial effusion (n = 11), as well as cor pulmonale in primary pulmonary arterial hypertension (n = 2). In one patient the first manifestation of AIDS was tubercular pericarditis; in two patients there was a likely connection to disseminated pneumocystis infection and toxoplasmosis, respectively. In 11 patients no specific cause was found for the cardiac involvement. Nine of the 14 patients (64%) had symptoms due to the cardiac involvement. These findings indicate that the incidence and clinical significance of cardiac involvement must be taken into account in any treatment concept for AIDS.
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PMID:[Cardiac manifestations in advanced HIV infection]. 818 20

The feasibility of on-site primary care services and their use by human immunodeficiency virus HIV-seropositive and seronegative injecting drug users within an outpatient methadone maintenance program are examined. A 16-month prospective study was conducted within an ongoing cohort study of HIV infection at a New York City methadone program with on-site primary care services. The study group consisted of 212 seropositive and 264 seronegative drug injectors. A computerized medical encounter data base, with frequencies of primary care visits and with diagnoses for each visit, was linked to the cohort study data base that contained information on patients' demographic characteristics, serologic status, and CD4+ T-lymphocyte counts. Eighty-one percent of the drug injectors in the study voluntarily used on-site primary care services in the methadone program. Those who were HIV-seropositive made more frequent visits than those who were seronegative (mean annual visits 8.6 versus 4.1, P < .001), which increased with declining CD4+ T-lymphocyte counts; 79 percent of those who were seropositive with CD4 counts of less than 200 cells per cubic millimeter received on-site zidovudine therapy or prophylaxis against Pneumocystis carinii pneumonia, or both. Common primary care diagnoses for patients seropositive for HIV included not only conditions specific to the human immunodeficiency virus but also bacterial pneumonia, tuberculosis, genitourinary infections, asthma, dermatologic disease, psychiatric illness, and complications of substance abuse; those who were seronegative were most frequently seen for upper respiratory infection, psychiatric illness, complications of substance abuse, musculoskeletal disease, hypertension, asthma, and diabetes mellitus. Vaginitis and cervicitis,other gynecologic diseases, and pregnancy were frequent primary care diagnoses among both seropositive and seronegative women.
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PMID:Utilization of on-site primary care services by HIV-seropositive and seronegative drug users in a methadone maintenance program. 839 79


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