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Query: UMLS:C0019693 (HIV)
 170,526 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

There is compelling evidence that micronutrients can profoundly affect immunity. We surveyed vitamin supplement use and circulating concentrations of 22 nutrients and glutathione in 64 HIV-1 seropositive men and women and 33 seronegative controls participating in a study of heterosexual HIV-1 transmission. We assayed antioxidants (vitamins A, C, and E; total carotenes), vitamins B6 and B12, folate, thiamin, niacin, biotin, riboflavin, pantothenic acid, free and total choline and carnitine, biopterin, inositol, copper, zinc, selenium, and magnesium. HIV-infected patients had lower mean circulating concentrations of magnesium (p < 0.0001), total carotenes (p = 0.009), total choline (p = 0.002), and glutathione (p = 0.045), and higher concentrations of niacin (p < 0.0001) than controls. Fifty-nine percent of HIV+ patients had low concentrations of magnesium, compared with 9% of controls (p < 0.0001). These abnormal concentrations were unrelated to stage of disease. Participants who took vitamin supplements had consistently fewer low concentrations of antioxidants, across HIV infection status and disease stage strata (p = 0.0006). Nevertheless, 29% of the HIV+ patients taking supplemental vitamins had subnormal levels of one or more antioxidants. The frequent occurrence of abnormal micronutrient nutriture, as found in these HIV+ subjects, may contribute to disease pathogenesis. The low magnesium concentrations may be particularly relevant to HIV-related symptoms of fatigue, lethargy, and impaired mentation.
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PMID:Micronutrient profiles in HIV-1-infected heterosexual adults. 862 65

The purpose of this study was to describe the frequency and duration of clinical features at the time of acute human immunodeficiency virus type 1 (HIV-1) disease in 218 patients with documented symptomatic primary HIV-1 infection. The mean duration of acute HIV-1 disease was 25.1 days (median, 20.0 days) and did not differ by gender, age, and risk factor. The frequency and mean duration of clinical features occurring in >50% of patients were as follows: fever, 77.1% and 16.9 days; lethargy, 65.6% and 23.7 days; cutaneous rash, 56.4% and 15 days; myalgia, 54.6% and 17.7 days; and headache, 50.9% and 25.8 days. Only 15.6% of patients presented with a typical mononucleosis-like illness (MLI) defined as fever, pharyngitis or sore throat, and cervical adenopathy, and 10% had no features of an MLI. A meningitis-like syndrome occurred in 20 patients (9.2%). Acute HIV-1 disease is more diverse than previously reported, and the absence of fever or other MLI features does not rule out acute HIV-1 disease.
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PMID:Acute human immunodeficiency virus type 1 disease as a mononucleosis-like illness: is the diagnosis too restrictive? 914 2

The housing status of persons with HIV/AIDS is a central issue in their care and prognosis. We conducted eight focus groups to explore the housing needs of special populations of persons with HIV/AIDS in New York State; these populations included substance users, ex-offenders, persons with documented histories of homelessness, and rural dwellers/migrant workers. For the focus groups, 52 participants were recruited from the clientele of health and social service agencies. A major theme was the potent effect that housing situations had on participants' health. Participants frequently attributed lowered T-cell counts and increased lethargy to the stress associated with governmental rules and paperwork. Lack of money, inadequacy of entitlements, and high costs of housing were the major barriers to securing stable and appropriate housing. Furthermore, participants experienced housing discrimination based on HIV status and experience with the criminal justice system or drugs.
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PMID:Housing issues of persons with AIDS. 966 75

RSV is the most important respiratory pathogen in infants and young children. About 1% of primary RSV infections result in hospitalization. The virus is spread by large droplets of secretions or contact with contaminated secretions. Infants infected with RSV may demonstrate poor feeding, rhinorrhea, apnea, lethargy, wheezing, and respiratory distress. Diagnosis may be made by clinical signs and symptoms (especially those observed during epidemics), by chest radiographs showing hyperinflation, or by rapid antigen detection with immunofluorescence of nasopharyngeal aspirates. Risk factors for severe disease accompanied by complications include chronic heart disease, chronic lung disease, immunodeficiency, HIV, and prematurity. Immunity is incomplete and of short duration, and reinfection is common. Treatment remains supportive and consists of oxygen administration, hydration, and diligent monitoring. Use of corticosteroids, bronchodilators, antibiotics, and ribavirin is controversial and is dependent largely on physician preference. Use of ribavirin should be reserved for patients who have severe underlying conditions associated with increased mortality rates. Intravenous RSV Ig has been replaced by palivizumab, which is generally recommended for infants at high risk for severe RSV, including those with a history of prematurity and those with chronic lung disease.
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PMID:RSV infection in infants and young children. What's new in diagnosis, treatment, and prevention? 1060 68

A 53-year-old woman with newly diagnosed HIV infection was treated with the nucleoside analogue antiretroviral agents lamivudine and stavudine and the protease inhibitor indinavir. An illness characterized by severe lethargy, persistent nausea and vomiting, lactic acidosis, hyperglycemia, and microvesicular hepatic steatosis developed. Her symptoms improved gradually after withdrawal of the antiretroviral agents. The illness can be explained by mitochondrial dysfunction caused by inhibition of mitochondrial DNA (mtDNA) polymerase by the nucleoside analogues. The patient was successfully treated with nonnucleoside reverse transcriptase inhibitors, which lack affinity for mtDNA polymerase.
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PMID:Lactic acidosis secondary to nucleoside analogue antiretroviral therapy. 1106 7

Tumor necrosis factor (TNF, cachectin), a cytokine secreted by macrophages and T-cells, mediates inflammatory and immune responses, and is associated with wasting in persons with malignancies or AIDS. In inflammation, TNF attracts and activates neutrophils, stimulating phagocytic function of neutrophils and macrophages. TNF also increases hepatic cell resistance to damaging parasitic effects; enhances endothelial permeability, causing edema; aids in wound healing by stimulating tissue and vascular growth; enhances lymphocytic activity through cytokine activation; acts with interleukin (IL) to produce fever, anorexia, lethargy and sleep; and possesses antitumor activity, particularly against the presumed origin of Kaposi's sarcoma, capillary endothelial cells. The host has an acute phase response (APR) following TNF- and IL-induced immunologic activation. TNF and IL decrease production and activity of lipoprotein lipase (LPL), resulting in reduced uptake and improper storage of fat; and they stimulate anabolism of fatty acids, causing hypertriglyceridemia. This "futile cycling" causes shuttling of fatty acids between adipose tissue and the liver, and use of muscle protein as the main fuel source. This, along with further muscular breakdown due to the increased caloric demands of fever, may affect cachexia. TNF benefits the HIV-infected through selective killing of HIV-infected cells, although effects may be dose and time dependent. The negative effects of TNF may be impeded by anti-cytokine therapy. Possible therapies include dietary N-3 fatty acid (fish oil), an inhibitor of TNF and IL production in vitro; pentoxifylline (Trental), another TNF production inhibitor; anti-TNF monoclonal antibodies; and soluble TNF receptors.
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PMID:Tumor necrosis factor: its role in HIV/AIDS. 1136 96

A review of data on HIV and depression fails to show any direct cause-and-effect relationships between the two, despite the fact that clinical depression is the most commonly seen psychiatric disorder in patients with HIV infection. Most of the HIV-positive individuals with depressive disorders were found to have a history of depression antedating their infection. Contradicting early reports of unusually high rates of depression among HIV patients, more recent studies show that depression levels are not higher for the seropositive versus the seronegative, nor do the levels increase over time or at different stages of the infection. Persons with HIV may be misdiagnosed as depressed because the somatic symptoms of the illness--fatigue, lethargy, weight loss, loss of appetite, and low libido--are also symptoms of depressive disorders. Practitioners are urged to distinguish loss of interest, per se, from loss of interest in activities due to medical problems. When HIV-infected patients are diagnosed as clinically depressed, they respond as well as seronegative patients to antidepressant medications, such as tricyclic antidepressants, serotonin reuptake inhibitors (SRRI's), and psychostimulants. Brief, focused psychotherapy can prove helpful for assisting HIV-positive patients through times of particular vulnerability: the confirmation of HIV infection, adjusting to the seropositive status, onset of physical symptoms, and a sudden decline in T-cell counts.
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PMID:Depressive disorder and HIV disease: an uncommon association. 1136 50

In persons living with HIV/AIDS, depression can cause a variety of psychological and physical symptoms; medical treatments are readily available. When normal emotions, such as sorrow, interfere with daily living, a person may be diagnosed with depression. The percentage of HIV-positive persons suffering from depression, the severity of depression, the effect of anti-HIV treatments on depression, and whether HIV causes depression, are provided. Depression in HIV-positive people is often difficult to diagnose because the person may be hospitalized or the symptoms may be a secondary effect of the medication. It is important to keep a record of the length, the symptoms, and the possible causes of the depression. Possible signs of depression include inability to sleep, repetitive thinking of death, lethargic movement, or difficulty concentrating or remembering. Treatments for depression include tricyclic antidepressants, monoamine oxidase inhibitors, and serotonin reuptake inhibitors.
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PMID:[Depression and HIV]. 1136 48

Toxoplasma gondii is a unicellular protozoan. The definitive hosts, cats, produce hardy oocysts and sporozoites. Ingestion by a nonfeline leads to the formation of tachyzoites acutely, which cause parasitemia and further dissemination, and bradyzoites, which lead to latent infection with the formation of tissue cysts in skeletal muscle, heart muscle, and central nervous system (CNS) tissue. Toxoplasmosis can be transmitted to humans by ingestion of tissue cysts in raw or inadequately cooked infected meat or in uncooked foods that have come in contact with contaminated meat, by inadvertent ingestion of oocysts and sporozoites in cat feces, or transplacentally. Immunocompetent adults and adolescents with primary infection are generally asymptomatic, but symptoms may include mild malaise, lethargy, and lymphadenopathy. Specific treatment for nonpregnant adults and adolescents is not required. Immunosuppressed patients may experience more severe manifestations, including splenomegaly, chorioretinitis, pneumonitis, encephalitis, and multisystem organ failure. These patients are also prone to reactivation of latent infection involving the CNS. All patients with human immunodeficiency virus infection and CD4 counts <100 cells per cubic millimeter should be treated prophylactically with pyrimethamine-sulfonamide. Congenital toxoplasmosis is marked by the classic triad of chorioretinits, intracranial calcifications, and hydrocephalus. Current studies have determined that prolonged treatment (1-2 years) of neonates with fansidar is important to prevent serious sequelae. Diagnosis of acute toxoplasmosis is mainly by antibody detection and generally only undertaken in pregnant patients with risk factors for transplacental transmission. All positive screening tests in pregnant women must be confirmed at a toxoplasma reference laboratory. Recent studies have shown that polymerase chain reaction testing of amniotic fluid is useful for identification or exclusion of fetal T. gondii infection. Ultrasound can be used as an adjunct to serological screening but cannot itself definitively diagnose disease. Early-first-trimester maternal infections are less likely to result in congenital infection, but the sequelae are more severe. Transplacental passage is more common when maternal infection occurs in the latter half of pregnancy, but fetal injury is usually much less severe. Typically, infected pregnant patients are treated with pyrimethamine-sulfonamide for positive PCR-amniotic-fluid testing and with spiramycin for negative PCR-AF testing.
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PMID:Toxoplasmosis. 1137 31

Treatment of tuberculous meningitis should begin with an anti-tuberculous regimen of at least three drugs: isoniazid, pyrazinamide, and rifampin. Early in the course of therapy, ethambutol or streptomycin may be of some added benefit. If the local incidence of drug resistance to Mycobacterium tuberculosis is greater than 4%, or is unknown, then a fourth drug (ethambutol or streptomycin) should be added. If the patient is from an area with organisms resistant to multiple drugs, or is likely to be infected with a multiply resistant organism for any reason, then the patient should be on enough drugs to insure that at least two active anti-tubercular drugs are included in the therapy. An expert should be consulted Length of therapy is not standardized. For sensitive organisms, a regimen of three drugs daily for 2 months, followed by two-drug therapy (isoniazid and rifampin) has been recommended. The American Thoracic Society (ATS) and the Centers for Disease Control (CDC) have recommended a minimum of 12 months of therapy for tuberculous meningitis. If cultures remain positive for extended periods, or signs or symptoms respond slowly, therapy should be extended to 18 months. Patients with HIV also may need longer courses of therapy. The severity of tuberculous meningitis can be classified based on a system devised by the British Medical Research Council. Stage I patients are fully conscious, rational, and do not have neurologic signs. Stage II patients are confused or have neurologic signs such as cranial nerve palsy or hemiparesis. Stage III patients are comatose or stuporous with more severe neurologic signs. Corticosteroids are recommended if the patient is mentally confused, has neurologic signs, or is comatose (Stages II and III). In patients with moderate disease (Stage II), corticosteroids appear to improve neurologic sequelae and survival. Dexamethasone 6 to 12 mg per day and prednisone 60 to 80 mg per day tapered over 4 to 8 weeks has been used. Symptoms of central nervous system (CNS) inflammation may recur if the corticosteroid taper is implemented too soon or too fast. Steroids and diuretics such as furosemide and acetazolamide are sometimes used to treat hydrocephalus. Ventriculoperitoneal or ventriculoatrial shunting may be required to relieve signs and symptoms of hydrocephalus.
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PMID:Tuberculosis Meningitis. 1148 56


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