Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0019693 (HIV)
 170,526 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

During infection with HIV, overt clinical or biochemical thyroid dysfunctions are rare. When present, thyroid failure generally results from the destruction of the thyroid gland by opportunistic infections such as Pneumocystis carinii, or tumoural processes such as KS. Less frequently, hypothalamic-pituitary failure due to central nervous system infections is involved. Some cases of thyroiditis with thyrotoxicosis or hypothyroidism due to Pneumocystis carinii have also been reported. Subtle alterations of thyroid function tests are more common in HIV infection and are sometimes already detectable in the early phase of the disease. Contrary to what is observed in severe non-thyroidal illnesses, the low T3 syndrome and the sick euthyroid syndrome are less marked; these changes are mainly present in the final stage of the disease, when anorexia and weight loss occur, and indicate a poor outcome. Unique abnormalities of thyroid function indices have also been recently documented. A progressive elevation in serum TBG--but not in other binding proteins such as CBG and SHBG--accompanying the decline of the CD4 lymphocyte count, and associated with a concomitant increase in the serum T4 value, has been reported. An unusual prolonged maintenance of normal T3 levels with a paradoxical decrease in serum rT3 values has also been recognized. Finally, a hypothyroid-like regulation of the pituitary-thyroid axis, possibly directed to limit hypermetabolism in HIV infection, has been observed. The recognition of these particular thyroid profiles is of clinical importance as serum TBG appears to be a specific marker of the progression of HIV infection and serum T3 a reliable prognostic indicator for AIDS.
 ...
PMID:Thyroid dysfunction in HIV infection. 781 Dec 24

Malnutrition and wasting are common in patients with HIV infection. Nutritional needs vary with the stage of HIV disease. Severe weight loss is associated with increased mortality in patients with AIDS and is multifactorial in development. Possible causes of weight loss include decreased food intake due to oral or GI pathology or anorexia, nutrient malabsorption, and systemic infections. Severe malabsorption is limited to patients with advanced HIV disease with CD4+ cell counts < 100 and usually < 50 cells/microliters. The spectrum of GI pathogens continues to broaden. For hypermetabolic patients, evaluation for systemic infection followed by effective antiinfective treatment is critical. For nonhypermetabolic patients, a variety of metabolic and endocrinological abnormalities may be present. It is important to recognize that micronutrient deficiencies often accompany macronutrient deficits. Providing appropriate nutritional support to patients with AIDS is fundamental to optimal medical care. Overall indications for nutritional support in a patient with AIDS are the same as in any other chronic disease. Nutritional repletion is well documented, and there are a variety of approaches to achieving appropriate intake, including volitional (megestrol or dronabinol therapy) and nonvolitional (feeding tubes and total parenteral nutrition). Parenteral nutrition should not be undertaken without preset limits. The value of nutritional pharmacology with supraphysiological doses of micronutrients has not been established.
 ...
PMID:Wasting syndrome: nutritional support in HIV infection. 781 45

Forty-five subjects with symptomatic human immunodeficiency virus type 1 (HIV-1) infection, CD4+ lymphocyte counts of > or = 150 x 10(6)/L, and Karnofsky scores > or = 60 were enrolled in a multicenter, randomized, controlled trial that compared zidovudine monotherapy and combination therapy for 48 weeks with zidovudine and interferon-alpha (IFN-alpha). Zidovudine with IFN-alpha (n = 25) had a favorable effect on CD4+ cell counts compared with zidovudine alone (n = 20). At all time points analyzed, the mean change from baseline was higher, reaching significance at week 24 (+10% versus -21%; P = .029). At week 48 the difference was -12% versus -45% (P = .07). Anti-CD3 monoclonal antibody-induced T cell reactivity improved temporarily in both groups. Serum HIV p24 antigen levels decreased maximally during the first 12 weeks of treatment. At weeks 0 and 48, polymerase chain reaction analysis for mutations at codons 67 and 215 of the HIV-1 reverse transcriptase gene conferring zidovudine resistance was conducted in 10 subjects receiving zidovudine and in 8 subjects receiving combination therapy. At week 48, 1 of 8 and 4 of 6 samples from the groups receiving zidovudine only or combination therapy, respectively, contained wild type virus at codon 215. Grade 3 or 4 toxicity was uncommon. Drug-related malaise and anorexia were observed more frequently in patients receiving both zidovudine and IFN-alpha.
 ...
PMID:Zidovudine and interferon-alpha combination therapy versus zidovudine monotherapy in subjects with symptomatic human immunodeficiency virus type 1 infection. 791 Aug 38

We report the case of a 30-years old HIV-infected woman who suffered from recurrent fever up to 41 degrees C, loss of appetite, loss of 8 kg body weight and swelling of the cervical and inguinal lymph nodes. The diagnostic work-up revealed infection with leishmania in gastric and duodenal biopsies. The parasites were also found in the inguinal lymph nodes and in the bone marrow of the patient. According to patient's history the infection was acquired on a holiday in southern spain. The patient was treated with pentavalent antimony in combination with interferon gamma. Visceral leishmaniosis in immuno-suppressed patients is discussed and therapeutic approaches are described.
 ...
PMID:[Visceral leishmaniasis with gastrointestinal involvement in a 30-year-old HIV infected patient]. 797 78

A number of reports over the last several years have linked a previously unidentified acid-fast organism with prolonged diarrhea in humans. Initially thought to be a cyanobacterium, the organism has been identified as a coccidian protozoan of the genus Cyclospora, and the name Cyclospora cayetanensis has been proposed. Organisms that resemble Cyclospora protozoa have been discovered in human stool samples around the world and have been isolated from children, immunocompetent adults, and human immunodeficiency virus (HIV)-seropositive individuals. The apparently waterborne organisms cause disease predominantly in summer months. In wet mounts of fresh stool specimens, the organisms are wrinkled spheres of 8-9 microns in diameter, with well-defined nonrefractile external walls and internal granular material, and resemble large oocysts of Cryptosporidium species. Organisms fluoresce under ultraviolet illumination. Formalin-preserved oocysts are variably acid-fast, and the results of staining with the modified carbolfuchsin technique (which is used to stain Cryptosporidium species) range from no staining to deep-red staining. The clinical syndrome is characterized by watery diarrhea (approximately 6 stools/day), nausea, anorexia, abdominal cramping, fatigue, and weight loss. Diarrhea appears to be self-limiting in the immunocompetent host but may be prolonged in patients with advanced HIV infection. Symptoms have abated in a handful of people treated with trimethoprim-sulfamethoxazole. Many questions remain to be answered about this newly identified pathogen.
 ...
PMID:Cyclospora: a newly identified intestinal pathogen of humans. 803 19

Gastrointestinal symptoms are commonly seen in patients with established AIDS. We examined the charts of 258 HIV-infected patients attending our HIV outpatient clinic to determine: (1) the frequency of gastrointestinal symptoms in unselected HIV-infected patients and (2) if there are any predictors of the development of symptoms in initially asymptomatic patients. We found the overall frequency of gastrointestinal symptoms at initial presentation in our ambulatory, predominantly homosexual population of HIV-infected patients was 35% (95% CI 30-40%) with 19% having anorexia, 15% weight loss, 14% diarrhea, and 5% dysphagia. There was no association between the presence of symptoms and stool parasites, which were found in 51% of patients. In 165 patients who were initially asymptomatic, 72% subsequently developed symptoms over 36 months of actuarial follow-up. Patients with initial T4 counts < 500 were more likely to develop symptoms. Patients with a greater degree of immunosuppression as indicated by a lower T4 count, are more likely to develop gastrointestinal symptoms.
 ...
PMID:Gastrointestinal symptoms in ambulatory HIV-infected patients. 810 92

Nutritional support of patients with HIV or acquired immune deficiency syndrome (AIDS) has many similarities to other disease states in that the same nutritional products and techniques are used. Some patients with HIV, and many with AIDS without secondary infection, experience a metabolic milieu similar to patients with cancer cachexia. In providing dietary counselling to the HIV patient, we encounter many of the obstacles that must be overcome to improve nutrition in cancer: anorexia, gastrointestinal discomfort, lethargy, and poor nutrient utilization, which limit the ability for nutritional repletion. When a secondary infection is superimposed on HIV, patients resemble more highly catabolic trauma patients or patients in the intensive care unit (ICU), where, despite aggressive efforts to feed, there is usually a net nitrogen wasting leading to the more rapid development of cachexia. However, even in this setting, feeding will limit substantially net catabolism when compared to total starvation. Because the nutritional needs of HIV patients vary greatly, individual strategies have to be designed as the patient moves through the stages of disease. Patients are generally able to consume adequate nutrition either as regular food or dietary supplements during the latency period of viral replication. Once secondary infections become prevalent, artificial diets administered by tube or by vein may be required during the period of active secondary infections, with dietary supplements often helpful during more quiescent periods. Patients with HIV are among the most challenging for clinicians providing nutritional support. Knowledge from treatment of patients with other diseases may be useful, but more data must be gathered on the unique aspects of aetiology and treatment of the anorexia, malabsorption, and ultimate wasting associated with AIDS.
 ...
PMID:Nutrition support and the human immunodeficiency virus (HIV). 811 86

The anti-tumor drug D-aspartate beta-hydroxamate (D-A beta H), selectively destroys HIV-1 infected peripheral blood mononuclear cells, but produces anorexia and nausea during prolonged treatment to AIDS patients. Consequently, based on the structural similarity between D-A beta H and the excitotoxins L-aspartate and NMDA, we have investigated the potential neurotoxic action and pharmacology of D-A beta H and of a series of chemically related anti-tumor drugs on rat primary neuronal/glial cultures. In this aim, after a 30 min exposure to D-A beta H (1-2 mM), cortical neurons were selectively destroyed within 24 h. The stereoisomer L-A beta H (0.5-2 mM) was highly neurotoxic for both glial and neuronal cells in mixed cultures but demonstrated no toxicity in glial cell cultures alone. Furthermore, for a series of D-A beta H analogues, VHS.121 and VHS.122 demonstrated a reduced but significant neurotoxicity, whereas VHS.124 and VHS.125 showed no significant neurotoxic effect, and in the case of VHS.125 also prevented D-A beta H and glutamate-mediated neurotoxicity. The related anti-tumor drugs L- or D-glutamate gamma-monohydroxamate or keto-glutamate gamma-monohydroxamate (< or = 2 mM) were not neurotoxic for cortical neurons. The neurotoxic effect of D-A beta H and L-A beta H was attenuated by the NMDA antagonists MK-801, TCP, memantine, ifenprodil, pentamidine and CGS-19755. alpha-Difluoromethylornithine, an inhibitor of polyamine biosynthesis, also protected cultures against the neurotoxicity of L-A beta H and D-A beta H.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Neurotoxic effect of the anti-HIV drug D-aspartate beta-hydroxamate for rat primary neuronal cultures: attenuation by N-methyl-D-aspartate (NMDA) antagonists. 811 99

A 33-year-old, HIV-1 positive, white, homosexual man was hospitalized in May, 1991, because of fever, cough, skin eruptions, anorexia, and weight loss during the previous 2 months. In October, 1990, he had traveled in Sumatra. On examination he was ill, tachypneic, normotensive with a temperature of 39.1 degrees Celsius. The spleen was substantially enlarged. Laboratory investigations showed: ALAT 72 U/I (normal 23 U/1), LDH 508 U/1 (normal 275 U/1). A bronchoscopy with bronchoalveolar lavage revealed yeast cells. Gastroscopy showed an ulcer in the hypopharynx and an erosion in the stomach. Biopsies of this ulcer demonstrated the presence of Penicillium marneffei. Biopsies of the liver showed the same organism. The patient was treated with amphotericin B induction therapy (1 dd 0.5 mg/kg for 21 days, total dose of 730 mg) in combination with flucytosine (3 dd 2500 mg, total dose 142 g in 19 days). In the following 2 weeks the temperature became normal, and the dyspnea and the skin eruptions disappeared, except for the mollusca contagiosa. The spleen diminished by 50%. LDH and ALAT became normal. Oral maintenance therapy followed with fluconazole (the first 3 months 400 mg daily, followed by 200 mg a day). 24 months later, no recurrence had been observed. Case 2 was a 28-year-old, HIV-infected, homosexual man, born in Suriname, who was hospitalized in October, 1991, with prolonged fever, dyspnea, and a painful throat. In March, 1991, he had traveled in rural Thailand. AIDS was diagnosed on the basis of cerebral toxoplasmosis in August, 1991. A biopsy of the ulcer in the oropharynx showed an active aspecific inflammation and also P. marneffei. Treatment with amphotericin B intravenously (0.5 mg/kg, total dose 1052 mg in 32 days) was commenced. The lesions in the oral cavity and throat, the lymph nodes, and the shortness of breath disappeared within a few days. Ten months later he died from emaciation caused by cryptosporidiosis.
 ...
PMID:Disseminated Penicillium marneffei infection as an imported disease in HIV-1 infected patients. Description of two cases and a review of the literature. 820 1

This study was designed to examine the effects of a pre-existing, clinically asymptomatic feline immunodeficiency virus (FIV) infection on a primary challenge with Toxoplasma gondii. Parenteral challenge of FIV-infected cats with tachyzoites of the ME49 strain of T. gondii caused a precipitous drop in all lymphocytes (CD4+, CD8+, and B cells) and generalized severe toxoplasmosis. The predominant postmortem lesions included acute and often fatal interstitial pneumonia, dominated histologically by macrophages, and multifocal to coalescing hepatic necrosis. Immunohistochemistry revealed numerous T. gondii antigen and tachyzoites in macrophages and other cell types in the lung lesions. The proliferative response of peripheral blood mononuclear cells to specific (T. gondii antigen) and nonspecific (Concanavalin A) mitogens was defective in the dually infected cats, suggesting marked immunosuppression. In contrast to the dually infected cats, cats infected only with T. gondii developed a transient, mild clinical disease characterized by anorexia, lethargy, and multifocal chorioretinitis. Lymphocyte changes in T. gondii-infected cats included an early pan-lymphopenia followed by reestablishment of all lymphocyte subset profiles. These cats also showed a reduced proliferative response to Concanavalin A at 1 week after challenge, but a measurable in vivo response to T. gondii antigens, as evidenced by in vitro lymphocyte proliferation in the absence of a mitogenic stimulus. These results show that infection of cats with FIV-NCSU, markedly enhances their susceptibility to a primary T. gondii infection and provides a model to study the mechanisms of the underlying immunological defect(s) occurring early after HIV infection that may predispose individuals to development of acquired immunodeficiency syndrome and associated diseases.
 ...
PMID:Feline immunodeficiency virus predisposes cats to acute generalized toxoplasmosis. 823 62


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>