Endocrine Manifestations of Human Immunodeficiency Virus (HIV) Infection

Marks, Jennifer B.

doi:10.1097/00000441-199108000-00009

Cited by 32 publications

(14 citation statements)

References 59 publications

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“…However, recent reports demonstrate that hyperkalemia occurred in patients with AIDSand Pneumocystis carinii pneumonia who were treated with high-dose Tmp-Smx (6)(7)(8). In most of those cases, a causal relation between the Tmp-Smxtreatment and hyperkalemia is suggested but not proven because of the simultaneous presence of complications such as renal failure, adrenal insufficiency, and hypoaldosteronism (9)(10)(11)(12). Recently, we experienced two cases with severe hypo-natremia and hyperkalemia associated with high-dose Tmp-Smxtherapy.…”

Section: Introductionmentioning

confidence: 99%

Severe Hyponatremia and Hyperkalemia Induced by Trimethoprim-Sulfamethoxazole in Patients with Pneumocystis carinii Pneumonia.

et al. 1995

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An antimicrobial agent trimethoprim-sulfamethoxazole (Tmp-Smx)does not usually cause electrolyte disturbances at regular doses, and few cases ofTmp-Smx-inducedelectrolyte imbalance have been reported in the English-language literature to date. Recently, however, we treated two patients with Pneumocystis carinii pneumoniawhodeveloped severe hyponatremia and hyperkalemia on administration of high-dose Tmp-Smx.These electrolyte disturbances were attributable to the direct effect of Tmp-Smxon the renal distal tubules, were reversible, and corrected by infusion of a sodium-enriched and potassium-free liquid. Therefore, it is suggested that even after electrolyte disturbances have occurred, high-dose Tmp-Smxtherapy may be continued for severe infectious diseases under appropriate electrolyte correction. (Internal Medicine 34: 96-99, 1995)

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Section: Introductionmentioning

confidence: 99%

Severe Hyponatremia and Hyperkalemia Induced by Trimethoprim-Sulfamethoxazole in Patients with Pneumocystis carinii Pneumonia.

et al. 1995

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“…The mechanism(s) responsible for the decline in testicular testosterone secretion is not yet clear, but the presence of FeLV in the Leydig cells could account for the primary testicular failure. This will eventually lead to the following clinical symptoms, i.e., decreased spermatogenesis, Leydig cell hypoplasia, and germ cell tumors (15, 17, 18, 50).…”

Section: Discussionmentioning

confidence: 99%

Induction of Feline Acquired Immune Deficiency Syndrome by Feline Leukemia Virus: Immuno- and Neuroendocrine Dysfunctions

Wang

Teng

1994

Experimental Biology and Medicine

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Young cats, when chronically infected with feline leukemia virus (FeLV), developed feline acquired immune deficiency syndrome (FAIDS). The syndrome was associated with a sequence of dysfunctions in the hypothalamic-pituitary-gonadal (HPG) and the immune system, manifested in the reduction of luteinizing hormone-releasing hormone (LHRH), follicle stimulating hormone (FSH), luteinizing hormone (LH), and testosterone in blood plasma. The average FSH and LH (in plasma or lymphocyte), testosterone, and LHRH concentrations in the 20 FeLV-infected cats were measured by radioimmunoassay. The results were compared with those of the 12 control cats that were not FeLV-infected. Four weeks after infection, the plasma LHRH concentration in the infected cats showed a 43% reduction. Five to six weeks after infection, the content of FSH and LH in lymphocyte was reduced by 50% and 28%, respectively, whereas, the plasma FSH and LH was reduced by 52% and 42%, respectively. A significant reduction in testosterone content was detected at Week 11 of infection. The onset of the immuno- and neuroendocrine dysfunctions in FAIDs cats followed this sequence: hypothalamus, lymphocyte, pituitary, adrenal gland, and gonads. Indirect immunofluorescence assay showed the presence of FeLV cytoplasmic antigens in the fibers of the hypothalamic preoptic region and the Leydig cells. The possible causal relationship between the dysfunction of the lymphocyte and HPG systems and the presence of FeLV was discussed.

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“…Altered organ function can be caused by HIV and opportunistic infection, medications, and malnutrition. 93 Many of the alterations related to the wasting syndrome may also be related to the processes of acute or long-term and later stage disease processes. However, normal mechanisms to conserve lean body mass in acute and chronic disease may be altered and result in the wasting syndrome and other complications.94 Zidovudine therapy may be of benefit in the maintenance of normal endocrine function.95 A lack of endocrine abnormalities in 10 asymptomatic HIV+ women has also been reported .96 Understanding the processes as well as timing of endocrine and other abnormalities in both males and females are essential to the success of nutritional maintenance and rehabilitation efforts.…”

Section: Metabolic Alterationsmentioning

confidence: 99%

Invited Review: A Review of Mechanisms of Wasting in HIV Disease

Fields-Gardner¹

1995

Nut in Clin Prac

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According to estimates, between 50% to 90% of patients infected with the Human Immunodeficiency Virus (HIV) will experience some form of malnutrition. The degree and types of malnutrition are attributed to alterations in nutrient intake, absorption, and metabolism. Causes for each of these changes are complex and multifactorial. Research on treatment modalities generally concentrates on a single mechanism and reports varying degrees of short-term benefit. Appetite stimulation along with special diets, oral supplements, and nonvolitional enteral or parenteral nutrient provision may improve nutrient intake and body weight. Therapies aimed at the rehabilitation and improvement of the pool of functioning protein stores, such as alteration of inflammatory response, restoration of hormonal balance, and exercise are under investigation. Longer term studies will allow researchers to observe effects of therapies on overall body functions. With the development of clinical standards of care, the maintenance and restoration of nutritional status is emerging as the foundation for HIV disease management.

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Endocrine Manifestations of Human Immunodeficiency Virus (HIV) Infection

Cited by 32 publications

References 59 publications

Severe Hyponatremia and Hyperkalemia Induced by Trimethoprim-Sulfamethoxazole in Patients with Pneumocystis carinii Pneumonia.

Severe Hyponatremia and Hyperkalemia Induced by Trimethoprim-Sulfamethoxazole in Patients with Pneumocystis carinii Pneumonia.

Induction of Feline Acquired Immune Deficiency Syndrome by Feline Leukemia Virus: Immuno- and Neuroendocrine Dysfunctions

Invited Review: A Review of Mechanisms of Wasting in HIV Disease

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