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Query: UMLS:C0001175 (AIDS)
 120,706 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Bacillary angiomatosis is known to be caused by a rickettsial organism; Rochalimaea henselae. This causative agent has been compared with different microorganisms and clinical conditions that appear in similar settings but that have been clearly differentiated from them; e.i. Cat-scratch disease (Afipia felis), Bartonella bacilliformis, other Rochalimaea sp., Kaposi;s sarcoma, Lobular capillary hemangioma, Angiosarcoma, and Epithelioid hemangioma. Clinically the bacillary angiomatosis (BA) skin lesions vary from a single lesion to thousands. The cutaneous lesion appears as a bright-red round papule, subcutaneous nodule, or as a cellulitic plaque. When the lesion is biopsied it tends to blanch-out, bleed, and cause pain. The patient might present with signs and symptoms of chills, headaches, fever, malaise, and anorexia with or without weight loss. The extracutaneous lesions found in BA tend to be from multiple organs affecting from the oral lesions to anal mucosal lesions to widespread visceral lesions. The sites of preferences for BA lesion manifestation tend to be the liver, spleen, lymph nodes, and bone. To diagnose bacillary angiomatosis the physician should prepare a differential diagnosis based primarily on its histopathological and clinical characteristics. To confirm the results from the stain, electron microscopy can identify the bacillus and pin-point the diagnosis of bacillary angiomatosis. The lesions presented by BA respond well to therapy with erythromycin 500mg four times daily for a duration of 2 weeks to 2 months. In case of intolerance to erythromycin the second line of drug that successfully treats the BA bacillus is doxycycline. If relapses of the BA lesion recur, then a prolonged antibiotic therapy is necessary and in AIDS patients the duration may be extended as life-long suppressive therapy.
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PMID:Bacillary angiomatosis: microbiology, histopathology, clinical presentation, diagnosis and management. 891 40

We report a case of a 22-yr-old man with AIDS who presented with abdominal pain, vomiting, and anorexia. Diagnosis of gastric toxoplasmosis was made on biopsy and immunohistochemistry. The patient's symptoms resolved after treatment of toxoplasmosis. We present a case of an unusual manifestation of a common infection in patients with AIDS.
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PMID:Gastric toxoplasmosis: case report and review of the literature. 893 38

Leptin, a hormone that is secreted by adipose tissue in proportion to fat stores, regulates energy balance and appetite. Recently, tumor necrosis factor and interleukin-1, cytokines that regulate the host response to infection, have been shown to acutely increase leptin levels, raising the possibility that leptin could mediate the anorexia of some infections. We measured leptin levels in patients with the acquired immunodeficiency syndrome and found that leptin levels were not increased relative to body fat in patients who were anorectic, were losing weight, or had a history of weight loss. Furthermore, leptin levels were not increased during secondary infection, suggesting that elevations in leptin do not play a key role in the anorexia of infections associated with acquired immunodeficiency syndrome.
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PMID:Serum leptin levels in the acquired immunodeficiency syndrome. 895 39

Weight gain is a well-known side-effect of megestrol acetate (MA) treatment. This effect has been studied systematically in cancer and AIDS patients with involuntary weight loss, anorexia or manifest cachexia, situations in which weight gain is desirable. Significant, positive effects on weight gain and on certain quality of life aspects, such as appetite, nausea, body image and mood have been reported for cancer patients treated with 160 mg to 1.600 mg daily and similar effects have been registered in AIDS patients if doses of about 400-800 mg are used. Maximal weight gain is normally achieved within 8 weeks. The weight gain is, unfortunately, mainly due to an increase in fat mass and partly due to edema and, therefore, no significant effects are reported as regards the Karnovsky index. If anorexia, nausea and a negative body image are major concerns and if the patient has a life expectancy of more than 3 months, MA is a reasonable treatment option. However, if the central problem is fatigue and a low Karnovsky index, especially in a patient with a short expected survival, MA, which is not inexpensive, is not likely to be of significant help.
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PMID:The effect of megestrol acetate on anorexia, weight loss and cachexia in cancer and AIDS patients (review). 906 97

We studied the effects of long-term (12 months) dronabinol in 94 late-stage acquired immunodeficiency syndrome (AIDS) patients (mean CD4 count of 45/mm3) who previously participated in a 6-week study (placebo versus dronabinol). All patients received dronabinol orally-2.5 mg twice daily (90%) or 2.5 mg once daily (10%). Appetite was measured using a visual analogue scale for hunger (VASH). Dronabinol was associated with consistent improvement in mean appetite. Patients previously treated with dronabinol continued to show improvement in VASH (percent change from baseline of 6-week trial: 48.6-76.1% at each month), whereas those previously treated with placebo exhibited substantial improvement in mean appetite, particularly during the initial 4 months of treatment (48.5-69.9%). Thereafter, dronabinol was associated with a VASH change at least twice baseline. Patients tended toward stable body weight for at least 7 months. Adverse events were primarily related to known central nervous system effects of dronabinol. These data support long-term, safe use of dronabinol for anorexia associated with weight loss in patients with AIDS.
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PMID:Long-term efficacy and safety of dronabinol for acquired immunodeficiency syndrome-associated anorexia. 922 37

A documented association exists between nutritional status and immunologic function, development, and outcome of infectious processes, and treatment-related toxicity and vital organ function. In persons with AIDS, nutritional deficits precipitate a cycle that results in a downward spiral of weight lost, malabsorption, diarrhea, anorexia, body image disturbance, and increased risk for morbidity and mortality. This article presents an overview of the malnutrition in HIV/AIDS patients. It critiques the current Centers for Disease Control's definitions of wasting syndrome, describes the incidence of weight loss, delineates the implications of untreated malnutrition, and traces the etiology of weight loss and contributing factors. This article serves as an introduction to HIV/AIDS related malnutrition. A subsequent article will review nursing implications and clinical management programs.
J Assoc Nurses AIDS Care
PMID:Malnutrition associated with HIV/AIDS. Part One: Definition and scope, epidemiology, and pathophysiology. 924 67

This nonrandomized, two-period crossover study was performed to assess whether concomitant administration of megestrol acetate influences the steady-state pharmacokinetics of zidovudine and its inactive 5'-O-glucuronide metabolite. Twelve HIV-positive, asymptomatic male volunteers received a 100-mg oral capsule dose of zidovudine at least 30 min before meals five times a day at 0700, 1100, 1500, 1900, and 2300 h on study days 1 to 3 and a single 100-mg dose at 0700 h on day 4. On days 5 to 17, 800 mg of megestrol acetate, as a 40-mg/ml aqueous suspension, was administered orally immediately before the 0700 h dose of zidovudine. On days 5 to 16, zidovudine was also administered at 1100, 1500, 1900, and 2300 h. Serial blood samples were collected for 12 h after the single 100-mg dose of zidovudine on days 4 and 17; trough samples were also obtained just before the 0700 h dose on days 2 to 4 and 15 to 17. Levels of zidovudine and its glucuronide in plasma were assayed by a validated radioimmunoassay. Statistical analysis of trough plasma level data indicated that steady-state levels of zidovudine and its glucuronide in plasma had been attained when pharmacokinetic assessments were made on days 4 and 17. When megestrol acetate and zidovudine were coadministered for 13 days, differences of -14, -6.5, and -4.6% in mean zidovudine peak concentration and areas under the curve at 0 to 4 and 0 to 12 h, respectively, +22.5% in mean trough concentration, +2.6% in mean plasma half-life, and no change in median time to peak were observed compared to conditions when zidovudine was administered alone; for zidovudine 5'-O-glucuronide the respective differences were -9, -7.3, -4.4, +2.3, and +10% and no change. None of the differences were statistically significant (P > 0.05). Concomitant therapy with megestrol acetate, at the dose employed to treat anorexia, cachexia, or an unexplained, significant weight loss in AIDS patients, did not alter the steady-state pharmacokinetics of zidovudine or its 5'-O-glucuronide metabolite.
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PMID:Pharmacokinetic interaction of megestrol acetate with zidovudine in human immunodeficiency virus-infected patients. 937 53

Two forms of recombinant interferon-alpha (IFN-alpha2a and IFN-alpha2b) have been approved by the Food and Drug Administration for a variety of clinical indications, including hairy cell leukemia, hepatitis, acquired immunodeficiency syndrome-related Kaposi's sarcoma, chronic myelogenous leukemia (IFN-alpha2a only), and adjuvant therapy for melanoma (IFN-alpha2b only), based on their proven clinical efficacy and acceptable safety profiles. The continued postmarketing monitoring of adverse reactions associated with IFN-alpha therapy has revealed some new toxicities. The most common adverse events associated with IFN-alpha therapy are flu-like symptoms, fatigue, anorexia, and central nervous system and psychiatric reactions. In particular, the incidence of depression has only recently been fully appreciated. Some of these side effects, particularly chronic fatigue, anorexia, and neuropsychiatric reactions, may become dose limiting. New approaches to minimize and manage the side effects of IFN-alpha therapy are needed.
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PMID:Safety profile of interferon-alpha therapy. 948 35

We conducted a small exploratory study to assess whether testosterone therapy is an effective treatment for clinical symptoms characteristic of hypogonadism in eugonadal men with AIDS. Treatment consisted of 12 weeks of bi-weekly intramuscular injections of testosterone cypionate. Twenty-three men enrolled in the study; mean age was 37 and 44% were ethnic minorities. All had an AIDS diagnosis and the mean CD4 cell count was 150 cells/mm3. All baseline serum testosterone levels were within the laboratory reference range and above 500 ng/dl. Diminished libido was an inclusion criterion, plus each patient had at least one additional symptom (low mood, low energy, loss of appetite and/or weight). Nineteen men completed the trial and a majority of patients responded with regard to libido (89%), mood (67%), energy (71%), and appetite (67%) as rated by the Clinical Global Impressions Scale. With the exception of appetite, self and clinician rated measures showed significant improvement in all symptom domains. Among the 14 study completers with significant weight loss, the average weight gain was 2.3 kg, with a 1.8 kg increase in body cell mass and no change in body fat. These results suggest that testosterone is as effective in treating these symptoms in eugonadal men with AIDS as we have found in our research with hypogonadal HIV+men.
Int J STD AIDS 1998 Jan
PMID:Testosterone therapy for clinical symptoms of hypogonadism in eugonadal men with AIDS. 951 14

The production of pro-inflammatory cytokines, such as interleukins 1 and 6 and tumour necrosis factors, occurs rapidly following trauma or invasion of the body by pathogenic organisms. The cytokines mediate the wide range of symptoms associated with trauma and infection, such as fever, anorexia, tissue wasting, acute phase protein production and immunomodulation. In part, the symptoms result from a co-ordinated response, in which the immune system is activated and nutrients released, from endogenous sources, to provide substrate for the immune system. Although the cytokine mediated response is an essential part of the response to trauma and infection, excessive production of pro-inflammatory cytokines, or production of cytokines in the wrong biological context, are associated with mortality and pathology in a wide range of diseases, such as malaria, sepsis, rheumatoid arthritis, inflammatory bowel disease, cancer and AIDS. Cytokine biology can be modulated by antiinflammatory drugs, recombinant cytokine receptor antagonists and nutrients. Among the nutrients, fats have a large potential for modulating cytokine biology. A number of trials have demonstrated the anti-inflammatory effects of fish oils, which are rich in n-3 polyunsaturated fatty acids, in rheumatoid arthritis, inflammatory bowel disease, psoriasis and asthma. Animal studies, conducted by ourselves and others, indicate that a range of fats can modulate pro-inflammatory cytokine production and actions. In summary fats rich in n-6 polyunsaturated fatty acids enhance IL1 production and tissue responsiveness to cytokines, fats rich in n-3 polyunsaturated fatty acids have the opposite effect, monounsaturated fatty acids decrease tissue responsiveness to cytokines and IL6 production is enhanced by total unsaturated fatty acid intake. There are a large number of potential cellular mechanisms which may mediate the effects observed. The majority relate to the ability of fats to alter the composition of membrane phospholipids. As a consequence of alterations in phospholipid composition, membrane fluidity may change, altering binding of cytokines to receptors and G protein activity. The nature of substrate for various signalling pathways associated with cytokine production and actions may also be changed. Consequently, alterations in eicosanoid production and activation of protein kinase C may occur. We have examined a number of these potential mechanisms in peritoneal macrophages of rats fed fats with a wide range of fatty acid composition. We have found that the total C18:2 and 20:4 diacyl species of phosphatidylethanolamine in peritoneal macrophages relates in a positive curvilinear fashion with dietary linoleic acid intake; that TNF induced IL1 and IL6 production relate in a positive curvilinear fashion to linoleic acid intake; that leukotriene B4 production relates positively with dietary linoleic acid intake over a range of moderate intakes and is suppressed at high intakes, while PGE2 production is enhanced. There was no clear relationship between linoleic acid intake and membrane fluidity, however fluidity was influenced in a complex manner by the type of fat in the diet, the period over which the fat was fed and the presence of absence of TNF stimulation. None of the proposed mechanisms, acting alone, can explain the positive effect of dietary linoleic acid intake on pro-inflammatory cytokine production. However each may be involved, in part, in the modulatory effects observed.
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PMID:Modulation of pro-inflammatory cytokine biology by unsaturated fatty acids. 955 30


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