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Query: UMLS:C0235394 (wasting)
 8,040 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Human immunodeficiency virus type 1 (HIV-1) has been clearly associated with a variety of new illnesses, including profound immunodeficiency (acquired immune deficiency syndrome [AIDS]), wasting syndromes (formerly termed AIDS-related complex [ARC]) and neurologic syndromes, including neuropathy, myelopathy and encephalopathy (often termed subacute encephalitis or AIDS dementia complex). HIV-1 preferentially infects T lymphocytes by binding to a membrane receptor protein, CD4, associated with helper function. The virus can also attack macrophages and, possibly, other cells such as neuronal cells, colonic epithelial cells and B lymphocytes. Infection of macrophages or monocytes may be involved in neurologic disease. Knowledge about HIV-1 has rapidly increased, and investigators have characterized its structure, ways in which it infects cells, replicates and is cytopathic for certain cells, and how the immune system responds to it. The ideal vaccine would prevent adsorption of the virus into the cell, but it is difficult to develop stable resistance because the virus has many antigenic patterns and mutates frequently. The results of vaccine trials in animals have not been promising, but work is being done with monoclonal antibodies. Antiviral therapies being investigated include those to prevent virus binding and entry, to inhibit reverse transcription, to inhibit the virus's life cycle and to restore immune competence in immunocompromised patients.
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PMID:Vaccine and antiviral strategies against infections caused by human immunodeficiency virus. 328 28

Infection of animal cells by a number of viruses generally results in an array of metabolic defects, including inhibition of host DNA, RNA, and protein synthesis, and morphological alterations known as cytopathic effects. For adenovirus infection there is a profound loss of cell structural integrity and a marked inhibition of host protein synthesis, the latter generally assumed necessary to enhance virus production. We examined the purpose of viral inhibition of cell translation and found that it was related in part to cytopathic wasting of infected cells. We show that viral shutoff of host translation promotes destruction of the intermediate filament network, particularly cytokeratins which are proteolysed at keratins K7 and K18 by the adenovirus late-acting L3 23-kDa proteinase. We found that if adenovirus is prevented from inhibiting cell translation, the intermediate filament network remains relatively intact, keratin proteins are still synthesized, and cells possess an almost normal morphological appearance and lyse poorly, reducing the release of nascent virus particles by several hundredfold. Remarkably, in tissue culture cells the accumulation of late viral structural proteins is only marginally reduced if host translation shutoff does not occur. Thus, a surprising major function for adenovirus inhibition of cellular protein synthesis is to enhance impairment of cellular structural integrity, facilitating cell lysis and release of progeny adenovirus particles.
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PMID:Adenovirus inhibition of cell translation facilitates release of virus particles and enhances degradation of the cytokeratin network. 751 Nov 74

Withering syndrome (WS) is an epizootic fatal wasting disease that is devastating California Channel Island populations of black abalone Haliotis cracherodii. Our studies suggest a strong pathogen-disease association. The pathogen is an intracellular prokaryote that infects epithelial cells lining the gut and enzyme secreting cells of the digestive diverticula. It multiplies by binary fission in round to oval, basophilic, membrane-bound colonies teeming in the cytoplasm. Infection of the digestive diverticula is accompanied by a complete loss of digestive enzyme granules and metaplasia of enzyme secretory cells to a morphology similar to epithelium lining the gut. Extensive infection of digestive diverticular cells and the resultant deficiency in digestive enzymes correlates to the degree of pedal muscle atrophy and the severity of signs associated with WS. Electron microscopically the intracellular pathogen is a rod-shaped, ribosome-rich, gram-negative, prokaryote with a trilaminar cell wall consistent with the order Rickettsiales. Microbiological and protozoological methods produced no patterns that implicated other types of microbes. Chemical analysis of tissue from animals from a population with WS did not support an association between WS and environmental pollutant exposure to polycyclic aromatic hydrocarbons, polychlorinated biphenyls, or chlorinated pesticides.
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PMID:Association of prokaryotes with symptomatic appearance of withering syndrome in black abalone Haliotis cracherodii. 759 33

The clinical and pathological features of 22 patients, 11 males and 11 females 17-70 years of age (48.0 +/- 16.0 years), with hepatic tuberculosis were reviewed. Five patients had no evidence of extrahepatic tuberculosis (local form), and 17 had the miliary form. The clinical features of the miliary and local forms were similar with pyrexia, abdominal pain, hepatomegaly and body weight loss as the main manifestations. The biochemical findings were also quite similar in reversed albumin and globulin (A/G) ratio (2.9/3.5 vs. 3.2/3.4 g/dl) and disproportionate elevation of alkaline phosphatase (ALP) in comparison with bilirubin values but lower levels of alanine aminotransferase (ALT) (40.4 +/- 51.0 vs. 170.8 +/- 209.4 U/l; p < 0.05) and ALP (208.5 +/- 138.9 vs. 389.5 +/- 271.1 U/l; p < 0.05) in the miliary form. Patients with the local form had higher albumin (3.2 +/- 0.8 vs. 2.9 +/- 0.7 g/dl), aspartate aminotransferase (AST) (160.4 +/- 221.7 vs. 65.9 +/- 69.7 U/l), and gamma glutamyl-transpeptidase (gamma GT) (217.0 +/- 144.0 vs. 136.0 +/- 92.1 U/l), although the differences were not significant. The histopathological features of the miliary form were also similar to the local form with granuloma, caseation, acid-fast bacilli, fatty change and portal fibrosis as the main findings. The local form revealed more severe signs of hepatocytic damage while the miliary form was more wasting. The results suggest that the miliary and local forms of hepatic tuberculosis had quite similar clinical presentations and pathological features. The biochemical tests suggesting hepatic tuberculosis were reversed A/G ratio and disproportionate elevation of ALP.
Infection
PMID:Hepatic tuberculosis: comparison of miliary and local form. 774 92

Infection due to the Mycobacterium avium complex (MAC) is the most common opportunistic disease of bacterial origin among patients with AIDS in the United States. The incidence of disseminated disease due to MAC (DMAC) has risen dramatically in recent years. The risk of developing DMAC increases as the CD4+ lymphocyte count declines to < 100/mm3. Preliminary analyses of several studies suggest that gender, racial or ethnic group, and individual risk factors for human immunodeficiency virus infection do not influence the incidence of DMAC but that prior Pneumocystis carinii pneumonia, the development of severe anemia, or the interruption of antiretroviral therapy may increase risk. Both the respiratory and the gastrointestinal tracts probably serve as portals of entry for MAC. Colonization may potentiate the risk of DMAC but does not always precede dissemination. Patients with AIDS and DMAC have a shorter duration of survival than do those with AIDS but without DMAC. While treatment for DMAC may extend survival, no well-controlled, prospective, randomized clinical trial has documented this point. Most patients with AIDS and DMAC have disseminated multiorgan disease; the most frequently described symptoms include fever, night sweats, weight loss or wasting, diarrhea, and abdominal pain. The most commonly identified laboratory abnormalities are anemia and elevated serum levels of alkaline phosphatase. Localized disease syndromes related to MAC infection occur less often.
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PMID:Disease due to the Mycobacterium avium complex in patients with AIDS: epidemiology and clinical syndrome. 820 73

It is widely assumed that infections are the principal cause and primary outcome determinant of the syndrome of Multiple Organ Failure (MOF) in critically ill patients. Infections are frequent in these patients, but the prevention and treatment of infections may not influence the course of MOF. This study tested the hypothesis that infections play a decisive role in the outcome of MOF. Data were gathered concurrently on all adult patients admitted over an 18-month period to a non-cardiac surgical ICU at a university hospital and recorded in a computer database. Sepsis was defined as a state characterized by at least three of the following: fever, tachycardia, leukocytosis or leukopenia, increased cardiac index, reduced systemic vascular resistance, and hypercatabolism manifested by nitrogen-wasting. The presence of an infection was not required for the diagnosis of sepsis. Mild sepsis was defined as the presence of three or four parameters. Severe sepsis was defined as the presence of five or six parameters. MOF was defined as the development of dysfunction of at least two of the following major organ systems: cardiac, gut, pulmonary, renal, cerebral, and hepatic. Of 749 admissions, 73 patients developed MOF. Thirty four (47%) had a documented source of infection, 37 (51%) had positive blood cultures, and all had sepsis. Hospital mortality was 66 percent (48 of 73 patients). Death could not be predicted by bacteremia (P > 0.25), nor by the presence of an infectious source (P = 1.0), but was strongly associated with severe sepsis (P < 0.0005).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The role of infection in outcome of Multiple Organ Failure. 823 94

Fungal infections account for a large number of AIDS-index diagnoses and complicate the course of most patients with HIV disease. Infection with Cryptococcus neoformans is the most commonly encountered deep-seated fungal infection in AIDS and represents a major threat to HIV-infected people worldwide. Although most patients with cryptococcosis present with meningitis, pulmonary disease may occasionally dominate the clinical picture. Treatment of symptomatic pulmonary cryptococcosis remains amphotericin-B with or without 5-flucytosine. The toxicity and difficulty of administration of amphotericin-B has engendered interest in treatment alternatives with the new triazoles. As HIV infection has become more common in the American heartland, it has overlapped areas endemic for Histoplasma capsulatum, Coccidioides immitis, and Blastomycosis dermatitidis. Disease from these deep-seated fungal pathogens, whether from de novo exposure or reactivation, has protean manifestations. Common to all is a protracted, febrile, wasting illness, with or without respiratory symptoms. Treatment of choice for all these infections remains amphotericin-B, followed by lifelong-maintenance therapy with a triazole. In this article I review the microbiology, epidemiology, presentation, diagnosis, and treatment of AIDS-associated deep-seated fungal infections.
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PMID:Pulmonary fungal infections in HIV-infected persons. 827 79

Infection with the human immunodeficiency virus (HIV) can lead to global alterations in metabolism as well as immunodeficiency. There is dysregulation of endocrine function in adults and children, the extent and magnitude correlating with disease progression. Some of the more prominent abnormalities occur in the thyroid, gonadal, and somatomedin axes. Clinical manifestations of these abnormalities are growth failure in children, which is one of the most sensitive indicators of disease progression, and a wasting syndrome in adults and children. Although there are case reports of growth hormone (GH) deficiency in HIV-infected children, most patients with growth failure have normal serum levels of GH and normal to low levels of insulin-like growth factor-I (IGF-I). Antiretrovial therapy can improve the growth rate in children for a period of time if there is a drop in viral titer, but as the viral load increases, the growth rate decreases again. Administration of GH or IGF-I to these patients can improve the growth rate and lean body mass, and in some patients improve immune function. Although studies on resting energy expenditure in HIV-infected patients have shown increases, these are not proportional to disease progression, but may be dependent upon cytokine activation and other abnormalities. Adult patients with wasting have been shown to have relatively normal total energy expenditure, but decreased intake. Appetite stimulants have been shown to have some benefit, but do not increase lean body mass. The most significant clinical benefit has come from administration of GH in short-term trials. GH and IGF-I are both able to inhibit apoptosis and reconstitute the immune system in rodents treated with ablative therapy. In addition, GH can modulate the marrow suppressive effects of zidovudine and may enhance its ability to inhibit viral reverse transcriptase. Current clinical trials are ongoing in both adults and children. GH and IGF-I may have a role in regimens intended for immune reconstruction, and could be useful as adjuvant therapy in selected patients with HIV infection.
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PMID:Use of human recombinant growth hormone and human recombinant insulin-like growth factor-I in patients with human immunodeficiency virus infection. 895 Jun 24

During September 1989-November 1991 in Peru, 207 infants, 0-3 months old at enrollment and living in a periurban shanty town in Lima, were followed to determine whether a child's first infection with Cryptosporidium parvum had an adverse effect on weight gain during the first month of infection and whether poor nutritional status was a risk factor for C. parvum. Infection with C. parvum occurred at least once in 45% (97) of the infants. Median age at onset of a first C. parvum infection was 16 months. The growth interval of only 57 (61%) of C. parvum infected children was evaluated. 36 (63%) children were asymptomatic. The remaining 21 infected children had diarrhea. Children with cryptosporidiosis, whether symptomatic or asymptomatic, gained less weight during the first month of infection than children without cryptosporidiosis. Children with symptomatic cryptosporidiosis gained 184 g less weight during the first month of infection than did children with asymptomatic cryptosporidiosis. Children with symptomatic cryptosporidiosis gained 342 g less during the first month of infection than did children who were not infected with C. parvum and did not have diarrhea. Children with asymptomatic cryptosporidiosis gained 162 g less during the first month of infection than did children who were not infected with C. parvum and did not have diarrhea. The adverse effect of C. parvum on weight gain was strongest in children younger than 12 months. Neither wasting nor underweight was a significant risk factor for C. parvum infection. Stunting tended to increase the risk of C. parvum infection but the effect was not statistically significant. These findings show that C. parvum infection has an adverse effect on growth. Asymptomatic cryptosporidiosis is of special concern, since it was more prevalent and thus probably would have more of an overall adverse effect on child growth in the community.
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PMID:Asymptomatic and symptomatic cryptosporidiosis: their acute effect on weight gain in Peruvian children. 900 12

Prophylactic hemodialysis has been employed in the treatment of 15 patients with acute renal failure due to acute tubular necrosis (12), bilateral renal cortical necrosis (two), and poststreptococcal glomerulonephritis (one). Dialyses, usually lasting six hours each, were begun before clinical evidence of uremia developed in each patient and/or before the nonprotein nitrogen reached 200 mg.%, and were repeated daily or often enough to maintain the nonprotein nitrogen below 150 mg.%. The hypothesis underlying this technic postulates (1) that wasting, sepsis and impaired wound healing in these patients may reflect tissue injury by the same dialyzable toxic agents which produce the uremic symptoms that are readily reversible by dialysis, and (2) that repeated dialyses should therefore prevent both clinical uremia and the later, often lethal sequelae. The results contrast dramatically with our own past experience in treating patients with acute renal failure with a carefully executed medical regimen together with hemodialysis on conventional indications. Except in one instance of crush injury with progressive intracerebral damage, and one brief occasion in another individual, these patients experienced a stable, convalescent clinical course, remained free of uremic symptoms or chemical imbalances, ate at least three meals daily which were unrestricted in amount and composition, and were ambulatory between dialyses unless confined to bed by associated disease. Wounds healed well. Infection either did not occur, or subsided after appropriate therapy. Fluid restriction was liberalized by means of ultrafiltration with dialysis. Regional heparinization of only the extracorporeal circuit eliminated actual or impending bleeding as a contraindication to dialysis. Chronic vessel cannulation made the frequent dialyses possible, but may have provided the route for repeated, transient bacterial contamination of the blood stream in the first hour of many dialyses. Marked anemia, despite reticulocytosis, moderate to mild weight loss and some mental deficit persisted in spite of the general clinical improvement and well-being. Three patients with tubular necrosis died after seven, 11 and 26 days of oliguria; both patients with bilateral renal cortical necrosis also succumbed, on the seventy-third and ninety-second days of renal failure, and after 29 and 40 dialyses, respectively. At autopsy, evidence of sepsis was conspicuously absent. The remaining 10 patients survived. Thus some, but not all, clinical manifestations of acute renal failure appear to be favorably influenced by prophylactic dialysis treatment. Our initial experience in this group of 15 patients does not of course prove that freedom from complications and a significantly better outlook for survival can be assured to patients with acute renal failure by these methods. However, it seems to offer a reasonable hope of this possibility which we cannot attach to management by medical measures alone, or by dialysis on conventional indications. If this hope is realized in greatly extended, subsequent series, then it seems inevitable that some form of prophylactic dialysis, or some equally effective alternative, should be adopted in treating the majority of patients with acute renal failure.
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PMID:Prophylactic hemodialysis in the treatment of acute renal failure. Annals of Internal Medicine, 53:992-1016, 1960. 984 96


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