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

An attempt is made to characterize the population of homeless street youth who are living marginally and to describe aspects of this population's dynamics, motivations, values, and aspirations. Street youth, ranging in age from birth to 21, are on the street for one reason or another--dire poverty in the home, which necessitates their working on the street to supplement the family income, because they have been rejected by parents or guardians, because they have left home due to violence in the home, drug or alcohol use by family members, or because of lack of a place where they feel they can be "themselves." These conditions make street youths particularly vulnerable to HIV infection, not to mention malnutrition, stress, and drug use. Their violently accelerated emotional maturation, ignorance, alcohol- and drug-induced confusion, together with the exploitation and sexual abuse of which they are often victims, are additional factors that contribute to sexual practices that may lead to HIV infection.
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PMID:Street youth and AIDS. 138 67

There are considerable data suggesting that breast milk and colostrum transmit HIV. The European Collaborative Study shows the risk of transmission of HIV from breast milk to infant to be about 28%. A study in Rwanda indicates that transmission is more likely to take place during viremia which occurs during primary HIV infection and later with progression to AIDS. Postnatal transmission in this study stood at about 60%. Breast feeding protects against diarrhea and respiratory infections. A study in Brazil demonstrates that infants who were not breast fed were at 14.2 and 3.6 higher risk of death from diarrhea and respiratory infections, respectively, than breast-fed infants. These risks are especially great where poverty, inadequate sanitation, and poor hygiene predominate. A study in Malaysia shows that infants living in a household with no piped water and no toilet and were not breast-fed faced a 5-fold risk of death after 1 week of age than breast-fed infants living under the same conditions. This risk continued to be high (2.5) for non-breast-fed infants living in a household with piped water and a toilet. In developed countries, affordable formula, clean water, and adequate facilities for sterilizing bottles allows HIV positive mothers to bottle feed their infants which should reduce the vertical transmission rate. In developing countries, however, bottle feeding is expensive and hazardous. Governments often cannot provide potable water and sanitation services. In addition, mathematical models demonstrate that for HIV positive mothers, the risk of infant death is lower in infants who breast feed than in those who do not. Thus, in those areas of the world where infectious diseases and malnutrition are the leading causes of infant death, health workers should promote breast feeding regardless of HIV status of the mothers.
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PMID:Breast feeding and HIV infection. 148 98

The physiopathology of malnutrition among AIDS, ARC and HIV infected children was reviewed. One-hundred eight-three newborns were studied, 152 of which were born at "La Fe" Maternity Hospital. Of these patients, 29% were LBW and 28% preterm. Transfused and hemophiliac patients were excluded from the study. Anorexia, vomiting, fever, infections of the respiratory and GI tracts and drug therapy were the most frequent factors affecting the nutritional status. Fifty-three newborns were infected with the HIV (29%). The children were classified into three groups (G). Group-I was formed by HIV+children > 18 months of age, G-II, P-2 class by children < 18 months of age and G-III was formed by those children that died of AIDS. The most common symptoms were chronic diarrhea and infections of the respiratory tract. Of the HIV+children > 18 months of age, 65% had a weight < the 10th percentile and 61% were < the 10th percentile for height. Of the children that died of AIDS, 80% were in the lower 10th percentile for both weight and height. Hemoglobin, T4/T8, total proteins, seroalbumin and calcium were also negatively affected. Those most severely affected were the dead patients, followed by P-2 < 18 months and finally the HIV+ > 18 months of age. The differences between G-I and G-II-G-III were statistically significant, p < 0.01. The biochemical quantification of the nutritional status was difficult due to the limited amount of blood available. HIV infected children require nutrition supplementation to maintain an adequate nutritional status. Among these patients, malnutrition is a multifactorial phenomenon.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Nutritional status in HIV infection in infancy]. 145 14

Diarrhea and weight loss are common features of pediatric and adult human immunodeficiency type 1 (HIV-1) infection, particularly in developing countries. We studied prospectively episodes of diarrhea in 559 children, ages 10 to 15 months, participating in a longitudinal study of perinatal HIV-1 infection in Kinshasa, Zaire. Children with HIV-1 infection had more frequent episodes of diarrhea and were more likely to present with fever or moderate or severe dehydration and to have persistent or fatal diarrhea. Of 9 HIV-1-positive infants with diarrhea, 3 had enteroadherence factor-positive Escherichia coli, compared with 5 of 74 HIV-1-negative children with diarrhea (P = 0.04); no other pathogen was associated with HIV-1 infection. In a logistic regression model diarrhea was significantly associated with HIV-1 infection in the child, moderate or severe malnutrition and symptoms of acquired immunodeficiency syndrome in the mother. Diarrhea among children with perinatal HIV infection in Zaire is more severe than among uninfected children and is associated with malnutrition and advanced disease in the mother.
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PMID:Diarrhea among African children born to human immunodeficiency virus 1-infected mothers: clinical, microbiologic and epidemiologic features. 146 10

For the sake of clarity and in agreement with the World Health Organization immunodeficiency classification, it is important to distinguish the congenital, inherited malformative lesions called generically 'thymic dysplasia' from the secondary, acquired changes, designated under the broad term of 'severe thymic atrophy'. Thymic dysplasia represents the archetype of thymic changes in cellular immunodeficiency, since there is no example of a thymic dysplasia associated with a normal T-cell function. Thymic dysplasia is observed in several inherited diseases, the most frequent of them being severe combined immunodeficiency. More than the depletion of lymphoid cells, the lack of differentiation of the thymic epithelium, responsible for the absence of Hassal's corpuscles, is the main and constant feature of this condition. Thymic dysplasia underscores the crucial role of the thymic epithelium in the normal differentiation of the T-cell population. Severe thymic atrophy is secondary to various causes, including prolonged protein malnutrition and immunosuppressive or cytotoxic drugs, graft versus host reaction and, chiefly today, chronic viral infection, especially with HIV-1. The morphological changes are similar and are characterized by a partial lymphoid depletion, involving mainly the CD1+ population, necrosis and calcification of epithelial cells, the frequent presence of plasma cells and, more significantly, fibrohyaline changes of the basement membrane of the vessels and thymic epithelium. The severity of the atrophic changes and the immunodeficiency-related manifestations depend on the duration of the aetiological factors and, more significantly, with their early occurrence, within the first months of life. The mechanisms underlying thymic atrophy are poorly understood. A primary impairment of lymphoid cells seems at present to be the most likely hypothesis.
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PMID:Thymic pathology in primary and secondary immunodeficiencies. 146 48

Participants at a 1992 WHO/UNICEF consultation meeting on HIV transmission and breast feeding weigh the risk of death from AIDS with the risk of death from other causes. Breast feeding reduces the risk of death from diarrhea, pneumonia, and other infections. Artificial or inappropriate feeding contributes the most to the more than 3 million annual childhood deaths from diarrhea. The rising prevalence of HIV infection among women worldwide results in more and more cases of HIV-infected newborns. About 33% of infants born to HIV-infected. Some HIV transmission occurs through breast feeding, but breast feeding does not transmit HIV to most infants HIV-infected mothers. Participants recommend that, in areas where infectious diseases and malnutrition are the leading causes of death and infant mortality is high, health workers should advise all pregnant women, regardless of their HIV status, to breast feed. The infant's risk of HIV infection via breast milk tends to be lower than its risk of death from other causes and from not being breast fed. HIV-infected women who do have access to alternative feeding should talk to their health care providers to learn how to feed their infants safely. In areas where the leading cause of death is not infectious disease and infant mortality is low, participants recommend that health workers advise HIV-infected pregnant women to use a safe feeding alternative, e.g., bottle feeding. Yet, the women and their providers should not be influenced by commercial pressures to choose an alternative feeding method. Health care services in these areas should provide voluntary and confidential HIV testing and counseling. Participants stress the need to prevent women from becoming HIV-infected by providing them information about AIDS and how to protect themselves, increasing their participation in decision-making in sexual relationships, and improving their status in society.
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PMID:HIV and breast-feeding. 147 85

In 37 intravenous drug users (IVDUs) in the first stages of HIV-infection (17 in stage II and 20 in stage III according to CDC), compared with 32 IVDUs HIV-negatives, we found a significant decrease in circulating leucocytes (p less than 0.01), lymphocytes (p less than 0.005), platelets (p less than 0.005), serum albumin (p less than 0.005), and C3 (p less than 0.02) and significant increase in serum gammaglobulins (p less than 0.0005) and IgG (p less than 0.0005). On the other hand no difference was observed in hemoglobin and in IgA levels; nevertheless an inverse relationship between serum IgA and CD4+ lymphocytes was present in HIV-positive (HIV+) patients (r = -0.34; p = 0.04). This observation agrees with that is observed in the advanced stages of HIV-infection, which presents an increase in IgA serum levels. In these stages this fact could be due to a decrease of secretory IgA, with a deficient barrier effect; the consequent recirculation of intestinal antigens should enhance the antibody production, as well as serum IgA. In the IVDUs HIV-infected a reverse correlation between albumin serum levels and the length of HIV-positivity (r = -0.44; p = 0.008) and a direct correlation between albumin serum levels and circulating CD4+ lymphocytes (r = 0.37; p = 0.05) were present. There was no direct linear relationship between albumin serum levels and creatinine, on the contrary to what was observed in the control group. The decrease of albumin levels could have a prognostic value as in other clinical conditions, in which it is associated with a higher mortality risk. Many factors could act to decrease albumin levels, but the most important one is perhaps the malnutrition of HIV-infected patients that can also be present in the first stages of infection, negatively influencing the associated immunodeficiency.
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PMID:Serum albumin and others parameters in intravenous drug users HIV-infected. 149 83

Freedom from infection is the result of many tiers of immune defenses that harmoniously interact to rid the body of microorganisms and their products, which are perceived as foreign. The ability to distinguish self from nonself is embodied in lymphocytes, which serve both effector and regulatory functions. Through the elaboration of cytokines and immunoglobulins, lymphocytes recruit nonspecific immune effectors, focus their activity, and modulate the intensity of the immune response. The phylogenetically more primitive complement system serves a similar function. Although congenital defects in immune function occur, by far the most common causes of immunodeficiency are acquired and occur in patients treated for cancer with myelosuppressive, cytolytic drugs and in transplant recipients treated with immunosuppressants. HIV infection and malnutrition are responsible for even larger numbers of immunocompromised patients worldwide. The nature and severity of infections that occur as a result of immunodeficiency vary as a function of the immune effector targeted and the degree to which it is dysfunctional. Granulocytopenia is well tolerated unless the absolute number of circulating cells falls below 500/mm3. Profound granulocytopenia and deficits of neutrophil function are often manifest as bacterial or fungal infections. Complement deficiency predisposes to infection with encapsulated bacteria such as pneumococci, meningococci, and Haemophilus influenzae. T cells play such a central role in the immune response that their derangement is associated with susceptibility to almost any potential pathogen. These patients often succumb to mortal opportunistic infections. Recent advances in hybridoma and recombinant DNA technology have provided us with immunologic reagents that enable us to manipulate the immune response. Anti-CD3 monoclonal antibody has permitted salvage of solid organ transplants in well-defined clinical settings. Monoclonal antibodies against TNF-alpha and lipopolysaccharide may alter the consequences of gram-negative sepsis. Alternatively, recombinant cytokines have been associated with clinically significant tumor regression in selected patients, presumably by enhancing the nascent antitumor immune response. The development of immunologic reagents such as these in concert with our growing understanding of the immune system may translate to improved care for immunocompromised patients.
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PMID:Immune function and dysfunction. A primer for the radiologist. 157 Mar 93

We report the development of severe hepatotoxicity in a patient on zidovudine therapy who received 3.3 g of acetaminophen in less than 36 hours. Three days later, the patient's serum aspartate aminotransferase level was 5,724 U/L, alanine aminotransferase was 3,124 U/L, lactate dehydrogenase was 12,675 U/L, alkaline phosphatase was 84 U/L, and total bilirubin was 20 mumol/L. These values substantially improved over the ensuing 4 days. Serologic results for hepatitis B, hepatitis A, and cytomegalovirus were all negative. The pattern and time sequence of transaminase elevation in this patient are consistent with acute acetaminophen hepatotoxicity, especially since zidovudine-induced hepatotoxicity is described as producing cholestasis rather than acute hepatitis. We hypothesize that our patient's susceptibility to acetaminophen-dependent hepatotoxicity may have been augmented by competitive utilization of glucuronidation by other drugs such as zidovudine and/or trimethoprim-sulfamethoxazole with subsequent increased cytochrome P450-dependent metabolism of acetaminophen. Additionally, due to malnutrition and/or to human immunodeficiency virus infection per se, our patient may have had decreased hepatic reserves of glutathione with which to conjugate the toxic acetaminophen product of the P450 system. Although severe acetaminophen-associated hepatotoxicity has not previously been reported in patients receiving zidovudine, we suggest that clinicians be aware of this potential interaction and counsel malnourished patients, especially those with concomitant hepatic disease, to exercise caution when taking both these medications.
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PMID:Severe hepatotoxicity in a patient receiving both acetaminophen and zidovudine. 836 34

Tryptophan (Trp) is an indispensable amino acid required for biosynthesis of proteins, serotonin and niacin. Indoleamine 2,3-dioxygenase (IDO) is induced by infections, viruses, lipopolysaccharides, or interferons (IFNs) and this results in significant catabolism of Trp along the kynurenine (Kyn) pathway. Intracellular growth of Toxoplasma gondii and Chlamydia psittaci in human fibroblasts in vitro is inhibited by IFN-gamma and this inhibition is negated by extra Trp in the medium. Similarly, growth of a number of human cell lines in vitro is inhibited by IFN-gamma and addition of extra Trp restores growth. Thus, in some in vitro systems, antiproliferative effects of IFN-gamma are mediated by induced depletion of Trp. We find that cancer patients given Type I or Type II IFNs can induce IDO which results in decreased serum Trp levels (20-50% of pretreatment) and increased urinary metabolites of the Kyn pathway (5 to 500 fold of pretreatment). We speculate that in vivo antineoplastic effects of IFNs and clinical side effects are mediated, at least in part, by a general or localized depletion of Trp. In view of reported increases of IFNs in autoimmune diseases and our earlier findings of elevated urinary Trp metabolites in autoimmune diseases, it seems likely that systemic or local depletion of Trp occurs in autoimmune diseases and may relate to degeneration, wasting and other symptoms in such diseases. We find high levels of IDO in cells isolated from synovia of arthritic joints. IFNs are also elevated in human immunodeficiency virus (HIV) patients and increasing IFN levels are associated with a worsening prognosis. We propose that IDO is induced chronically by HIV infection, is further increased by opportunistic infections, and that this chronic loss of Trp initiates mechanisms responsible for the cachexia, dementia, diarrhea and possibly immunosuppression of AIDS patients. In these symptoms, AIDS resembles classical pellagra due to dietary deficiency of Trp and niacin. In preliminary studies, others report low levels of Trp and serotonin, and elevated levels of Kyn and quinolinic acid in AIDS patients. The implications of these data in cancer, autoimmune diseases and AIDS are discussed.
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PMID:Implications of interferon-induced tryptophan catabolism in cancer, auto-immune diseases and AIDS. 172 46


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