Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0021051 (immunodeficiency)
 71,517 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Infectious complications in cirrhotic patients can cause severe morbidity and mortality. Bacterial infections are estimated to cause up to 25% of deaths in cirrhotic patients. The most frequent are urinary tract infection, spontaneous bacterial peritonitis, respiratory tract infection, and bacteremia. It has been said that cirrhosis is the most common form of acquired immunodeficiency, exceeding even AIDS. The specific risk factors for infection in cirrhotic patients are low serum albumin, gastrointestinal bleeding, intensive care unit admission for any cause, and therapeutic endoscopy. Certain infectious agents are more virulent and more common in patients with liver disease. These include Vibrio, Campylobacter, Yersinia, Plesiomonas, Enterococcus, Aeromonas, Capnocytophaga, and Listeria species, as well as organisms from other species. Spontaneous bacterial peritonitis is a frequent, severe, life-threatening complication of patients with ascites. Current observations and recommendations regarding treatment and prophylaxis are reviewed. A brief synopsis of miscellaneous infections encountered in cirrhotic patients is also included.
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PMID:Infectious complications of cirrhosis. 1146 97

Hepatitis C virus (HCV) is one of the leading causes of chronic liver disease. It was first identified in 1989, as being distinct from hepatitis A and hepatitis B. The HCV does not attack the immune system, but rather causes an inflammatory reaction that is localized within the liver, involving the entire organ. About 80% of patients with acute hepatitis C will develop chronic HCV, of which about 20-30% will progress to cirrhosis and its consequences, over 10-20 years. After 20-40 years, a smaller proportion of patients with chronic disease will develop hepatocellular carcinoma. The course and outcome of the disease vary considerably. In some individuals, spontaneous remission occurs over a few years; in others, the disease is more severe, progressing to cirrhosis and end-stage liver disease. Despite biochemical and pathological confirmation of the diagnosis, patients are often asymptomatic for many years. Hepatic failure occurs late in the disease. Factors suggesting a poor prognosis include high serum transaminase levels, active cirrhosis on liver biopsy, and an increased viral load (HCV RNA), as well as associated medical conditions such as alcoholic liver disease, hepatitis B viral (HBV) infection, or human immunodeficiency virus (HIV). Nutrition has been recognized as a prognostic indicator in patients with chronic liver failure. However, standardized approaches for the diagnosis and classification of malnutrition in this population have not been consistently applied before implementing nutrition intervention. Common criteria for the assessment of malnutrition, weight and body mass index (BMI) for example, do not give accurate data in patients with chronic liver disease, complicated by ascites and edema. In addition, the chronic inflammatory reaction of liver failure progresses slowly, so that subtle nutritional deficits are not obvious at early stages of the disease. A review of the literature has been undertaken to identify current nutritional guidelines for patients with hepatitis C as well as chronic hepatitis.
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PMID:Nutritional guidelines for persons infected with the hepatitis C virus: a review of the literature. 1151 51

Chemokines are implicated in the pathogenesis of alcoholic liver disease and human immunodeficiency virus-1 (HIV-1) infection. Thus, this work examined the regulation of chemokines --i.e., cytokine-induced neutrophil chemoattractant (CINC) and macrophage inflammatory protein-2 (MIP-2)--produced by hepatocytes after HIV-1 glycoprotein 120 (gp120) vaccination in Wistar rats fed with ethanol for 30 weeks. HIV-1 gp120 in complete Freund's adjuvant was given by intrainguinal route at a dose of 5 g/kg, followed by two booster shots in incomplete Freund's adjuvant at a weekly interval. Samples were taken 1 week after the last injection was given. Results show that anti-HIV-1 gp120 antibody titer was suppressed by 40% in the ethanol-fed rats, compared with findings in the parallel controls. However, serum CINC and MIP-2 levels were more elevated in the ethanol-fed rats than in the pair-fed group. The likely sources of these chemokines are the hepatocytes. After HIV-1 gp120 treatment, isolated hepatocytes obtained from the ethanol-fed group produced more CINC and MIP-2 than did those of pair-fed rats. Concomitantly, mRNA expression for these two chemokines and hepatic sequestration of neutrophils were upregulated. Ethanol feeding alone suppressed chemokine release, but it did not alter mRNA expression in isolated hepatocytes. Administration of Freund's adjuvant (without HIV-1 gp120) did not induce chemokine release in vivo and did not prime isolated hepatocytes for enhanced chemokine production in vitro. These results show that chronic ethanol intoxication affects the ability of the host to respond to HIV-1 gp120 vaccination.
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PMID:Chronic ethanol intoxication enhances the production of cytokine-induced neutrophil chemoattractant and macrophage inflammatory protein-2 by hepatocytes after human immunodeficiency virus-1 glycoprotein 120 vaccination. 1152 80

The objective of this study was to develop an anthropometry-based prediction model for the assessment of bone mineral content (BMC) in children. Dual-energy X-ray absorptiometry (DXA) was used to measure whole-body BMC in a heterogeneous cohort of 982 healthy children, aged 5-18 years, from three ethnic groups (407 European- American [EA], 285 black, and 290 Mexican-American [MA]). The best model was based on log transformations of BMC and height, adjusted for age, gender, and ethnicity. The mean +/- SD for the measured/predicted in ratio was 1.000 +/- 0.017 for the calibration population. The model was verified in a second independent group of 588 healthy children (measured/predicted In ratio = 1.000 +/- 0.018). For clinical use, the ratio values were converted to a standardized Z score scale. The whole-body BMC status of 106 children with various diseases (42 cystic fibrosis [CF], 29 juvenile dermatomyositis [JDM], 15 liver disease [LD], 6 Rett syndrome [RS], and 14 human immunodeficiency virus [HIV]) was evaluated. Thirty-nine patients had Z scores less than -1.5, which suggest low bone mineral mass. Furthermore, 22 of these patients had severe abnormalities as indicated by Z scores less than -2.5. These preliminary findings indicate that the prediction model should prove useful in determining potential bone mineral deficits in individual pediatric patients.
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PMID:Z score prediction model for assessment of bone mineral content in pediatric diseases. 1154 35

In hepatitis C virus (HCV) infection, virus load and the risk for HCV-related end-stage liver disease (ESLD) are increased among persons with human immunodeficiency virus (HIV) coinfection. To clarify these relationships, 42 hemophilic patients who developed ESLD and random samples from 164 hemophilic patients with HCV infection alone and 146 with HCV-HIV coinfection were tested for HCV load and genotype. HCV genotype was unrelated to HIV and age. In contrast, HCV load was higher with older age (P(trend)=.0001) and with HIV coinfection (6.2 vs. 5.9 log(10) genome equivalents/mL, P=.0001). During 16 years of follow-up of dually infected patients, ESLD risk was unrelated to HCV load overall (P(trend)=.64) or separately to HCV genotype 1 and genotypes 2 or 3 (P(trend)> or =.70). Irrespective of virus load, incidence of ESLD was marginally increased 2-fold (95% confidence interval, 0.8-5.6) with HCV genotype 1. Understanding the discordance between HCV load and ESLD, despite HIV's link to each of these, may help clarify the pathogenesis of HCV-related disease.
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PMID:Lack of association of hepatitis C virus load and genotype with risk of end-stage liver disease in patients with human immunodeficiency virus coinfection. 1159 46

Hepatitis C virus (HCV) has become a major contributor to morbidity and mortality in patients with human immunodeficiency virus (HIV). It is estimated that 30% to 50% of patients with HIV are coinfected with HCV. Advances in antiretroviral therapy and improved life expectancy of HIV patients have resulted in an emergence of HCV-induced liver disease as a leading cause of significant morbidity and death in this population. Clinically, hepatitis C is a more severe disease in HIV-infected individuals, characterized by rapid progression toward end-stage liver disease. Highly active antiretroviral therapy is the mainstay of current acquired immunodeficiency syndrome management. One of the limiting side effects of combination therapy for HIV is hepatotoxicity, which is more common and often more serious in patients with underlying liver disease. Management of coinfected patients has no strict guidelines, but it is generally accepted that HIV infection needs to be treated before HCV. Hepatitis C in coinfected individuals is probably best treated using combination therapy (interferon alpha and ribavirin). It appears that combination therapy can safely be administered to this population and that previous concerns about ribavirin/zidovudine antagonism are unsubstantiated in clinical practice. Although initial results using only interferon alpha showed poor results in HIV coinfected patients, combination therapy seems to be as effective as in the general population. All HIV-HCV coinfected patients should be vaccinated against hepatitis B and hepatitis A; vaccines are safe and effective.
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PMID:Hepatitis C and human immunodeficiency virus coinfections. 1160 51

Oxidative stress has been observed in HIV-1 infection and alcoholic liver disease. The formation of reactive oxygen species (ROS) contributes to cell injury through apoptosis and/or necrosis and secretion of proinflammatory cytokines and chemokines. The major sources of ROS and chemokines are the Kupffer cells. During chronic ethanol consumption they are primed and activated for enhanced formation of pro-inflammatory factors, probably as a result of ethanol-induced translocation of gut-derived endotoxin into the circulation. Pro-inflammatory factors produced in the liver stimulate neutrophilic and/or lymphocytic infiltration to this organ. The presence of inflammatory cells in the liver may compromise the hepatocytes to injury by releasing cytotoxic factors, i.e., ROS, cytolytic proteases. Kupffer cells also interact with the glycoprotein 120 of SIV and HIV-1, which can induce oxidative stress and chemokine release. CD4+ lymphocytes that are infected with the virus generate intracellular ROS, which in turn leads to apoptosis and cell death. Downregulation of CD4+ cells contributes to immunodeficiency, while enhanced sequestration of inflammatory cells in the liver during chronic ethanol use with or without HIV-1/SIV may result in hepatocyte injury and exacerbation of alcoholic liver disease.
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PMID:Free radicals, chemokines, and cell injury in HIV-1 and SIV infections and alcoholic hepatitis. 1174 25

Interactions between human immunodeficiency virus (HIV) and hepatitis C virus (HCV) have been widely studied before the introduction of highly active antiretroviral therapies (HAART). We reviewed the potential impact of HAART on hepatitis C as well as the interactions between HIV and HCV therapies. Physicians should be aware of the potential risk of: (i) symptomatic liver disease in HCV-HIV-coinfected patients at the era of triple antiretroviral therapy; (ii) potential liver deterioration paralleling immune restoration; (iii) lack of impact of triple antiretroviral therapy on HCV load; and (iv) potential drug-related hepatitis which may modify the natural history of HCV-related liver disease. Liver biopsies should be performed regularly in these patients in order to identify patients with severe liver disease who require early initiation of anti-HCV therapy under close monitoring of their immune status. Treatment is, to date, based on the combination of ribavirin and interferon with an expected sustained response rate around 25%. An important unresolved issue is to better delineate the temporal place of anti-HCV and anti-HIV antiviral therapies. At least in coinfected patients with significant liver disease, namely necro-inflammatory activity and/or fibrosis >or= 2, we believe that anti-HCV therapy is the priority since it lessens the risk of drug-induced hepatitis and of hepatitis due to immune restoration.
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PMID:Hepatitis C and human immune deficiency coinfection at the era of highly active antiretroviral therapy. 1185 97

The use of highly active antiretroviral therapy (HAART) has extended the lifespan of patients infected with human immunodeficiency virus (HIV). As the prognosis of HIV infection has improved, liver disease associated with hepatitis C virus (HCV) has become clinically significant in patients with HIV, liver failure being a frequent cause of death in this population. HIV infection may accelerate the course of liver disease in patients co-infected with HCV, so infection with HCV should be treated like any other opportunistic disease in these patients. Nowadays, combination therapy with interferon-alpha and ribavirin is the standard treatment for chronic hepatitis C in HIV-negative patients. Preliminary results of combination therapy in HIV/HCV co-infected patients have been promising, showing a sustained response rate in 40% of these patients. Patients with higher CD4 counts and lower HCV/HIV viral load and those infected with HCV genotype 3a have a better response to therapy. Potential drug interactions between HAART therapy and interferon and ribavirin treatment emphasize the importance of initiating treatment of HCV infection in HIV-positive individuals as soon as possible and ideally before the need for anti-HIV therapy. Recent case reports have suggested that liver transplantation might be an appropriate procedure in HIV patients with undetectable HIV viral load, high CD4 counts and HCV advanced liver disease. However, the limited amount of available information and the complexities of drug interactions between HAART therapy and immunosuppressive drugs oblige us to be prudent within considering such a procedure.
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PMID:Hepatitis C in HIV-infected patients--therapeutic approach. 1195 20

Highly active anti-retroviral therapy(HAART) for human immunodeficiency virus(HIV) has delayed the disease progression. The advances prompted us to undertake liver transplantation in a 41-year-old man with hemophilia B, HIV infection, and hepatitis C(HCV) end-stage liver disease. The donor was the patient's elderly brother. His right liver was implanted by the standard method. Two months after the operation, interferon alfa and ribavirin were administered for HCV infection. HCV was eradicated two weeks after the treatment. The HIV viral load is persistently negative and HAART has not been started so far. Utilizing a organ from living relatives should be one of the options to resolve the concern around the utilization of a scarce public source from cadavers for patients who may not have an equivalent survival to HIV negative patients.
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PMID:[Living donor liver transplantation in a patient with HIV]. 1196 92


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