Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019158 (hepatitis)
 30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of measles are relatively mild in well-nourished children, but are associated with high mortality in those who are malnourished and in those who have other diseases. Complications may include bacterial pneumonia, bronchitis, otitis media, gastroenteritis, myocarditis, hepatitis, and encephalomyelitis. The Expanded Program on Immunization was introduced to India in 1978, but measles immunization did not commence until 1985 under the Universal Immunization Program. Total district coverage was achieved in 1990, followed by a peak immunization coverage figure of 90.9% in 1991. Coverage rates declined, however, to 85.8% in 1992-93. Impressive though they may be, these coverage rates obfuscate the reality that measles remains a major cause of morbidity and childhood mortality in India. Coverage levels remain under 50% in many tribal and remote areas, with 49,453 notified cases at the time of printing. Overall case fatality rates for the country are in the range of 2-15% due to a synergistic relationship between malnutrition and infection. One must therefore not rest in the fight against measles. Sudden outbreaks should be reported immediately and vitamin A supplements and immunization supplies readied in anticipation of epidemic. The many reasons why vaccine coverage rates remain low in some areas include the failure of many parents, health personnel, and some doctors to regard measles as a serious disease; restrictive vaccine administration directives requiring the presence of a physician; physician reticence to open a 10-dose vial for 1-2 patients; and parental and physician reluctance to immunize children who are slightly ill or where minor adverse side reactions such as fever and rash may be anticipated.
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PMID:Measles is down but not out. 1217 72

Infections remain among the major causes of disease, hospitalization and death in uremic patients, especially in those treated by dialysis. Several pathophysiologic factors enhance this infectious risk: (1) breakdown of protective barriers; (2) affinity of bacteria for foreign materials; (3) bioincompatibility; (4) uremic toxin retention; (5) deficiency and resistance to vitamin D; (6) carriership of germs, and (7) malnutrition. Twenty to 30% of dialysis patients develop infection, and 20-30% of these die from their infection. Sepsis is significantly more frequent, and mortality secondary to sepsis is 50 times higher than in the normal population. Bacteremia (prevalence 1 episode/100 patient-months) is mainly caused by Gram-positive species, especially in vascular access-related infection and infection of unknown origin. Among these Gram-positive germs, staphylococci play a predominant role. The most frequent and most morbid viral infections are associated with hepatitis. Whereas the incidence of hepatitis B decreases, hepatitis C has become the major variant. The incidence of tuberculosis has increased up to 15 times, and in the Western world it mainly affects patients who immigrated from endemic areas. Fungal infections are also frequent, especially in the setting of peritoneal dialysis. In conclusion, infections remain a frequent and morbid problem in dialysis patients. Preventive measures should be applied more vigorously.
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PMID:Incidence of infectious morbidity and mortality in dialysis patients. 1220 97

Morbidity from pregnancy complications was 19.6% of inpatients in 1990 in Bangkok Metropolis. This study examines the impact of local customs on prenatal, delivery, and postpartum care; the factors affecting use of health services for prenatal care and delivery; and the nature of women's involvement in IEC for maternal health. Data was obtained from a community survey in May 1992 among 526 ever married women, 15-40 years old, from low-income communities in Bangkok Metropolis. In-depth interviews with hospital personnel were conducted at two general hospitals and three health centers, and focus groups were conducted in two communities. Findings show that Hospital A received 220 old and 80 new prenatal patients daily; Hospital B accommodated 130 old and 50 new ones. According to nurses, the major hospital problem was doctors' attitudes toward nurses. Comprehensive services were available at both hospitals. Hospital B encountered patient health problems of minor malnutrition, syphilis, and hepatitis, while Hospital A treated diarrhea and high blood pressure problems. A lack of medical personnel was reported in both settings. Low level of education was reported as related to noncompliance. Incorrect practices were identified as adherence to food taboos that led to deficiencies, consumption of whiskey with traditional medicine, which contaminated breast milk, and discarding mother's first milk. At health centers, which included family planning, doctors only saw high risk patients; complications generally were for swelling, high blood pressure, and vaginal bleeding. Not all centers had a prenatal care diagnostic manual or licensed nurses. Obstacles to delivery of health care included a lack of nurses, refusals at referral centers by low level personnel, and a poor rapport between nurses and patients, which improved with bribes. Poorly educated patients had trouble understanding their health condition. Nurses and focus groups reported that services were not convenient for patients. Migration interfered with keeping appointments. Male doctors were preferred to female doctors as nicer to patients.
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PMID:Health services providers and users' opinions on maternal health services in Bangkok metropolis. 1231 92

The archives of the blood bank of the hospital of Dr. Louis Manual Morillo King, in the city of La Vega, Dominican Republic, were reviewed to identify all children who had been given blood transfusion during the period of July 1983 to July 1987 in order to identify HIV and the surface antigen of hepatitis B (HBsAg). Those who were released were visited in their homes for administration of HIV and hepatitis tests. Positive tests were confirmed by another test (AUSYME MONOCLONAL and Western Blot). Mothers were also tested to detect vertical transmission. 256 patients had been transfused, of whom 61 died. 80 of the 195 remaining patients could not be located. Of the 115 patients located, 52 had died in their homes after release from the hospital. Thus, the sample comprised 63 patients: 36 were 0-3 years old, 21 were 4-7 years old, and 6 were 8-11 years old. 50 lived in rural and 13 in urban areas. 56 patients had one transfusion and 4 had two transfusions. 28 patients had transfusion for anemia, 19 for malnutrition, 7 for sepsis, 6 for various reasons (meningitis, pleuritis, pneumonia), and 3 for sickle cell disease. 47 patients had been transfused at the hospital using the blood bank, 13 used blood from relatives, and 3 received blood from friends. Out of the 63 samples processed, 2 patients presented seropositivity for hepatitis B, while none were seropositive for HIV. Among the 2 patients who were seropositive for hepatitis B, the mother of one of them was also seropositive.
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PMID:[Human immunodeficiency virus and hepatitis B virus in children transfused in the Dr. Luis Manuel Morillo King Hospital]. 1234 60

Azathioprine is commonly prescribed for autoimmune hepatitis and inflammatory bowel disease. An acute gastroenteritis-like syndrome has been ascribed to azathioprine use, but chronic diarrhea has not. We report a patient with autoimmune hepatitis who developed severe small-bowel villus atrophy and chronic diarrhea after azathioprine was initiated (50 mg/day). We present a case report of a patient followed up prospectively. Duodenal mucosal histology and expression of brush border enzyme dipeptidyl peptidase IV and peptide transporter PepT1 messenger RNA levels were determined before and after azathioprine discontinuation. Chronic diarrhea developed several weeks after the initiation of azathioprine and resulted in micronutrient depletion and severe protein-calorie malnutrition, which was unresponsive to oral pancreatic enzyme therapy or a gluten-free diet. Severe malabsorption required parenteral nutrition support for longer than 1.5 years; this was complicated by unstable blood glucose control, acute calculous cholecystitis, catheter sepsis, and severe venous thrombosis. When the temporal association between azathioprine and diarrhea was identified, the drug was tapered while the patient consumed an unrestricted diet. Within 2 weeks after azathioprine was discontinued, diarrhea had completely resolved, and parenteral nutrition was discontinued. Mucosal biopsies obtained before and 4 months after azathioprine discontinuation showed complete reversal of severe duodenal villus atrophy and marked up-regulation of mucosal dipeptidyl peptidase IV and PepT1 messenger RNA. The patient has subsequently maintained normal liver function tests on low-dose prednisone alone, with normal stools and stable nutritional status for longer than 4 years. Azathioprine can induce severe small-bowel villus atrophy, diarrhea, and malabsorption that is reversible with drug discontinuation.
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PMID:Severe villus atrophy and chronic malabsorption induced by azathioprine. 1280 28

Ethanol toxicity on liver is a function of duration of alcoholism, amount of daily intake of alcohol and patient's nutrition. The threshold of alcohol toxicity on the liver is about 40 g of ethanol daily in men and 20-30 g in women, however liver cirrhosis develops in no more than 8-20% of patients exceeding this values. Ethanol is oxidized in the liver to acetaldehyde--a compound considerably more toxic than ethanol itself. Despite small amount of alcohol dehydrogenase (ADH) found in gastric mucosa, the metabolism of ethanol in this site may have an important hepatoprotective effect. The oxidation of ethanol is associated with a change of hepatocyte redox homeostasis, which leads to a number of metabolic disorders such as lactic acidosis, hyperlipidaemia and hyperuricaemia. Chronic ethanol consumption does not influence ADH activity, but has a profound stimulatory effect on microsomal enzymes, in particular cytochrome CYP2E1. This fact is responsible for development in alcoholic liver associated with rise of oxygen consumption, excessive production of free radicals and increased metabolism of ethanol, vitamin A and testosterone. Ethanol and acetaldehyde have a deleterious effect, both the direct and indirect, on hepatocytes e.g., generating radical oxygen species and damaging intestinal mucosal barrier. Cellular oxidative stress that is caused by both an excess of free radicals and the antioxidatives' deficiency (glutathion, vitamin E, phosphatidylcholine), may be the principal factor responsible for progression of alcoholic liver disease. Among other factors accelerating alcohol-related liver lesion there are certain drugs, high fat diet, infection with HCV and genetic factors (female sex, enzymatic polymorphic forms of ADH and ALDH, hemochromatosis). Great importance in pathogenesis of necrotic and inflammatory hepatic events is being attributed to portal endotoxaemia and cytokines induced within the liver, in particular TNF-alpha and interleukin 8. These cytokines play a key role in development of alcoholic hepatitis, which clinical severity ranges from subclinical to fatal forms. Apart from abstinence, the treatment of alcohol liver disease is based on hyperalimentation, since alcoholism is generally associated with protein malnutrition. In severe forms of alcohol hepatitis corticosteroids are recommended.
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PMID:[Alcoholic liver disease]. 1290 Dec 71

Deficiency of citrin encoded by SLC25A13 causes adult-onset type II citrullinemia (CTLN2) and idiopathic neonatal hepatitis (NICCD). So far we have diagnosed 126 (3) CTLN2 and 103 (4) NICCD patients in Japan (and other countries). From preliminary population analysis of the known nine SLC25A13 mutations, we found that the carrier frequency is high in China (1/79), Taiwan (1/98), and Korea (1/50) as well as Japan (1/69), suggesting that many patients with citrin deficiency exist in East Asia.
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PMID:Screening of nine SLC25A13 mutations: their frequency in patients with citrin deficiency and high carrier rates in Asian populations. 1468 Sep 84

There has been increasing interest in the development of effective agents that can be safely used to promote anabolism in the clinical setting for patients with chronic wasting conditions as well as in the prevention and treatment of frailty associated with loss of muscle tissue in aging (sarcopenia). One such agent is the anabolic androgenic steroid (AAS) oxandrolone, which has been used in such clinical situations as HIV-related muscle wasting, severe burn injury, trauma following major surgery, neuromuscular disorders and alcoholic hepatitis for over 30 years. In the US, oxandrolone is the only AAS that is US FDA-approved for restitution of weight loss after severe trauma, major surgery or infections, malnutrition due to alcoholic cirrhosis, and Duchenne's or Becker's muscular dystrophy. Our review of the use of oxandrolone in the treatment of catabolic disorders, HIV and AIDS-related wasting, neuromuscular and other disorders provides strong evidence of its clinical efficacy. Improvements in body composition, muscle strength and function, status of underlying disease or recovery from acute catabolic injury and nutritional status are significant in the vast majority of well designed trials. However, oxandrolone has not yet been studied in sarcopenia.Unlike other orally administered C17alpha-alkylated AASs, the novel chemical configuration of oxandrolone confers a resistance to liver metabolism as well as marked anabolic activity. In addition, oxandrolone appears not to exhibit the serious hepatotoxic effects (jaundice, cholestatic hepatitis, peliosis hepatis, hyperplasias and neoplasms) attributed to the C17alpha-alkylated AASs. Oxandrolone is reported to be generally well tolerated and the most commonly documented adverse effects are transient elevations in transaminase levels and reductions in high density lipoprotein cholesterol level.However, optimal risk:benefit ratios for oxandrolone and other agents in its class will need to be refined before widespread clinical acceptance of AASs as a therapeutic option in sarcopenia and other chronic wasting conditions.
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PMID:The anabolic androgenic steroid oxandrolone in the treatment of wasting and catabolic disorders: review of efficacy and safety. 1502 46

Apart from infectious or viral hepatitis, other most common non-infectious causes of hepatitis are alcohol, cholestatic, drugs and toxic materials. The most common mode that leads to liver injuries is antituberculosis drug-induced hepatitis. The severity of drug-induced liver injury varies from minor nonspecific changes in hepatic structure to fulminant hepatic failure, cirrhosis and liver cancer. Patients receiving antitubercular drug frequently develop acute or chronic hepatitis. The time required for the metabolites to reach hepatotoxic levels is much earlier with isoniazid plus rifampicin treatment than isoniazid alone and this has been shown to be synergistic rather than additive. Antituberculosis drug (ATT)-inducible cytochrome P-4502E1 (CYP2E1) is constitutively expressed in the liver. Recent studies show that polymorphism of the N-acetyltransferase 2 (NAT2) genes and glutathione-S-transferase (GST) are the major susceptibility risk factors for ATT-induced hepatitis. The hepatic NAT and GST are involved in the metabolism of several carcinogenic arylamines and drugs. The NAT2 enzyme has a genetic polymorphism in human. N-acetyltransferase 2 genes (NAT2) have been identified to be responsible for genetic polymorphism of slow and rapid acetylation in humans. Slow acetylators of NAT2 prove to develop more severe hepatotoxicity than rapid acetylators making it a significant risk factor. Deficiency of GST activity, because of homozygous null mutations at GSTM1 and GSTT1 loci, may modulate susceptibility to drug and xenobiotic-induced hepatotoxicity. Polymorphisms at GSTM1, GSTT1 and NAT2 loci had been linked to various forms of liver injury, including hepatocellular carcinoma.
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PMID:Antituberculosis drug-induced hepatitis: risk factors, prevention and management. 1533 88

Deficiency of citrin, a liver-type mitochondrial aspartate-glutamate carrier (AGC), encoded by the SLC25A13 gene on chromosome 7q21.3, causes autosomal recessive disorders: adult-onset type II citrullinemia (CTLN2) and neonatal hepatitis associated with intrahepatic cholestasis (NICCD). So far, we have described 12 SLC25A13 mutations: 11 were from Japan and one from Israel. Three mutations found in Chinese and Vietnamese patients were the same as those in Japanese patients. In the present study, we identified a novel mutation IVS6+1G>C in a Japanese CTLN2 patient and widely screened 12 SLC25A13 mutations found in Japanese patients in control individuals from East Asia to confirm our preliminary results that the carrier frequency was high in Asian populations. Mutations 851-854del and 1638-1660dup were found in all Asian countries tested, and 851-854del associated with 290-haplotype in microsatellite marker D7S1812 was especially frequent. Other mutations frequently detected were IVS11+1G>A in Japanese and Korean, S225X in Japanese, and IVS6+5G>A in Chinese populations. We found a remarkable difference in carrier rates in China (including Taiwan) between north (1/940) and south (1/48) of the Yangtze River. We detected many carriers in Chinese (64/4169 = 1/65), Japanese (20/1372 = 1/69) and Korean (22/2455 = 1/112) populations, suggesting that over 80,000 East Asians are homozygotes with two mutated SLC25A13 alleles.
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PMID:Frequency and distribution in East Asia of 12 mutations identified in the SLC25A13 gene of Japanese patients with citrin deficiency. 1605 47


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