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)

Hepatitis-Associated (Australia) Antigen (HAA) was detected in 13 (5.8%) of 223 patients with Down's syndrome and in 14 (3.7%) of 378 patients with other forms of mental retardation. The frequency of HAA was 2.4 per cent in 127 noninstitutionalized patients with Down's syndrome, and 10.4 per cent in 96 institutionalized patients. The frequency of HAA with Down's syndrome was lower on the average in Japan than in the United States or Germany. HAA was detected in one (1.3%) of 78 mothers of infants with Down's syndrome. Our study suggests that maternal exposure to HAA, as reflected by the presence of either HAA or anti-HAA, was not associated with the subsequent birth of an infant with Down's syndrome.
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PMID:Hepatitis-associated (Australia) antigen and Down's syndrome. 12 83

Data obtained concerning Hepatitis B as a possible couse of Down's syndrome, neonatal hepatitis, and the occurrence of Hepatitis A and B in institutionalized Down's syndrome and matched non-Down's syndrome retarded patients was summarized. The results of our studies indicated that Hepatitis B infection during pregnancy was not related to the genetic changes associated with Down's syndrome. It was further indicated that in institutionalized patients the incidence of Hepatitis B infection in both Down's syndrome and other mentally retarded patients was similar. Within the institition we studied, the incidence of Hepatitis B varied among wards. This ward variation seemed to be related to age at time of institutionalization and degree of mental retardation. Those patients with most retardation and those institutionalized at an early age were placed on wards with highest incidence of Hepatitis B antigenemia.
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PMID:Hepatitis and Down's syndrome. 12 5

Institutionalized patients with Down syndrome and matched controls with other causes of mental retardation were tested by immune adherence hemagglutination for the presence of antibody to hepatitis A antigen (anti-HA). Altogether 75.1% (175 of 233) exhibited presence of anti-HA, with no differences by sex or age. Patients reactive for hepatitis B surface antigen (HBsAg) or its antibody (anti-HBs) were reactive for anti-HA significantly more frequently than those with a negative reaction for these markers. In contrast to serologic markers of hepatitis type B, prevalence of anti-HA does not depend on the cause of mental retardation or on the age at primary infection. The rate of anti-HA positivity was found to be closely correlated with duration of institutionalization. The study confirmed that many closed institutions for the mentally retarded are hyperendemic for hepatitis type A and that formation of anti-HA is not greatly affected by either immune deficiency or immune immaturity.
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PMID:Antibody to hepatitis A antigen in institutionalized mentally retarded patients. 13 79

Twenty-seven infants with cytomegalovirus hepatitis were followed up for 15-40 months after onset of the illness. They had recovered from the hepatitis, but microcephaly was present in 2 (7.4%), sensorineural hearing loss in 5 (18.5%), quadriplegia, mental retardation, ventricular septal defect and tooth defects in 1 (3.7%) each. The patients with congenital infection had more severe and complex defects, some with perinatal infection had mild defects, those with postnatally acquired infection had no sequelae. The mean MDI and frequency of expressive language delay in the former group differed significantly from those of the other 2. Five patients still excreted cytomegalovirus in the urine at follow-up.
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PMID:Effects of cytomegalovirus hepatitis on growth, development and nervous system of infants. A follow-up study. 165 27

The institutionalized population and staff in a centre for the mentally retarded were tested retrospectively, and 1.6% hepatitis Bs antigen and 0.6% hepatitis Be antigen carriers were found among persons with mental retardation. The 40 subjects, residents and staff, with most risk of acquiring hepatitis B were given vaccination. The immunogenicity of the H-B-Vax vaccine was followed up prospectively and, in 7.5% of the vaccinated persons, even re-vaccination gave an unsatisfactory result.
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PMID:Hepatitis B carriers in a centre for the mentally retarded in Finland and immunogenicity of hepatitis B vaccine. 214 93

In 1980, 18 institutionalized children, carriers of hepatitis B virus (HBV), were enrolled into two special education schools, and staff and students were monitored for HBV markers. Eleven HBV exposures were observed and those exposed were given hepatitis B immune globulin. After 3.5 years, no remaining staff showed serological evidence of HBV infection but three of 61 susceptible students did so. The three students probably acquired the infection outside the school. At the conclusion of the project, one school located in the community decided not to institute a vaccine program for students or staff. The other school, located inside the mental retardation institution, established an organized vaccine initiative. Indications for use of hepatitis vaccine in schools should be individualized to accommodate for differences in student and staff interaction, physical design of the school, and number and behaviors of HBsAg carrier students.
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PMID:Hepatitis B virus transmission in a public school: effects of mentally retarded HBsAG carrier students. 382 68

In 1814, George Maton, first recognized that a mild illness characterized by rash, adenopathy, and little or no fever was a discrete entity. Henry Veale, in 1866, named the disease rubella. The illness attracted little attention until 1942, when Norman Gregg noticed that first-trimester maternal rubella caused serious birth defects. The full spectrum and impact of rubella embryopathy remained unclarified until rubella virus was isolated in tissue culture in 1962 by two independent groups: Parkman, Buescher, and Artenstein; and Neva and Weller. Using the new tools of the virus laboratory, many investigators concentrated on the consequences of a severe rubella epidemic in 1964, which affected approximately 1% of pregnancies. Newly recognized transient manifestations of congenital rubella infection (CRI) include neonatal thrombocytopenic purpura, hepatitis, bone lesions, and meningoencephalitis and late-emerging sequelae such as diabetes mellitus and progressive rubella panencephalitis added to the cataract, heart disease, mental retardation, and deafness previously defined as due to CRI. Sharp contrasts were documented between the patterns of virus excretion and immune response of postnatal vs. congenital rubella. Licensure and widespread distribution of attenuated rubella virus vaccines in 1969 have prevented epidemic rubella. Pockets of illness remain, even in the United States. Continued effort will be required to eliminate the rubella problem.
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PMID:The history and medical consequences of rubella. 389 Jan 5

Valproic acid is a useful antiepileptic drug, with occasional gastrointestinal side effects. Hepatotoxicity is the most serious adverse reaction and, although rare, it can be fatal. Risk factors for hepatotoxicity are an age of less than two years, polytherapy and mental retardation; it has been rarely reported in adults. We report three mentally retarded adult patients receiving polytherapy, who developed valproic acid induced hepatotoxicity. Two patients had a symptomatic hepatitis with a concomitant paradoxical increase in seizure frequency and one an asymptomatic alteration of hepatic function tests. After discontinuing the drug, the hepatitis subsided. We conclude that hepatotoxicity must be considered as a possible side effect of valproic acid and we suggest some recommendations for its early detection.
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PMID:[Hepatotoxicity induced by valproic acid in adults. Report of 3 cases]. 808 69

Complete loss of N-glycosylation is lethal in both yeast and mammals. Substantial deficiencies in some rate-limiting biosynthetic steps cause human congenital disorders of glycosylation (CDG). Patients have a range of clinical problems including variable degrees of mental retardation, liver dysfunction, and intestinal disorders. Over 60 mutations in phosphomannomutase (encoded by PMM2) diminish activity and cause CDG-Ia. The severe mutation R141H in PMM2 is lethal when homozygous, but heterozygous in about 1/70 Northern Europeans. Another disorder, CDG-Ic, is caused by mutations in ALG6, an alpha 1,3glucosyl transferase used for lipid-linked precursor synthesis, yet some function-compromising mutations occur at a high frequency in this gene also. Maintenance of seemingly deleterious mutations implies a selective advantage or positive heterosis. One possible explanation for this is that production of infective viruses such as hepatitis virus B and C, or others that rely heavily on host N-glycosylation, is substantially inhibited when only a tiny fraction of their coat proteins is misglycosylated. In contrast, this reduced glycosylation does not affect the host. Prevalent functional mutations in rate-limiting glycosylation steps could provide some resistance to viral infections, but the cost of this insurance is CDG. A balanced glycosylation level attempts to accommodate these competing agendas. By assessing the occurrence of a series of N-glycosylation-compromising alleles in multi-genic diseases, it may be possible to determine whether impaired glycosylation is a risk factor or a major determinant underlying their pathology.
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PMID:Balancing N-linked glycosylation to avoid disease. 1153 Feb 12

Childhood tuberculous meningitis is associated with serious long-term sequelae, including mental retardation, behavior disturbances, and motor handicap. Brain damage in tuberculous meningitis results from a cytokine-mediated inflammatory response, which causes vasculitis and obstructive hydrocephalus. Thalidomide, a potent tumor necrosis factor alpha inhibitor, was well tolerated and possibly showed some clinical benefit in children with tuberculous meningitis during a pilot study. The purpose of the present study was to assess the effect of adjunctive thalidomide in addition to standard antituberculosis and corticosteroid therapy on the outcome of tuberculous meningitis. Thalidomide (24 mg/kg/day orally) or placebo was administered in a double-blind randomized fashion for 1 month to patients with stage 2 or 3 tuberculous meningitis. The study was terminated early because all adverse events and deaths occurred in one arm of the study (thalidomide group). Thirty of the 47 children enrolled received adjunctive thalidomide, of whom 6 (20%) developed a skin rash, 8 (26%) hepatitis, and 2 (6%) neutropenia or thrombocytopenia. Four deaths (13%) occurred in patients with very severe neurologic compromise at baseline; two deaths were associated with a rash. Motor outcome after 6 months of antituberculosis therapy was similar in the two groups, even though the thalidomide group showed greater neurologic compromise on admission. In addition, the mean IQ of the two treatment groups did not differ significantly (mean IQ thalidomide group 57.8 versus mean IQ control group 67.5; P = .16). These results do not support the use of adjunctive high-dose thalidomide therapy in the treatment of tuberculous meningitis.
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PMID:Adjunctive thalidomide therapy for childhood tuberculous meningitis: results of a randomized study. 1516 89


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