Neurologic complications in children with enterovirus 71 infection. (41/3380)

BACKGROUND: Enterovirus 71 infection causes hand-foot-and-mouth disease in young children, which is characterized by several days of fever and vomiting, ulcerative lesions in the oral mucosa, and vesicles on the backs of the hands and feet. The initial illness resolves but is sometimes followed by aseptic meningitis, encephalomyelitis, or even acute flaccid paralysis similar to paralytic poliomyelitis. METHODS: We describe the neurologic complications associated with the enterovirus 71 epidemic that occurred in Taiwan in 1998. At three major hospitals we identified 41 children with culture-confirmed enterovirus 71 infection and acute neurologic manifestations. Magnetic resonance imaging (MRI) was performed in 4 patients with acute flaccid paralysis and 24 with rhombencephalitis. RESULTS: The mean age of the patients was 2.5 years (range, 3 months to 8.2 years). Twenty-eight patients had hand-foot-and-mouth disease (68 percent), and 6 had herpangina (15 percent). The other seven patients had no skin or mucosal lesions. Three neurologic syndromes were identified: aseptic meningitis (in 3 patients); brain-stem encephalitis, or rhombencephalitis (in 37); and acute flaccid paralysis (in 4), which followed rhombencephalitis in 3 patients. In 20 patients with rhombencephalitis, the syndrome was characterized by myoclonic jerks and tremor, ataxia, or both (grade I disease). Ten patients had myoclonus and cranial-nerve involvement (grade II disease). In seven patients the brain-stem infection produced transient myoclonus followed by the rapid onset of respiratory distress, cyanosis, poor peripheral perfusion, shock, coma, loss of the doll's eye reflex, and apnea (grade III disease); five of these patients died within 12 hours after admission. In 17 of the 24 patients with rhombencephalitis who underwent MRI, T2-weighted scans showed high-intensity lesions in the brain stem, most commonly in the pontine tegmentum. At follow-up, two of the patients with acute flaccid paralysis had residual limb weakness, and five of the patients with rhombencephalitis had persistent neurologic deficits, including myoclonus (in one child), cranial-nerve deficits (in two), and ventilator-dependent apnea (in two). CONCLUSIONS: In the 1998 enterovirus 71 epidemic in Taiwan, the chief neurologic complication was rhombencephalitis, which had a fatality rate of 14 percent. The most common initial symptoms were myoclonic jerks, and MRI usually showed evidence of brainstem involvement.  (+info)

Genetic polymorphisms of N-acetyltransferase 1 and 2 and risk of cigarette smoking-related bladder cancer. (42/3380)

Aromatic amines from cigarette smoking or occupational exposure, recognized risk factors for bladder cancer, are metabolized by N-acetyltransferases (NAT). This study examined the association of (NAT) 1 and 2 genotypes with the risk of smoking-related bladder cancer. A total of 74 pathologically confirmed bladder cancer patients and 184 controls were serially recruited from the National Taiwan University Hospital. History of cigarette smoking and other risk factors for bladder cancer was obtained through standardized questionnaire interview. Peripheral blood lymphocytes were collected from each subject and genotyped for NAT1 and NAT2 by DNA sequencing and polymerase chain reaction-restriction fragment length polymorphism methods. Allele frequency distributions of NAT1 and NAT2 were similar between cases and controls. There was a significant dose-response relationship between the risk of bladder cancer and the quantity and duration of cigarette smoking. The biological gradients were significant among subjects carrying NAT1*10 allele or NAT2 slow acetylators, but not among NAT2 rapid acetylators without NAT1*10 allele. The results are consistent with the hypothesis that NAT1 and NAT2 might modulate the susceptibility to bladder cancer associated with cigarette smoking.  (+info)

Breast cancer risk associated with genotype polymorphism of the estrogen-metabolizing genes CYP17, CYP1A1, and COMT: a multigenic study on cancer susceptibility. (43/3380)

Estrogen has been proposed to trigger breast cancer development via an initiating mechanism involving its metabolite, catechol estrogen (CE). To examine this hypothesis, we conducted a multigenic case-control study to determine whether polymorphisms of the genes responsible for CE formation via estrogen biosynthesis (CYP17) and hydroxylation (CYP1A1) and CE inactivation (COMT) are associated with an elevated risk for breast cancer in Taiwanese women, and whether the association between genotype and risk may be modified by estrogen exposure. One hundred and fifty breast cancer patients and 150 healthy controls were recruited. PCR-based RFLP assays were used to determine the genotypes of estrogen-metabolizing genes. The breast cancer risk associated with individual susceptibility genotypes varied among the three genes and was highest for COMT, followed by CYP1A1 and CYP17. After simultaneous consideration of all three genes and other well-established risk factors of breast cancer, the COMT genotype remained the most significant determinant for breast cancer development and was associated with a 4-fold increase in risk (95% confidence interval, 1.12-19.08). Furthermore, a trend of increasing risk for developing breast cancer was found in women harboring higher numbers of high-risk genotypes (P = 0.006), including the high activity CYP17 (CYP17 A2/A2), high inducibility CYP1A1 (CYP1A1 MspI vt/vt), and low activity COMT (COMT L/L) genotypes. The association of risk with the number of susceptibility genotypes was stronger in women with prolonged estrogen exposure (indicated by a higher number of estrogen exposure years or a higher number of estrogen exposure years between menarche and first full-term pregnancy), women with higher estrogen levels (implied by early menarche), and women with a higher body mass index (> or = 22.5). On the basis of comprehensive profiles of estrogen metabolism, this study supports the possibility that breast cancer can be initiated by estrogen exposure.  (+info)

A point mutation in the albumin gene in a Chinese patient with familial dysalbuminemic hyperthyroxinemia. (44/3380)

Familial dysalbuminemic hyperthyroxinemia (FDH) is an autosomal dominant disorder characterized by euthyroid hyperthyroxinemia. However, FDH has not been reported in Chinese or African patients. Here, we report the first case of FDH in a Chinese patient. A 69-year-old Chinese man was found to have increased serum total T(4) concentrations (198-242nmol/l; normal range 58-148nmol/l) and free T(4) concentrations (>58pmol/l; T(4) analog method, normal range 9-28pmol/l). Serum total T(3) and TSH concentrations were normal. The patient was misdiagnosed as hyperthyroid and was later suspected to have a TSH-producing tumor by the finding of a pituitary microadenoma, which was eventually proven to be a non-functional pituitary 'incidentaloma'. Electrophoretic analysis of the patient's serum proteins demonstrated enhanced albumin binding of [(125)I]T(4). Serum free T(4) concentrations were normal (16-19pmol/l, normal range 9-26pmol/l) when a two-step method was used. Direct sequencing of the albumin gene showed a guanine to adenosine transition in the second nucleotide of codon 218, resulting in a substitution of histidine (CAC) for the normal arginine (CGC) in one of the two alleles in the patient. The point mutation was further confirmed by HphI digestion of exon 7 of the albumin gene. The patient's son was not affected. Our studies demonstrated that the point mutation of the albumin gene in a Chinese patient with FDH was similar to that found in western white families, but differed from that in a Japanese family in whom a guanine to cytosine transition at the same position was found.  (+info)

The advisability of implementing cholesterol screening in school-age children and adolescents with a family history of cardiovascular disease and hyperlipidaemia. (45/3380)

BACKGROUND: The family basis of coronary heart disease is well recognized and it is important for family physicians to assess whether children have elevated cholesterol levels. OBJECTIVES: We aimed to evaluate the advisability of implementing cholesterol screening in children with a family history of cardiovascular disease and hyperlipidaemia. METHODS: We conducted a cross-sectional study in Taiwan from February to June 1996. There were 47,800 students in the population. A total of 4520 students were recruited by two-stage sampling. All the participants were required to fill out a structured questionnaire. RESULTS: The response rate was 92.5%. Our results show that 16-18% of the children had a positive family history of cardiovascular disease or hyperlipidaemia. Children with a family history of hyperlipidaemia were significantly more likely to have elevated total cholesterol and low-density lipoprotein cholesterol than those without such a history (both odds ratios: 1.4, P < 0.05). Positive predictive values of hyperlipidaemia were less than 13% based on family history. More than 75% of children with abnormal lipid levels would be missed. CONCLUSIONS: The data suggest that parents' self-reported family history is an ineffective means of identifying children with elevated serum lipid levels in Taiwan. Further research and modification of current National Cholesterol Education Program Panel guidelines for selective cholesterol screening in children may be warranted.  (+info)

Economic transition and changing relation between income inequality and mortality in Taiwan: regression analysis. (46/3380)

OBJECTIVE: To examine the changing relation between income inequality and mortality through different stages of economic development in Taiwan. DESIGN: Regression analysis of mortality on income inequality for three index years: 1976, 1985, and 1995. SETTING: 21 counties and cities in Taiwan. MAIN OUTCOME MEASURES: All age mortality and age specific mortality in children under age 5. RESULTS: When median household disposable income was controlled for, the association between income inequality and mortality became stronger in 1995 than in 1976. Especially, the association between income inequality and mortality in children aged under 5, with adjustment for differences in median household disposable income, changed from non-significant in 1976 to highly significant in 1995. In 1995, the level of household income after adjustment for income distribution no longer had a bearing on mortality in children under 5. CONCLUSION: The health of the population is affected more by relative income than by absolute income after a country has changed from a developing to a developed economy.  (+info)

Seroepidemiology of Helicobacter pylori infection among preschool children in Taiwan. (47/3380)

Helicobacter pylori is associated with chronic antral gastritis that is related to duodenal ulcer, gastric ulcer, and probably gastric adenocarcinoma. Infection with H. pylori during childhood is considered an important risk factor for gastric carcinoma in adult life. To examine the epidemiologic characteristics of H. pylori infection among preschool children in central Taiwan, a community-based survey was carried out in 54 kindergartens in 10 urban townships, 10 metropolitan precincts, and 2 aboriginal townships randomly selected through stratified sampling. Serum specimens of 2,551 healthy preschool children (3-6 years old) randomly sampled from study kindergartens were screened for antibodies to H. pylori by latex agglutination and ELISA methods. Multivariate-adjusted odds ratios (ORs) with their 95% confidence intervals (CIs) were estimated by multiple logistic regression analysis. A total of 207 subjects were antibody-positive, giving a prevalence of 8.1%. The overall seropositive rates were 4.5% in 3-year-old group, 4.4% in 4-year-old group, 9.4% in 5-year-old group, and 11.7% in 6-year-old group. The older the age, the higher the seroprevalence (OR = 3.2, 95% CI = 1.5-6.8 for 3-year-old children versus the 6-year-old children). Seroprevalence was not different between boys and girls. The aboriginal townships had a seroprevalence greater than the urban townships and metropolitan precincts (OR = 2.6, 95% CI = 1.9-3.7). The larger the number of siblings, the higher the seroprevalence (OR = 2.4, 95% CI = 1.0-5.8 for those with no sibling versus those with > or = 3 siblings). In the multiple logistic regression analysis, the seroprevalence of H. pylori remained significantly increased with age, aboriginal township, and large sibship size after multivariate adjustment. A poor water supply system, sewage disposal, and other environmental hygiene in the aboriginal townships might have played some role in infection with H. pylori. The early childhood transmission among siblings might also be an important determinant of H. pylori seropositivity in Taiwan.  (+info)

Heterogeneous Helicobacter pylori isolates from H. pylori-infected couples in Taiwan. (48/3380)

Helicobacter pylori strain diversity was investigated in 55 H. pylori seropositive couples in Taiwan in biopsy samples from the antrum and corpus. Two DNA typing methods were used to characterize 90 isolates from 25 couples. In only 1 of the 25 couples was the same strain colonized from both partners. Comparison of isolates from 2 sites in each of 40 patients showed that 9 pairs were distinct but might be related. Peptic ulcer occurred in 77.8% of these 9 patients compared with 29% of 31 patients with the same predominant strain in 2 biopsies (P=.025). Random amplified polymorphic DNA and sequence analyses of 2 closely related isolates from 1 patient support the hypothesis that development of genetic diversity of H. pylori results from horizontal genetic exchange during long-term colonization of mixed bacterial populations.  (+info)