Abstract-Omega-3 fatty acids have potential antiatherogenic, antithrombotic, and antiarrhythmic properties, but their role in coronary heart disease remains controversial. To evaluate the association of omega-3 fatty acids in adipose tissue with the risk of myocardial infarction in men, a case-control study was conducted in eight European countries and Israel. Cases (nϭ639) included patients with a first myocardial infarction admitted to coronary care units within 24 hours from the onset of symptoms. Controls (nϭ700) were selected to represent the populations originating the cases. Adipose tissue levels of fatty acids were determined by capillary gas chromatography. The mean (ϮSD) proportion of ␣-linolenic acid was 0.77% (Ϯ0.19) of fatty acids in cases and 0.80% (Ϯ0.19) of fatty acids in controls (Pϭ0.01). The relative risk for the highest quintile of ␣-linolenic acid compared with the lowest was 0.42 (95% confidence interval [CI] 0.22 to 0.81, P-trendϭ0.02). After adjusting for classical risk factors, the relative risk for the highest quintile was 0.68 (95% CI 0.31 to 1.49, P-trendϭ0.38). The mean proportion of docosahexaenoic acid was 0.24% (Ϯ0.13) of fatty acids in cases and 0.25% (Ϯ0.13) of fatty acids in controls (Pϭ0.14), with no evidence of association with risk of myocardial infarction. In this large case-control study we could not detect a protective effect of docosahexaenoic acid on the risk of myocardial infarction. The protective effect of ␣-linolenic acid was attenuated after adjusting for classical risk factors (mainly smoking), but it deserves further research.
Chromium intake may increase insulin sensitivity, glucose tolerance, and the ratio of high density lipoprotein cholesterol to low density lipoprotein cholesterol. However, the epidemiologic evidence on the association between chromium and cardiovascular disease is very limited. To determine whether low toenail chromium concentrations were associated with risk of nonfatal myocardial infarction, the authors conducted an incident, population-based, case-control study in eight European countries and Israel in 1991-1992. Cases (n = 684) were men with a first diagnosis of myocardial infarction recruited from the coronary units of participating hospitals. Controls (n = 724) were men selected randomly from population registers (five study centers) or through other sources, such as hospitalized patients (three centers), general practitioners' practices (one center), or relatives or friends of cases (one center). Toenail chromium concentration was assessed by neutron activation analysis. Average toenail chromium concentrations were 1.10 mug/g in cases (95% confidence interval: 1.01, 1.18) and 1.30 mug/g in controls (95% CI: 1.21, 1.40). Multivariate odds ratios for quintiles 2-5 were 0.82 (95% CI: 0.52, 1.31), 0.68 (95% CI: 0.43, 1.08), 0.60 (95% CI: 0.37, 0.97), and 0.59 (95% CI: 0.37, 0.95). Toenail chromium concentration was inversely associated with the risk of a first myocardial infarction in men. These results add to an increasing body of evidence that points to the importance of chromium for cardiovascular health.
Data regarding the outcome of children with chronic hepatitis B after seroconversion are scarce. We describe the long-term evolution of these patients. One hundred and three children with antibody against hepatitis B e antigen and normal alanine aminotransferase (ALT) levels were followed for 0.6 to 12.5 years (mean, 6.3 years). Paired liver biopsies (before and after seroconversion) were available in 83 cases. Final biopsies were obtained 0.5 to 12.5 years (mean, 4.5 years) after seroconversion. ALT levels remained normal in most of the children (79%) throughout the follow-up. All children, except five who lost hepatitis B surface antigen, had serum viral DNA detected by polymerase chain reaction. When comparing baseline and final liver biopsies, a significant improvement (P F .001) was found in the histological activity index and in the necrosis, cytolysis, inflammation, and fibrosis scores. The histological diagnosis improvement in the final biopsy was significantly related (P F .001) to the time from seroconversion to the biopsy performance. All children had viral DNA on their final liver biopsy. In summary, seroconversion and ALT normalization are quite stable findings in children, and no differences in the long-term outcome between treated and untreated children were found. In light of the histological outcome, it seems unnecessary to perform a follow-up liver biopsy in these cases.(HEPATOLOGY 1999;29:572-575.)Although the long-term outcome of patients with chronic hepatitis B (HBV) after hepatitis B e antigen to antibody (anti-HBe) seroconversion and normalization of serum alanine aminotransferase (ALT) levels has already been reported, 1-6 these reports include a relatively small number of liver biopsies. Thus, the information about the liver histological activity and hepatitis B virus DNA (HBV-DNA) status is scarce. In addition, the time when a liver biopsy should be taken after seroconversion to anti-HBe, to definitively establish the histological status, has not yet been defined. Furthermore, differences in the long-term outcome between hepatitis B surface antigen (HBsAg)-carriers who seroconvert to antiHBe spontaneously and those who do so because of interferon-␣ treatment have not been conclusively shown, especially in children with chronic HBV.We studied the long-term outcome of children with chronic HBV who had seroconverted to anti-HBe, either spontaneously or as a result of interferon-␣ treatment, by comparing the baseline and final liver biopsies obtained at different time periods after ALT normalization and by determining the liver HBV-DNA status. PATIENTS AND METHODS Patients.Patients with chronic HBV under 18 years of age who attended our pediatrics department between 1978 and 1996 were retrospectively eligible if the following inclusion criteria were fulfilled: (1) Strictly documented seroconversion to anti-HBe with serum HBV-DNA clearance (as detected by dot-blot hybridization) and normal ALT levels on two consecutive occasions, 6 months apart; (2) Histologic evidence of chronic hepatitis ...
We recently showed that alkaptonuria (AKU) is caused by loss-of-function mutations in the homogentisate 1,2 dioxygenase gene (HGO). Herein we describe haplotype and mutational analyses of HGO in seven new AKU pedigrees. These analyses identified two novel single-nucleotide polymorphisms (INV4+31A-->G and INV11+18A-->G) and six novel AKU mutations (INV1-1G-->A, W60G, Y62C, A122D, P230T, and D291E), which further illustrates the remarkable allelic heterogeneity found in AKU. Reexamination of all 29 mutations and polymorphisms thus far described in HGO shows that these nucleotide changes are not randomly distributed; the CCC sequence motif and its inverted complement, GGG, are preferentially mutated. These analyses also demonstrated that the nucleotide substitutions in HGO do not involve CpG dinucleotides, which illustrates important differences between HGO and other genes for the occurrence of mutation at specific short-sequence motifs. Because the CCC sequence motifs comprise a significant proportion (34.5%) of all mutated bases that have been observed in HGO, we conclude that the CCC triplet is a mutational hot spot in HGO.
It has been proven that chronic hepatitis B virus (HBV) infection may have a progressive course ending in liver cirrhosis or hepatocellular carcinoma. 1,2 Interferon alfa (IFN-␣) has been used as therapy for this disease, leading to a sustained loss of HBV DNA and hepatitis B e antigen (HBeAg) (and seroconversion to anti-HBe) and biochemical improvement (normalization of alanine transaminase [ALT] values) in around 25% to 40% of the treated patients. 2-10 However, the remaining patients do not achieve a response, including those patients who relapse after achieving an initial response and patients who do not respond. These patients may potentially benefit from another cycle of IFN-␣ treatment.Attempts in pilot studies of retreatment with IFN-␣ for previous nonresponders provided no definite conclusions on its possible efficacy in chronic HBV. 11 No controlled trial evaluating the benefits of retreatment of chronic HBV with IFN-␣ has been published. The objective of our study has been to determine whether a second course of IFN-␣, given during 6 months, is safe and acceptable, and whether it results in a significantly higher treatment response (loss of HBeAg and HBV DNA) than no treatment in previously nonresponder patients with chronic HBV. PATIENTS AND METHODSStudy Design. This study was designed as a multicenter (see Appendix) randomized controlled trial in patients who failed to respond to a previous cycle of IFN-␣. Assuming that patients with no treatment show a 5% response, and patients with retreatment 25% (a 20% difference), 7 a total number of 145 patients was needed to detect a significant difference at the 5% level with a power of 80%, taking into account a possible 25% drop-out rate during the study. The inclusion period started in April 1992 and ended in December 1996. At that time, 62 patients who were HBeAg-and HBV DNA-positive in serum with abnormal ALT values (documented at least 3 times within the 6 months screening period) and a chronic HBV 12 documented in a liver biopsy obtained within 1 year before inclusion had been enrolled. The patients should have undergone a previous treatment of only one course of any type of IFN-␣ treatment (recombinant or lymphoblastoid) for at least 12 weeks with a minimum of 13.5 million units (MU) per week 8,13 ; at the end of the first IFN-␣ cycle ( at least 6 months before enrollment in this study) patients should have been HBeAg-positive.The following patient exclusion criteria were used: (1) evidence of any other type of liver disease, i.e., anti-hepatitis C virus or anti-hepatitis D virus positive, alcohol, ascites, bleeding varices, or Abbreviations: HBV, hepatitis B virus; HBeAg, hepatitis B virus e antigen; ALT, alanine transaminase; HBsAg, hepatitis B virus surface antigen; IFN-␣, interferon alfa.From the
Despite the much greater genetic defect, cognitive status is slightly better preserved in patients with juvenile-onset HD. Cognitive impairment in patients with juvenile- and late-onset HD differs in the severity of visual and prefrontal deficits. Functional disability in patients with late-onset HD depends more on global cognitive status, while in patients with juvenile-onset HD, it is conditioned more by motor deficits and prefrontal dysfunction.
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