Intrahepatic thrombotic events have been postulated to play a key role in the pathogenesis of hepatic fibrosis. Genetic and acquired thrombotic risk factors may therefore contribute to the varying rates of fibrosis progression observed in patients with chronic hepatitis C virus (HCV) infection. The aim of this study was to assess the impact of inherited mutations in factor V and factor II (prothrombin) on hepatic fibrosis progression rates in individuals infected with HCV. Two hundred and ten Irish women infected with HCV genotype 1b, contracted from a single source (HCV-contaminated anti-D immunoglobulin) were genotyped for the factor V Leiden G1691A and prothrombin G20210A polymorphisms, and compared with Irish Caucasoid controls. Index and subsequent liver biopsies were scored (Ishak scoring system) by a single pathologist. Statistical analysis was performed using SPSS. Factor V Leiden and prothrombin G20210A heterozygosity were determined in 3.7% and 1.85%, respectively, of the study population. There was no association between these polymorphisms and fibrotic score on the index biopsy, or degree of change in fibrotic score on subsequent biopsies. The mean fibrotic score for factor V wild type was 1.06 vs 0.71 for the heterozygotes (P = 0.89). The mean change in fibrotic scores between subsequent biopsies was 0.72 for factor V wild type vs 0.50 for heterozygotes (P = 0.68). Similarly, there was no significant difference in fibrotic score for those with the prothrombin G20210A polymorphism (P = 0.936). Alanine aminotransferase levels for factor V wild type were significantly lower than those for the heterozygotes, 45.9 vs 57 (P = 0.032). Factor V Leiden and prothrombin G20210A heterozygosity rates were infrequently detected in this HCV cohort and were similar to rates seen in a Caucasian Irish control population. In this cohort, neither factor V Leiden nor prothrombin G20210A polymorphisms had a significant impact on fibrotic scores or degree of change between subsequent biopsies. These data do not support a key role for thrombotic risk factors in fibrogenesis in HCV-infected patients.
AFTER examining many samples of liquid milk in the years 1881 to 1888, Vieth192 noticed that the proportions of ash, protein and anhydrous lactose were approximately in the ratio 1 to 5 to 6; subsequently: he stated that the ratio 2 to 9 to 13 was more exact. These later figures are quoted in standard text-books4y5 and are used as a basis for calculating the amount of non-fatty milk solids in ice-cream and dairy products. In the absence of interfering substances, non-fatty milk solids are derived by multiplying the anhydrous lactose content by 24/13 or the protein content by 24/9.When we applied this principle to the calculation of non-fatty milk solids in ice-cream samples of known and unknown composition, the results obtained by using the two factors generally disagreed, and, as New Zealand milk powder was an ingredient of most of the samples, twenty-two such powders were examined. The samples were taken a t random from different deliveries in the period April until September, 1959, and information on the time and place of manufacture and the breed of cow was not available. Fifteen powders were spray-dried, the remainder were rollerdried. Lactose was determined by Lane and Eynon's methods after clarification with zinc acetate and potassium ferrocyanide solutions7 ; protein was determined by the Kjeldahl method. RESULTSThe Vieth ratios for nineteen of these powders were-Anhydrous lactose . . .. . . 11-70 (standard deviation 0.14) Protein .
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