Hybrid external fixation in treatment of proximal tibial fractures: a good outcome in AO/ASIF type-C fractures.

INTRODUCTION: The treatment of proximal tibial fractures is often challenging, and internal fixation is occasionally associated with problems in wound healing due to frequently co-existing soft tissue injuries. External fixation of these fractures have yielded satisfactory results, but some studies have reported problems in the achievement and maintenance of fracture reduction. The purpose of the present study was to evaluate the performance of a hybrid external fixator in the treatment of different types of proximal tibial fractures. MATERIALS AND METHODS: Thirty-three proximal tibial fractures, of which 20 were high energetic, were treated with a hybrid external fixator (Tenxor Strker-Howmedica) in the acute phase. Fracture categorisation was done according to AO/ASIF, and the reduction was performed most often by closed means or through mini-open reduction (26/78.8%). The patients were followed up to an average of 12.7 months (range 10-22) and were evaluated with radiographs and clinical examinations. RESULTS: Five AO/ASIF type-C intraarticular fractures had a poor postoperative reduction, and were thus treated with internal fixation in a second operation. Of the remaining 28 patients, local and transient pin tract infection was observed in seven patients, and one had septic arthritis of the knee. All 13 C1 and five of six C2/C3 fractures united in mean time of 15.1 weeks, whereas three of nine type-A fractures failed to unite, albeit an adequate reduction, and needed a second operation (odds ratio 11.4, 95% CI 1.0-143, compared with type-C fractures). For the remaining six type-A fractures, the mean healing time was 24 weeks (mean difference 8.9, 95% CI 6-12 weeks compared with type-C fractures). Age over 48 and the presence of an open fracture, but not fracture type, gender, or the level of injury energy, correlated to a poor subjective outcome. CONCLUSIONS: The hybrid external fixation method we have used is safe, and type-C1 fractures are particularly suitable to be treated with this method. However, even C2/C3 fractures may be candidates for this method, but a meticulous fracture reduction should be performed. Type-A fractures are liable to healing problems when the fixator is used as a rigid complex.

Promoter polymorphism of the CD14 endotoxin receptor gene as a risk factor for alcoholic liver disease.

Twin concordance studies indicate that genetic factors influence the individual susceptibility for alcoholic liver disease (ALD). Both clinical and experimental data suggest that Kupffer cell activation by gut-derived endotoxins and other bacterial products is an important pathogenic factor. Activated Kupffer cells release proinflammatory cytokines, a process that is regulated by the CD14 endotoxin receptor (CD14). Recently, a C-->T (-159) polymorphism in the promoter region of the CD14 gene was detected and found to confer increased CD14 expression. In the present study, the association of CD14 promoter polymorphism with different forms of ALD was examined in 3 separate autopsy series. Among 442 men with valid alcohol-consumption data, 381 men had been moderate or heavy alcohol consumers. The allele frequency of the CD14 promoter genotype, determined by a modified cycle minisequencing technique, was 0.34 (CC), 0.51 (CT), and 0.16 (TT). The T allele was found to be associated with advanced ALD, i.e., with alcoholic hepatitis (odds ratio [OR]: 2.48; P = .018), and especially with cirrhosis (OR: 3.45; P = .004), but not with fatty liver, periportal fibrosis, or bridging fibrosis. The overall age-adjusted risk for cirrhosis was 3.08 (P = .01) for the carriers of the CT genotype, and 4.17 (P = .005) for the homozygous TT genotype. These results suggest that in the relatively isolated Finnish population, the T allele confers increased risk of alcoholic liver damage. In particular, TT homozygotes are at a high risk to develop cirrhosis.

Polymorphism in the cytochrome P450 2E1 gene and the risk of alcoholic liver disease.

BACKGROUND/AIMS: To study the genetic susceptibility to alcoholic liver disease, we investigated the association between genetic polymorphism in the cytochrome P450 2E1 gene and the occurrence of alcoholic liver disease. METHODS: Four previously described restriction fragment length polymorphisms (RFLPs) in the cytochrome P 450 2E1 gene were analyzed by restriction endonuclease (Dra I, Msp I, Pst I and Rsa I) digestion of polymerase chain reaction amplified DNA segments. Polymorphisms in these loci were compared to the occurrence of fatty liver, alcoholic hepatitis and liver fibrosis in 319 males comprising total abstainers, moderate alcohol consumers and chronic alcoholics. RESULTS: The allelic frequencies for each RFLP in this series were: 0.89 and 0.11 (Dra I), 0.98 and 0.02 (Msp I) and 0.99 and 0.01 (Pst I and Rsa I). The distribution of the alleles did not vary significantly between the different consumption groups. The allelic frequencies among patients with fatty liver, alcoholic hepatitis or liver fibrosis were not significantly different from the allelic frequencies among patients with normal liver histology. Comparison of different genotypes among moderate alcohol consumers (n = 43) or chronic alcoholics (n = 243) with or without liver disease showed no statistically significant associations. However, the rare polymorphic (d2) allele in the Dra I RFLP was found slightly more often among moderate consumers as well as alcoholics with alcoholic liver disease. CONCLUSIONS: These results indicate that the Msp I, Pst I and Rsa I RFLPs were very rare in the Finnish population, suggesting at most minor contribution to the inherited susceptibility to alcoholic liver disease. Polymorphism in the Dra I locus was more common in this study population, but showed no statistically significant association with alcoholic liver disease.

Glutathione-S-transferase GST M1 "null" genotype and the risk of alcoholic liver disease.

The present study was conducted to investigate possible association between the occurrence of glutathione-S-transferase GST M1 "null" genotype and alcoholic liver disease (ALD). The"null" genotype indicating absent activity of class mu glutathione transferase was assessed in 33 abstainers, 43 moderate alcohol consumers, and 313 heavy alcohol consumers by polymerase chain reaction. The genotypes were compared with occurrence of alcoholic fatty liver, alcoholic hepatitis, and alcoholic liver fibrosis. The "null" genotype was found among 44.7% of patients in the series, with no significant differences between different consumption groups: controls, 36.4%; moderate consumers, 39.5%; and heavy consumers, 46.3%. Occurrence of GST M1 "null" genotype was not associated with occurrence ALD among moderate alcohol consumers. Frequency of the "null" genotype was, however, statistically nearly significantly [p = 0.07, odds ratio (OR) = 1.75] lower among heavy consumers with normal liver histology than in alcoholics with ALD. Furthermore, when compared with heavy consumers without ALD, the "null" genotype was nearly significantly more frequent among heavy consumers with at least slight liver fibrosis (p = 0.05, OR = 1.8) and statistically significantly more frequent among among alcoholics with advanced liver fibrosis (p < 0.025, OR = 2.3). Results of the present Finnish association study suggest that homozygous deletion of the GST M1 gene may indicate increased susceptibility to develop irreversible liver damage in response to the toxic effects of ethanol. Significant association was found between the occurrence of the "null" genotype and the occurrence of alcoholic liver cirrhosis.

Cytokeratin inclusions in alcoholic liver disease and their relation to the amount of alcohol intake.

In the present study, the frequency and the distribution pattern of immunoreactive hepatocytic cytokeratin (CK) inclusions was investigated using the monoclonal antibody (MAb) CAM 5.2 detecting CKs 8, 18 and 19. The CK antigenicity of the inclusions was confirmed on frozen sections with MAbs for the CKs 7, 8, 17, 18 and 19. The frequency of hepatocytic CK aggregates was compared to the presence of non-alcoholic and alcoholic liver disease (ALD) as well as to the average all-year daily ethanol intake of 195 consecutive males subjected to medico-legal autopsy. Hepatocytic CK inclusions were infrequent in patients with normal liver histology, portal fibrosis and/or portal inflammation. In ALD, however, inclusions were observed in 35.6% of patients with fatty liver, in 63.2% of patients with alcoholic hepatitis, in 30.8% of patients with bridging fibrosis and in 60.0% of patients with liver cirrhosis. In all specimens studied, the inclusions were reactive only for CKs 8 and 18, CKs 7, 17, and 19 being unreactive. The frequency of inclusion bodies increased, paralleling increasing average all-year daily alcohol consumption. Compared to non-drinkers, a daily intake of between 40 and 80 g of absolute alcohol was associated with a statistically significantly (relative risk, RR = 6.6) increased risk of formation of aggregates. Similarly, daily consumption exceeding 80 g was related to increased (RR = 6.0) frequency of CK aggregates. The frequency of full-blown "classical" Mallory bodies (MBs) was, however, increased (RR = 8.9) only in patients with a daily intake exceeding 160 g.(ABSTRACT TRUNCATED AT 250 WORDS)

Alcohol consumption and alcoholic liver disease: evidence of a threshold level of effects of ethanol.

The effects of long-term moderate or "social" alcohol consumption (10-80 g daily intake) on the incidence of features of alcoholic liver disease (ALD) were delineated in a consecutive autopsy series of 210 males. The subjects' daily intake, as well as duration of alcohol consumption, was determined by an interview with the spouse or a close acquaintance and compared with semiquantitative histological scores for stage of ALD. No significant increase in the incidence of features of ALD could be related to all-year daily intake of ethanol below 40 g (40 g equals 1.1 liter of beer, 0.44 liter of wine, and 0.11 liter of spirits). However, daily intake between 40-80 g increased relative liver weight on average 3.1 g/kg of body weight (p < 0.02), the frequency of fatty liver from 11.7 to 47.2% [relative risk (RR) = 4.4], and the frequency of mainly slight alcoholic hepatitis up to 16.7% (RR = 7.5). The incidence of both bridging fibrosis and liver cirrhosis increased significantly (RR = 8.8) only when daily intake exceeded 80 g. Amounts of ethanol exceeding 80 g did not relate to further increases in incidence of bridging fibrosis or liver cirrhosis. These findings suggest that, in males, daily ingestion of ethanol below 40 g for a period of 25 years does not increase the risk of alcohol-related liver disease.(ABSTRACT TRUNCATED AT 250 WORDS)

Delayed increases in liver cirrhosis mortality and frequency of alcoholic liver cirrhosis following an increment and redistribution of alcohol consumption in Finland: evidence from mortality statistics and autopsy survey covering 8533 cases in 1968-1988.

Changes in the legal restrictions for alcohol consumption in 1969 liberated purchasing and marketing of low-alcohol beer. Subsequently, within the space of 5 years, the per capita consumption of absolute alcohol increased from 4.2 to 6.5 liters. To evaluate the possible effects of this change upon liver cirrhosis mortality as well as prevalence of liver cirrhosis in autopsy series, we surveyed mortality statistics and data from 8,533 medicolegal autopsies in 1968 through 1988. Liver cirrhosis mortality statistics revealed a highly significant (p less than 0.001) increase from 6.4 to 13.7 per 100,000 during the period, and similarly, the prevalence of liver cirrhosis in the autopsy series showed a highly significant (p less than 0.001) increase from 3.0% to 6.1%. More specifically, this increase was attributable to a highly significantly (Chi-square 15.4, p less than 0.001) increased proportion of alcoholic liver cirrhosis occurring at a younger age and almost exclusively in males. The stepwise mode of increase as well as the changes in sex and age distribution of cirrhosis since 1969 could be interpreted as an effect of distribution of consumption to a new generation of consumers. The forensic autopsy series seemed to reflect changes in per capita consumption with a shorter time lag than with mortality statistics. Additionally, only 7% of the 448 cirrhotics singled out from this material exhibited liver cirrhosis as a cause of death and were thus also included in the official mortality statistics, suggesting the greater accuracy of our forensic autopsy series.