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Most epidemiological surveys have confirmed the association of low HDL-cholesterol and high triglyceride levels with cholesterol gallstones. Our objective was to analyze the relationship between plasma lipid levels and common polymorphisms of ABCB11 (encoding the bile salt export pump, BSEP) and ABCB4 (encoding the phospholipid transporter into bile, MDR3) genes. Plasma lipids were measured in 108 index patients of sib pairs with gallstones and in 260 controls. Using PCR-based assays with 5'-nuclease and fluorescence detection (TaqMan), the ABCB11 coding SNP p.A444V and four haplotype-tagging SNPs covering the ABCB4 gene (c.504C > T, c.711T > A, p.R652G, rs31653 in intron 26) were genotyped. Plasma lipids were compared in carriers of the common versus rare allele of these polymorphisms using Student's t test and Pearson's correlation. BMI and triglyceride levels were higher and HDL-cholesterol levels were lower in affected siblings than in controls. Among cases, triglyceride and cholesterol levels were higher in carriers of the common versus rare (hetero/homozygous carriers) allele of the SNPs p.A444V of ABCB11 and C.504C > T of ABCB4. HDL-cholesterol was lower in carriers of the common allele of rs31653. In controls, significant differences of cholesterol and HDL-cholesterol levels were found in carriers of ABCB4 polymorphisms. Our results do not support the hypothesis of a link between ABCB4 and ABCB11 polymorphisms, lithogenic dyslipidemia, and gallstone risk.

Background: The role of ABCG5 and ABCG8 genes in the determination of plasma lipid levels is currently under intensive investigation. The aim of this study was to evaluate plasma lipid levels in sibling pairs with gallstones and to assess their correlation with common gene polymorphisms in the ABCG5/ABCG8 genes., Methods: Plasma levels of cholesterol, HDL-cholesterol, and triglycerides were measured in 68 patients belonging to 34 sibling pairs with gallstones (affected sibling pairs, mean age 56.3 years) and in 68 gallstone carriers with stone-free siblings (age/gender-matched controls in a ratio of 2:1 with the index patients of the study group). Four and one non-synonymous sequence variants in ABCG8 and ABCG5 genes, respectively, were determined in the affected sibling pairs, employing allelic discrimination with 5' nuclease assays., Results: Plasma triglyceride levels were higher and HDL-cholesterol levels lower in the index patients than in controls. Plasma lipid levels were correlated in the members of the affected sibling pairs. Triglyceride levels were higher in carriers of the common alleles for ABCG5 Q604E and ABCG8 D19H sequence variants, and HDL-cholesterol was lower in carriers of the common alleles for ABCG5 Q604E than in carriers of the rare alleles., Conclusions: The significantly different plasma lipid levels in siblings with gallstones versus controls, as well as the correlation of plasma lipids in affected sibling pairs, confirm the genetic influence in gallstone disease. Polymorphisms in ABCG5/ABCG8 genes might contribute to the genetic variation in plasma lipid levels and in cholesterol saturation of the bile.

We report the case of a young female patient, admitted for a recent ascites of unknown origin. The acute onset was with colicky abdominal pain and peritoneal effusion, which led to the suspicion of perforated ulcer. A diagnostic laparoscopy was performed which showed free peritoneal fluid and normal abdominal viscera. At upper gastro-intestinal endoscopy, performed a few days later, patchy erythema in the antral region and duodenal edema were revealed. Duodenal biopsies showed marked eosinophilic infiltration. The ascitic fluid was straw coloured, sterile with 90% eosinophils. Eosinophilic gastroenteritis was suspected, but differential diagnosis required the exclusion of migrant parasites. The stool exams were negative but serology for Toxocara antibodies was positive. The treatment with albendazole (Zentel 400 mg twice a day for 5 days) led to the disappearance of signs and symptoms. The eosinophilic infiltrate of the gut was absent in duodenal biopsies taken two months later.

The authors proposed to assess the prevalence of anti-Hp antibodies (IgG class) in patients with ischemic heart disease. The study included 93 patients distributed into two groups: a) group A--61 patients with ischemic heart disease; b) group B--32 controls. The Hp infection diagnosis was established by determination of the Hp antibodies in the peripheral blood. Hp infection was correlated with the following factors: (a) smoking, alcohol consumption, antiinflammatory drugs intake and water source; (b) biological parameters (fibrinogen, alpha1-globulins, cholesterol, triglycerides, thrombocyte count). In the patients with ischemic heart disease the prevalence of the Hp infection was 78.3%, and in controls 56.2% (p<0.05). The patients consuming alcohol and smoking had a significantly higher prevalence than controls. Antiinflammatory drugs and water source did not influence the prevalence of the Hp infection. Among the biological parameters, fibrinogen and alpha1 globulins were significantly increased in the Hp-positive patients with ischemic heart disease. In conclusion, the serum prevalence of anti-Hp antibodies was higher in the patients with ischemic heart disease, smokers and alcohol consumers than in health individuals.

The paper reports the clinical case of a 58 -year-old male patient admitted for diarrhea (6-7 stools/day, diffuse abdominal pain, borborygma, weight loss (20 kgs in two years), asthenia and fatigue. Physical examination evidenced a poor nutritional state (body mass index 19 kg/m2). The abdomen was slightly distended. Biological tests evidenced moderate/severe anemia, hypoproteinemia and hypoalbuminemia. Endoscopic examination evidenced oedematous duodenal mucosa with white-yellowish deposits. Histology (HE stain) revealed the presence of foamy cells and the PAS-staining of the duodenal mucosa evidenced PAS-positive macrophages and numerous intracellular bacilli. Penicillin therapy 2 x 1 million U/day for 14 days, followed by tetracycline 4 x 250 mg/day improved the clinical picture, the patient had only one stool per day and gained weight. After 7 months of treatment the general condition was good and the patient had gained 17 kgs, the duodenal mucosa was normal. HE staining did not evidence foamy cells and no PAS-positive macrophages could be found.