Phosphorus Supplementation Mitigated Food Intake and Growth of Rats Fed a Low-Protein Diet

BACKGROUND: Low protein intake is associated with various negative health outcomes at any life stage. When diets do not contain sufficient protein, phosphorus availability is compromised because proteins are the major sources of phosphorus. However, whether mineral phosphorus supplementation mitigates this problem is unknown, to our knowledge. OBJECTIVE: Our goal was to determine the impact of dietary phosphorus supplementation on food intake, weight gain, energy efficiency, body composition, blood metabolites, and liver histology in rats fed a low-protein diet for 9 wk. METHODS: Forty-nine 6-wk-old male Sprague-Dawley rats were randomly allocated to 5 groups and consumed 5 isocaloric diets ad libitum that varied only in protein (egg white) and phosphorus concentrations for 9 wk. The control group received a 20% protein diet with 0.3% P (NP-0.3P). The 4 other groups were fed a low-protein (10%) diet with a phosphorus concentration of 0.015%, 0.056%, 0.1%, or 0.3% (LP-0.3P). The rats' weight, body and liver composition, and plasma biomarkers were then assessed. RESULTS: The addition of phosphorus to the low-protein diet significantly increased food intake, weight gain, and energy efficiency, which were similar among the groups that received 0.3% P (LP-0.3P and NP-0.3P) regardless of dietary protein content. In addition, phosphorus supplementation of low-protein diets reduced plasma urea nitrogen and increased total body protein content (defatted). Changes in food intake and efficiency, body weight and composition, and plasma urea concentration were highly pronounced at a dietary phosphorus content <0.1%, which may represent a critical threshold. CONCLUSIONS: The addition of phosphorus to low-protein diets improved growth measures in rats, mainly as a result of enhanced energy efficiency. A dietary phosphorus concentration of 0.3% mitigated detrimental effects of low-protein diets on growth parameters

Prognostic factors in patients with advanced cholangiocarcinoma: Role of surgery, chemotherapy and body mass index

AIM: To study the factors that may affect survival of cholangiocarcinoma in Lebanon

Propafenone hepatotoxicity: Report of a new case and review of the literature

Propafenone is a class Ic antiarrhythmic drug. It is a beta-adrenergic blocker that causes bradycardia and bronchospasm. It is metabolized primarily in the liver. Its bioavailability and plasma concentration differ among patients under long-term therapy. They are genetically determined by the hepatic cytochrome P-450 2D6. Hepatic toxicity is highly uncommon. To date, only eight patients were reported in the reviewed world literature. In this article, one new case will be reported emphasizing the importance of medication history taking in patients presenting with new-onset liver enzymes abnormalities

Prevalence and clinical relevance of Helicobacter pylori cagA and vacA genes in Lebanese patients with gastritis and peptic ulcer disease

Background: The prevalence and clinical relevance of H. pylori cagA and vacA virulence genes in the pathogenesis of disease phenotype was assessed by a novel approach for this organism consisting of determination and comparisons of H. pylori gene transcription levels directly in gastric biopsies according to disease phenotype.Methodology: Gastric mucosal biopsies were collected from patients with peptic ulcer disease (PUD), gastritis, and normal mucosa in an academic medical center in Lebanon. H. pylori was detected in these biopsies by rapid urease (CLO™) test and PCR amplification of the ureA gene. H. pylori virulence genes, their transcription and transcription levels were determined respectively by PCR, RT-PCR and real time RT-PCR. Results: Forty-five percent of patients were H. pylori positive by PCR of the ureA gene, 37.5% of whom had cagA and 59.4% vacA.Conclusions: The cagA and vacA genes were detected more frequently in PUD patients with significantly higher transcription levels than in gastritis and normal mucosa