Association of Hypomagnesemia and Liver Injury, Role of Gut-Barrier Dysfunction and Inflammation: Efficacy of Abstinence, and 2-Week Medical Management in Alcohol Use Disorder Patients.

(1) We investigated the involvement of serum magnesium level in early alcoholic liver disease (ALD), gut barrier dysfunction, and inflammation in alcohol use disorder (AUD) patients; and lastly, the efficacy of 2-week abstinence and medical management to alleviate hypomagnesemia. (2) Forty-eight heavy drinking AUD patients (34 males (M)/14 females (F)) participated in this study. Patients were grouped by serum alanine aminotransferase (ALT) level (a marker of liver injury) as group 1 (Group 1 (Gr.1); ALT ≤ 40 U/L, 7M/8F, without any indication of early-stage ALD) and group 2 (Group 2 (Gr.2); ALT > 40 U/L, 27M/6F or early-stage ALD). These patients were sub-divided within each group into patients with normal magnesium (0.85 and more mmol/L) and deficient magnesium (less than 0.85 mmol/L) levels. All participants were assessed at baseline (BL) and received standard medical management for 2 weeks with reassessment at the treatment end (2w). (3) Female participants of this study showed a significantly lower baseline level of magnesium than their male counterparts. Gr.2 patients showed a greater propensity in the necrotic type of liver cell death, who reported higher chronic and recent heavy drinking. Magnesium level improved to the normal range in Gr.2 post-treatment, especially in the hypomagnesemia sub-group (0.77 ± 0.06 mmol/L (BL) vs. 0.85 ± 0.05 mmol/L (2w), p = 0.02). In Gr.2, both apoptotic (K18M30) and necrotic (K18M65) responses were significantly and independently associated with inflammasome activity comprising of LBP (Lipopolysaccharide binding-protein) and TNFα (Tumor necrosis factor -α), along with serum magnesium. (4) In AUD patients with liver injury, 2-week medical management seems to improve magnesium to a normal level. This group exhibited inflammatory activity (LBP and TNFα) contributing to clinically significant hypomagnesemia. In this group, the level of magnesium, along with the unique inflammatory activity, seems to significantly predict apoptotic and necrotic types of hepatocyte death.

Preparative Fasting Orders for Medical/Surgical Interventions and Imaging Studies: Time to Review and Revise!

PURPOSE OF THE REVIEW: Preparative fasting orders arose out of a purported need to enhance imaging studies, reduce interference of food with intended medical/surgical interventions, and protect the patient from vomiting and aspiration pneumonia. This review discusses the frequency, appropriateness, and efficacy of fasting orders in meeting those needs and whether their use should be modified in the future. RECENT FINDINGS: Nil per os (NPO) orders are overused, as they are often inappropriate, typically excessive, and routinely create barriers which may increase risk for patients. Fasting orders are used more often for medical procedures than for surgical operations or imaging studies. One fourth of NPO orders are inappropriate, and the intended procedure or study is canceled 20% of the time usually for a change in plans or scheduling error and rarely because of patient eating. Nausea/vomiting associated with contrast media or imaging studies is rare, self-limited, and not linked to preparatory fluid or food ingestion. Prolonged fasting reduces patient cooperation and satisfaction, and may contribute to a higher rate of complications. Each institution should review and revise preparative fasting orders. Drinking of fluids should be allowed without restriction. Truncated periods of solid food restriction may be required due to technical reasons related to specific imaging studies, and for procedures or surgical operations which require sedation or general anesthesia. Inappropriate and prolonged fasting should be avoided, as they create barriers to adequate nutritional therapy and impose added risk with regard to patient outcomes.

Deferasirox induced liver injury in haemochromatosis.

Durg-induced liver injury is a common side-effect of many medicines. It is particularly problem when the original condition under treatment is already causing liver damage. This report describes the hepatotoxicity induced by Deferasirox in a patient with haemochromatosis with a discussion of possible pathogenetic mechanism.