(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.
Introduction: Hypomagnesemia has been documented in alcohol-associated liver disease (ALD). This study aims to characterize hypomagnesemia in alcoholic hepatitis (AH) patients and identify its response with liver injury and severity markers. Materials and Methods: A total of 49 male and female AH patients with an age range of 27–66 years were enrolled in this study. Patients were grouped by MELD: MiAH (mild AH < 12 [n = 5]), MoAH (12 ≤ moderate AH ≤ 19 [n = 13]), and SAH (severe AH ≥ 20 [n = 31]). Patients were also evaluated by MELD grouping as non-severe (MELD ≤ 19 [n = 18]) and severe (MELD ≥ 20 [n = 31]). Data were collected on demographics (Age; BMI), drinking history (AUDIT; LTDH), liver injury (ALT; AST), and liver severity (Maddrey’s DF; MELD; AST:ALT). Serum magnesium (SMg) levels were tested as SOC lab (normal ≥ 0.85 ≤ 1.10 mmol/L). Results: SMg was deficient in each group; the lowest in the MoAH patients. The true positivity of SMg values were at a good performance level when compared between severe and non-severe AH patients (AUROC: 0.695, p = 0.034). We found that the SMg level < 0.78 mmol/L could predict severe AH (sensitivity = 0.100 and 1-specificity = 0.000) at this true positivity, and subsequently analyzed patients with SMg < 0.78 mmol/L (Gr.4) and ≥0.78 mmol/L (Gr.5). Between Gr.4 and Gr.5, there were clinically as well as statistically significant differences in disease severity as defined by MELD, Maddrey’s DF, and ABIC scores. Conclusions: This study demonstrates the utility of SMg levels to identify AH patients who may have progressed to severe status. The extent of magnesium response in AH patients also corresponded significantly with the prognosis of liver disease. Physicians suspecting AH in patients with recent heavy drinking may use SMg as an indicator to guide further testing, referrals, or treatment.
Introduction: Colorectal cancer (CRC) is the second leading cause of cancer-related deaths amongst men and women together in the United States. Screening colonoscopies have been proven to reduce CRC mortality. However, the efficacy of colonoscopies can be hindered by poor bowel preparation due to poor visualization and a higher likelihood of missing polyps and other colonic lesions including CRC. Per ASGE, adenoma detection rate (ADR) for combined male and female population is 25%. This retrospective study aims to identify the ADR for patients with inadequate bowel preparation noted during colonoscopies at our institution to emphasize the importance of quality bowel preparation. Methods: During the years 2018-2020, a total of 250 inadequately prepared colonoscopies were examined at University of Louisville Hospital for our study. 28 colonoscopies were excluded due to being aborted prior to the procedure brown stool being present on exam. 14 colonoscopies did not have pathology reports and were also excluded. The study was a retrospective single-center cohort study reviewing risk factors in patients with inadequate bowel preparation noted during colonoscopy. A Boston Bowel Preparation Scale (BBPS) was used with score of , 6 (inadequate preparation) and $6 (adequate preparation).Results: This study specifically examined the adenomatous detection rate for patients with poor colonoscopy preparation. Of these, 27 patients with screening colonoscopy indications had adenomatous or highrisk polyps with an ADR of 10.8%. This was well below the ASGE quality indicator for ADR for screening colonoscopies. 18 non-screening colonoscopies had an ADR of 7.2%. Additionally, there was a total of 91 the patients who came back for repeat colonoscopy within a 3-year time span after having poor bowel preparation or aborted procedure initially. 2 patients were missing pathology reports and excluded. 29 patients were found to have adenomatous or high-risk polyps for a total of 32.5% of patients with repeat colonoscopy who initially had poor bowel preparation or aborted procedure. Conclusion: Having a BBPS score of 5 or less considerably decreased ADR compared to ASGE standards. It is critically important that patients who have poor bowel prep return for repeat colonoscopy due to high risk of missing adenomatous or high-risk polyps as shown by the follow-up data. ADR is far below the endoscopist expectation without adequate bowel preparation in both screening and non-screening colonoscopies.
Introduction: Hepatic epithelioid hemangioendothelioma (EHE) is a malignant tumor of vascular origin with an estimated incidence of one in a million. The tumor derives its name from the characteristic composition of dendritic and endothelial cells with epithelioid morphology. Mostly asymptomatic, EHE is usually an incidental radiographic diagnosis that can mimic other liver tumors such as metastasis, hepatocellular carcinoma (HCC), angiosarcoma, or cholangiocarcinoma. We present a case of incidental diagnosis of hepatic EHE masquerading as multifocal liver metastasis. Case Description/Methods: An 80-year-old man with coronary artery disease presented with 5 days of diarrhea and black stools. He was taking bismuth subsalicylate in an attempt to ease diarrhea. Labs showed mild anemia with hemoglobin (Hb) of 13.1 g/dL with normal platelets and INR. A CT abdomen with contrast showed mild hepatomegaly and multiple space-occupying lesions in the liver concerning for metastatic cancer. The patient thereby underwent an EGD and colonoscopy which was negative for a primary GI malignancy. Ultrasound-guided liver biopsy was then pursued. Immunohistochemical stains performed on the core biopsy showed that the cells were positive for CD31, CD34 and ERG and were negative for cytokeratin-20, CDX-2, TTF-1, arginase, and glypican-3. Focal staining was noted with cytokeratin AE1/AE3 and cytokeratin-7. Special stain for mucicarmine was negative. These findings were consistent with diagnosis of hepatic EHE. His diarrhea resolved and Hb remained stable. He was discharged with outpatient oncology follow-up. (Figure ) Discussion: Hepatic EHE is typically diagnosed incidentally. However, the course of EHE may range from indolent to aggressive disease with distant metastases. Suspicion for EHE may arise when a patient is discovered to have multiple liver lesions with no identifiable primary cancer. Liver biopsy is required for diagnosis as EHE has unique histologic, immunohistochemical, and molecular characteristics. Treatment options are typically chosen based on the extent of the disease. EHE confined within the liver has been treated with liver resection, liver transplantation, radiofrequency ablation, or simply a wait and watch method. Patients with extrahepatic involvement have been treated with systemic therapy including a variety of cytotoxic chemotherapy, immune therapy, or targeted therapy. As EHE remains exceptionally rare, prompt diagnosis should be followed by a multidisciplinary discussion for individualized care.
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