Drug-induced enteritis and colitis are commonly included in the differential diagnosis for inflammatory bowel disease and olmesartan, an angiotensin-II receptor blocking antihypertensive medication, has been implicated in numerous cases. Typical findings of olmesartan-associated enteropathy mimic that of celiac disease with histology revealing villous blunting or atrophy, though a minority of patients present with an inflammatory phenotype that may be characterized by erythematous patches, cobblestoning, and ulceration. We present a case of olmesartan-associated enteropathy in a 79-year-old woman who initially presented with severe malabsorption and was found to have features initially concerning for upper gastrointestinal Crohn's disease.

Direct oral anticoagulants, such as dabigatran, rivaroxaban, apixaban, and edoxaban, are becoming more popular for the prevention of stroke and treatment of venous thromboembolism, although their effectiveness relies on adequate gastrointestinal absorption. However, in the setting of malabsorption, such as after bariatric surgery, short bowel syndrome, or during the course of active inflammatory bowel disease, the pharmacokinetic profile of the drugs can be altered. Recent literature indicates that, although rivaroxaban and apixaban are effective in stable patients after bariatric surgery, such as sleeve gastrectomy or Roux-en-Y gastric bypass, dabigatran is not effective because it requires the acidic environment of the stomach for adequate absorption. However, in the setting of severe malabsorption, such as very short bowel syndrome, the gold standard, which is warfarin, is recommended because the effect of the drug can be monitored. Guidelines recommend avoiding the use of direct oral anticoagulants during the acute postoperative period, which is defined as 0-4 weeks, and using drug-specific assays, such as antiXa or dilute thrombin time, to ensure adequate absorption.

Pancytopenia is a significant haematological finding with a broad differential, ranging from benign conditions to life-threatening malignancies. Copper deficiency is a recognised but uncommon cause of non-clonal cytopenias. We report a case of copper deficiency in a woman in her 80s who presented with urolithiasis and was found to have acute pancytopenia. A thorough evaluation identified undetectable copper levels despite the absence of classic risk factors such as gastrointestinal surgery, malabsorptive disorders or zinc supplementation. Our patient's copper deficiency was most likely multifactorial arising from insufficient dietary intake and chronic mild gastrointestinal dysfunction. Emerging evidence suggests that hypocupremia may be more common than previously appreciated, and clinicians should consider copper deficiency in the differential diagnosis of pancytopenia.

S-adenosyl-L-homocysteine (SAH), the product inhibitor of S-adenosyl-L-methionine-dependent methyltransferases, and its degradation product homocysteine (Hcy) are evolutionarily conserved master regulators of methylation metabolism, which is mediated by more than 200 methyltransferases in humans. Hyperhomocysteinemia (HHcy), characterized by elevated levels of Hcy in the blood, is an independent risk factor for atherosclerosis, a strong predictor of cardiovascular mortality and can cause associated pathology by interfering with methylation-dependent processes. Here, we developed a Drosophila melanogaster fly dietary model of HHcy and a Drosophila melanogaster genetic SAH accumulation model and compared them to corresponding Saccharomyces cerevisiae yeast models to reveal evolutionarily conserved methylation pattern changes responsive to elevation of Hcy levels. Feeding Drosophila an Hcy-containing diet or growing yeast on Hcy-supplemented medium, similarly to genetically blocking SAH degradation, led to SAH accumulation, developmental delay and growth defects. Furthermore, dietary or genetically induced SAH accumulation caused impaired phospholipid and protein methylation in both model organisms. Identification and functional characterization of evolutionarily conserved SAH-dependent methylation targets responsive to elevation of Hcy and/or SAH levels will reveal mechanisms of SAH toxicity in HHcy and help to decipher their role in associated pathologies.

Celiac disease (CD) is a chronic immune-mediated enteropathy characterized by gluten-induced small intestinal mucosal injury and a broad spectrum of clinical manifestations. Emerging evidence suggests that CD may also be associated with gastric mucosal abnormalities, including Helicobacter pylori-negative chronic gastritis (HPNCG). This study aimed to investigate the clinical, laboratory, and histopathological features of patients with CD complicated by HPNCG and to identify factors associated with this condition. A total of 60 patients with CD were retrospectively enrolled and divided into 2 groups: CD alone (n = 26) and CD with HPNCG (n = 34). Demographic characteristics, gastrointestinal symptoms, comorbidities, laboratory parameters, and histopathological findings were compared between groups. Univariate and multivariate logistic regression analyses were performed to identify factors independently associated with CD complicated by HPNCG. Receiver operating characteristic curve analysis was used to evaluate discriminatory performance. Among the 60 patients, 45.0% were male and 55.0% were female, with a mean age of 41.8 ± 15.2 years. Compared with the CD-alone group, patients with CD and HPNCG had significantly higher prevalence of abdominal bloating (61.8% vs 30.8%, P = .018), anemia (58.8% vs 26.9%, P = .013), osteopenia/osteoporosis (38.2% vs 15.4%, P = .048), and liver function abnormalities (23.5% vs 3.8%, P = .036). Histopathologically, Marsh grade IIIb-IIIc (88.2% vs 61.5%, P = .019) and moderate-to-severe chronic gastric inflammatory infiltration (64.7% vs 34.6%, P = .022) were more frequent in the CD with HPNCG group. Multivariate logistic regression identified Marsh grade IIIb-IIIc as the only factor independently associated with CD complicated by HPNCG (odds ratio = 3.96, 95% confidence interval: 1.05-14.91, P = .042). Receiver operating characteristic analysis showed that Marsh grade IIIb-IIIc alone yielded an area under the curve of 0.73, while the combined model achieved an area under the curve of 0.81. Patients with CD complicated by HPNCG present with a heavier burden of gastrointestinal symptoms, nutritional impairments, and mucosal injury compared to those with CD alone. Severe duodenal villous atrophy, reflected by Marsh grade IIIb-IIIc, is independently associated with HPNCG in CD and may serve as a clinically useful indicator for identifying this high-risk subgroup.

Cardio-facio-cutaneous (CFC) syndrome is a rare, multiple congenital anomaly disorder in which individuals commonly experience faltering growth; however, systematic analysis of growth parameters in this disorder has not been performed. We recruited 69 participants with CFC through CFC International and collected data on assessing height, weight, and body mass index (BMI). We found that the height-for-age and weight-for-age Z-scores were consistently lower in individuals with CFC than in the reference population and that children with CFC experience growth restriction from infancy to adulthood. Our findings show that as individuals age, their height Z-scores remain constant (-2 to -3 SD). However, over time, their weight shows a progressive decrease from average. There were no significant differences between the mean Z-scores of the growth parameters based on an individual's history of enteral feeding, gene associated with diagnosis, nor growth hormone deficiency status. This implies that feeding modality and severity of feeding difficulties may not be directly related to growth. Other factors could be responsible, such as malabsorption of nutrients, constitutional growth delay, hormonal deficiencies or resistance, or cardiac abnormalities. Our study is one of the first to systematically characterize growth parameters and analyze the association of clinical covariates with these parameters in individuals with CFC syndrome. Accurate assessment of growth in this rare condition will allow providers to recognize outliers of growth in their patients with CFC when compared to other individuals with CFC and make necessary referrals and recommendations, which may ultimately improve outcomes.

Environmental enteric dysfunction, universal in young children exposed to poor sanitation and hygiene, impairs growth and development through malabsorption and as a driver of chronic systemic inflammation (CSI). In an open-label, randomized, four-arm, phase II clinical trial, infants with birthweight ≥2000 g in Homa Bay County, western Kenya receive live, multi-strain Bifidobacterium spp. and Lactobacillaceae pro/synbiotics from 0 to 6 months. CSI (plasma α1-acid glycoprotein >1 g/L) at age 6 months (primary outcome) occurs in 60/138 (43%) controls versus 4/144 (3%; risk ratio [RR], 0.06; 95% confidence interval [CI], 0.02-0.17) infants in the Labinic synbiotic arm, 3/132 (2%; RR = 0.05; 95% CI, 0.02-0.16) in the Lab4b synbiotic arm, and 3/141 (2%; RR, 0.05; 95% CI, 0.02-0.15) in the Lab4b probiotic arm. Biomarkers of gut health and growth hormones also improve, and no serious adverse events are attributed to the interventions. Pro/synbiotics safely and markedly reduce CSI in a highly disadvantaged population, warranting further investigation of health impacts. The trial is registered at https://pactr.samrc.ac.za; identifier: PACTR202003893276712.