Basidiobolomycosis Mimicking Fistulizing Crohn's Disease: A Case Report From Saudi Arabia.

Gastrointestinal basidiobolomycosis (GIB) is a rare, emerging fungal infection caused by Basidiobolus ranarum, which requires a high index of clinical suspicion for early diagnosis and management. It is prevalent in hot and humid regions, and its clinical manifestations may mimic inflammatory bowel disease (IBD), malignancy, and tuberculosis (TB). This often results in the disease being missed or incorrectly diagnosed. We present the case of a 58-year-old female patient from the southern region of Saudi Arabia who presented with persistent non-bloody diarrhea for four weeks and was found to have GIB. This condition is associated with significant morbidity and mortality if not diagnosed and treated in a timely manner. The optimal therapeutic strategy for managing this rare infection has not yet been established. Most patients described in the literature have received a combination of pharmaceutical and surgical therapy. Including GIB in the differential diagnosis of gastrointestinal disorders that do not fit the diagnosis may help with its early diagnosis and management.

Randomized trial comparing general anesthesia with anesthesiologist-administered deep sedation for ERCP in average-risk patients.

BACKGROUND AND AIMS: General anesthesia (GA) or monitored anesthesia care (MAC) is increasingly used to perform ERCP. The definitive choice between the 2 sedative types remains to be established. This study compared outcomes of GA with MAC in ERCP performed in patients at average risk for sedation-related adverse events (SRAEs). METHODS: At a tertiary referral center, patients with American Society of Anesthesiologists (ASA) class ≤III were randomly assigned to undergo ERCP with MAC or GA. The main outcome was a composite of hypotension, arrhythmia, hypoxia, hypercapnia, apnea, and procedural interruption or termination defined as SRAEs. In addition, ERCP procedural time, success, adverse events, and endoscopist and patient satisfaction were compared. RESULTS: Of 204 randomized, 203 patients were evaluated for SRAEs (MAC, n = 96; GA, n = 107). SRAEs developed in 35% of the MAC cohort (34/96) versus 9% in the GA cohort (10/107), which was statistically significant (P < .001). Mean induction time for GA was significantly longer than that for MAC (10.3 ± 10 minutes vs 6.5 ± 10.8 minutes, respectively; P < .001). ERCP procedure time, recovery time, cannulation time and success, and procedure-related adverse events were not statistically different between the 2 sedative groups. The use of GA improved endoscopist and patient satisfaction (P < .001). CONCLUSION: GA is safe with fewer SRAEs than MAC in patients with ASA scores ≤III undergoing ERCP. Apart from prolonging induction time, use of GA does not change the procedural success or ERCP-related adverse events and offers greater endoscopist and patient satisfaction. Hence, GA is a consideration in patients undergoing ERCP in this population group. (Clinical trial registration number: NCT04099693.).

Mechanisms of hepatotoxicity of chloroacetonitrile - an end product of water chlorination.

Chloroacetonitrile is a disinfectant by-product of chlorination of drinking water and is considered as a direct-acting mutagenic and carcinogenic agent. Time-course and dose-response studies were performed to examine the mechanism of chloroacetonitrile-induced hepatotoxicity. In the time-course study, animals were scarified at 2, 4, 6 and 12 h after a single oral dose of chloroacetonitrile (38 mg/kg, p.o.). In the dose-response study, rats were scarified at 2 h after a single oral dose of chloroacetonitrile (9, 19, 38, and 76 mg/kg). In the time-course study chloroacetonitrile induced a significant decrease of hepatic glutathione, and activities of glutathione-S-transferase, glutathione proxidase and superoxide dismutase accompanied with an increase of hepatic malondialdehyde, plasma cytokines (IL-6 & 10 and TNF-α), serum aminotransferases and total bilirubin after 2 h of administration. Maximal alteration of the estimated parameters was observed at 4 h and returned to normal value at 6 h and/or 12 h after chloroacetonitrile treatment. Moreover, the alterations in oxidant, antioxidant parameters, inflammatory cytokines and the liver function tests were dose dependant. Histopathological findings supported the biochemical results. These data indicate that the mechanism of chloroacetonitrile-induced hepatotoxicity may be mediated through depletion of antioxidants, induction of oxidative stress and inflammatory cytokines.