Introduction: Cholangioscopy is an important tool in the evaluation of indeterminate biliary strictures allowing for direct visualization of strictures and targeted biopsies. We present an unusual case of painless jaundice where cholangioscopy played a crucial role in making the diagnosis. Case Description/Methods: A 76-year-old male with a past medical history of hypertension and diabetes mellitus, and a past surgical history of a laparoscopic cholecystectomy ten years prior to presentation was referred for one week of painless jaundice, darkening of urine, and pruritus. He denied any weight loss, abdominal pain, nausea, or vomiting. Laboratory evaluation was significant for a total bilirubin of 14.8, direct bilirubin of 7.6, AST 40, ALT 56, and alkaline phosphatase of 128. Magnetic resonance cholangiopancreatography was obtained, which revealed a poorly defined soft tissue lesion at the junction of the intrahepatic and extrahepatic common hepatic duct (CHD) with intrahepatic ductal dilation (IHD). Multiple small filling defects within the dilated ducts were also noted, suggestive of choleliths. The patient was referred for endoscopic ultrasound (EUS) and endoscopic retrograde cholangiopancreatography (ERCP). EUS revealed IHD and a benign appearing porta hepatis lymph node with no endosonographic evidence of pancreatic mass or cysts. The lymph node at the porta hepatis was sampled using fine needle aspiration (FNA). ERCP was then performed, revealing a single stenosis at the level of the CHD with IHD. Cholagioscopy was performed, which revealed an inflammatory-appearing stenosis of the CHD with embedded suture material and a cholelith proximal to the stenosis (Figure). The stenosis was biopsied and dilated with a 4 mm balloon dilator. An 8.5 x 10 cm plastic biliary stent was placed with subsequent flow of bile. FNA cytology and pathology of the CHD stricture were both negative for malignancy. Discussion: Our patient likely sustained a bile duct injury during his prior cholecystectomy, which was repaired with suture, leading to an inflammatory stricture and obstructive jaundice. We had a high suspicion pre-procedure for malignancy given this patient's presentation, and as such cholangioscopy was crucial in determining the etiology of this patient's stricture. Our case highlights the importance of cholangioscopy in the evaluation of indeterminate biliary strictures, particularly in patients whom have undergone biliary surgery.
Figure 1. A demonstrates a PRISMA flow diagram showing the patient selection process.Table 1. Comparison of demographics and Narcotic treatment of patients who used and did not use NSAIDs Variables NSAID use (n545) No NSAID use (n590) P value Age, mean 6 SD 51.9 6 16.4 57.9 6 18.1 0.06 Female, n (%) 21/45 (46.7) 4/90 (4.44) 0.81 White race, n (%) 38/45 (84.4) 71/90 (78.9) 0.9 Non-Hispanic ethnicity, n (%) 44/45 (97.8) 87/90 (96.7) 0.54 Urban resident, n (%) 32/45 (71.1) 52/90 (57.8) 0.13 Narcotic Rx at discharge, n (%) 38/45 (84.4) 66/90 (73.3) 0.14 Attempt to reach provider, n (%) 8/44 (18.2) 12/84 (14.3) 0.56
Case Description/Methods: A 59-year-old man with left-sided ulcerative colitis presented with acute-onset left hand weakness, numbness, facial droop, and slurred speech. He had a remote 4-pack year tobacco history and left-sided ischemic stroke 3 years ago in the setting of cocaine use. At that time, workup was unrevealing with normal cardiac function and no hyperlipidemia. He since reported complete abstinence from cocaine and continued on a statin and aspirin. His ulcerative colitis was diagnosed 8 months prior to presentation. He required multiple hospitalizations with inadequate response to oral mesalamine and intermittent intravenous steroids. He switched to infliximab but rapidly developed high anti-drug antibody titers. He started tofacitinib 10mg twice daily due to strong patient preference for an oral agent and concerns of developing antibodies against additional biologics. Five days after initiation, he presented with the neurologic symptoms above, which were mild and did not require tPA or thrombectomy. Computed tomography and magnetic resonance imaging revealed acute ischemic stroke in the posterior right frontal lobe. Low-density lipoprotein level was 40mg/dL; urine drug screen was negative. Expanded workup including hypercoagulability labs, echocardiogram, and 30-day cardiac loop monitor did not suggest a specific stroke etiology. He transitioned to ustekinumab. (Figure ) Discussion: While tofacitinib has shown elevated MACE risk compared to TNF inhibitors in rheumatoid arthritis, no studies have yet examined these outcomes in ulcerative colitis or parsed risk of stroke from composite cardiovascular events. This case highlights the rapidity with which stroke can occur after tofacitinib initiation in ulcerative colitis in a patient with underlying risk factors. Non-composite outcome data are essential to guide shared decisionmaking using patient-specific risk factors. Evolving safety profiles must be carefully balanced against patient preferences for oral therapies.[2767] Figure 1: Recurrent acute ischemic stroke within one week of tofacitinib initiation. Magnetic resonance imaging reveals a focus of acute restricted diffusion (approximately 1.4 x 1.8 cm) within the posterior right frontal lobe (middle cerebral artery territory).
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