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Turmeric is popularly used as a naturopathic supplement associated with myriad benefits and has long been generally regarded as safe. However, increasing reports of turmeric-associated liver injury have emerged over recent years. This case presents a female patient without significant past medical history who presents with signs and symptoms of acute hepatitis after consuming a turmeric-containing tea. Her case adds to a growing body of evidence that dosage safety, manufacturing, and pharmacologic delivery practices for turmeric supplements should be investigated.

McCune-Albright syndrome (MAS) is a genetic disorder characterized by polyostotic fibrous dysplasia, precocious puberty, and café-au-lait spots. In this case, a patient presented with precocious puberty in the setting of an ovarian mass and late development of café-au-lait macules, confounding the final diagnosis of MAS. A 3-year-old girl presented with vaginal bleeding. She had a previous episode of vaginal bleeding, breast budding, and a right ovarian cyst at 5 months of age. Work-up at that time showed no abnormal findings, though past medical history was notable for two fractures. Physical exam was significant for increased height (89th percentile), increased weight (99th percentile), bilaterally elevated breast mounds with palpable breast tissue and darkened areolae (Tanner stage 3), and residual blood in the vaginal introitus. Notable labs included low FSH and high ultrasensitive estradiol. Pelvic MRI showed a right ovarian cyst, which, in the context of precocious puberty, raised the suspicion for a juvenile granulosa cell tumor. Follow-up pelvic MRI demonstrated features that instead suggested an ovarian response to hormonal stimulation. On a subsequent visit several months later, the patient had small café-au-lait macules on the chest and right buttock, which were not present on the initial evaluation. Further workup revealed advanced bone age on an x-ray at 6 years 10 months, and multifocal polyostotic fibrous dysplasia involving bilateral femurs and right tibia. Failure to include MAS in the differential had led to unnecessary oophorectomy. It is crucial to identify MAS as a cause of peripheral precocious puberty to guide proper management.

Introduction: Median arcuate ligament syndrome (MALS), also known as celiac artery compression syndrome, is a rare anatomic disorder (2:100,000) that is more prevalent in women (4:1 ratio) with thin body habitus. Average age of presentation is 30 to 50 years old. It is characterized by weight loss, postprandial abdominal pain, nausea, and vomiting. We present a case of MALS in a 68-year-old male with nonspecific GI symptoms. Case Description/Methods: 68-year-old male with history of alcohol use and ex-lap presents with postprandial dull abdominal pain left to the umbilicus and radiates to the back. Accompanied by early satiety, and 10-20 lbs of unintentional weight loss over one-year. He had normal bowel movements with no melena or hematochezia. He took opioids, pantoprazole, and over the counter pain medications with some relief. He was evaluated with esophagogastroduodenoscopy, colonoscopy, abdominal ultrasound and a computed tomography (CT) of the abdomen and pelvis with contrast. These investigations did not yield any significant findings. CTA abdominal aorta with runoff was ordered due to concern of chronic mesenteric ischemia. It showed focal stenosis of the origin of the celiac axis with minimal post stenotic dilation. Patient was referred to vascular surgery who performed laparoscopic robot assisted median arcuate ligament release. Surgery was converted to open supra-umbilical laparotomy due to difficult visualization of the celiac artery origin. A thick band compressing the anterior surface of the celiac artery was freed. Post-surgery, patient had relief of his abdominal pain and has been recovering well (Figure). Discussion: Median arcuate ligament syndrome is a diagnosis of exclusion. It usually presents with nonspecific symptoms, and many patients can be asymptomatic and be found incidentally. It is believed that MALS causes inflammation and compression of the celiac plexus causing the symptoms. MALS is difficult to diagnose, especially in the absence of a standardized algorithm to aid in diagnosis and treatment. Our case was unique as our patient did not match with the typical demographics of patients with MALS. He was a male, in his 60's, with average weight. Clinicians should keep a high suspicion of MALS with patients who have postprandial abdominal pain and weight loss with negative initial workup. Diagnosis could be made by ultrasound, CT imaging, or CTA and MRA. Definitive management involves surgery with 85% of patients experiencing postop pain relief in one study.[3572] Figure 1. CTA Image.

Introduction: Turmeric, a plant prevalent in South Asia, is often marketed to be safe, with many benefits including antioxidant and anti-inflammatory effects. Hepatotoxicity, a rare adverse effect, has only been documented in a few case reports. Here we present a case of turmeric Drug Induced Liver Injury (DILI) with normalization of liver function tests after its cessation. Case Description/Methods: A 62-year-old female with a history of hypertension presented with nausea and generalized abdominal pain for five days. She denied taking medications other than hydrochlorothiazide. Further interview noted that she initiated turmeric tea over the preceding three weeks. On physical exam, she had scleral icterus and right upper quadrant tenderness. Laboratory workup showed AST 1510 U/L, ALT 1889 U/L, total bilirubin 13.9 mg/dL, direct bilirubin 8.1 mg/dL, ALP 134 U/L, LDH 542 U/L, with an ALT/LDH ratio of 3.49. INR was normal. Ultrasound revealed findings consistent with acute hepatitis. Ferritin, ceruloplasmin, and acetaminophen levels were normal. Alpha-1-antitrypsin, anti-mitochondrial, and anti-smooth muscle antibodies were unremarkable. Viral serologies were normal. The patient improved with turmeric cessation, with complete resolution of abnormal liver enzymes on follow-up. Discussion: Turmeric, previously considered safe, has now been reported to be associated with DILI in a few case reports. Our case adds to the growing body of evidence supporting turmeric induced DILI. Although we could not uncover the exact dose, we do establish a high probability of adverse effects from turmeric using the validated Roussel Uclaf Causality Method (RUCAM) scoring system. Our patient scored 9, with a score .8 representing a high probability. Turmeric induced DILI is thought to be both dose dependent and associated with formulations that contain supplements or nanoparticles that increase turmeric's bioavailability. Lombardi et al. and Sohal et al. for example both report several cases of acute hepatitis associated with turmeric preparations developed with piperine (black pepper), which has been shown to increase the absorption of turmeric by 2000%. In our case, the patient's turmeric tea also included black pepper, which likely explains the hepatotoxicity. This case underscores the importance of supplement history, with an emphasis on turmeric, when evaluating for potential causes of DILI.