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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.

Adipocytokines are hormones released from adipose cells. Their functions range from regulating hunger to regulating the metabolic effects of insulin. What role these hormones play in metabolic health and diabetes have not been studied in the Hispanic population. The present study examines associations between leptin, resistin and adiponectin levels in obesity and metabolic health in a Mexican-American border population, with a specific focus on leptin. We hypothesized that 1) Obese subjects display higher leptin levels, regardless of metabolic health and 2) Metabolically healthy subjects display higher leptin levels, regardless of obesity status. To study the association of plasma adipocytokines with weight and metabolic health, we performed a cross-sectional, retrospective study using patient data collected by the Cameron County Hispanic Cohort in Brownsville, Texas. Obesity is BMI ≥ 30 kg/m2. We determined metabolic health status by assessing the presence of the following four criteria: elevated blood pressure (SBP ≥ 130 mmHg and/or DBP ≥ 85 mmHg), elevated triglycerides ≥ 150 mg/dL, low HDL cholesterol (males < 40 mg/dL; females < 50 mg/dL), and elevated fasting glucose ≥ 100 mg/dL (or use of hypoglycemic medications). The presence of < 2 of these criteria defined a subject as “metabolically healthy”. We categorized the patients into four groups: metabolically healthy normal weight (MHNW, n = 245), metabolically healthy obese (MHO, n = 107), metabolically unhealthy normal weight (MUHNW, n = 97), and metabolically unhealthy obese (MUHO, n = 187). We excluded persons < 18 years of age, current smokers, subjects with major cardiovascular events or active malignancy, and subjects using confounding medications. We conducted comparisons of log-transformed adipocytokine concentrations data between the groups using multivariable linear regression after adjusting for sex, age, BMI and hypertension. Leptin was significantly higher in MHO compared to MHNW (p < 0.0001) and MUHNW (p = 0.02), and significantly higher in MUHO compared to MUHNW (p = 0.01) and MHNW (<0.0001). Resistin was higher in MUHNW (p = 0.01) and MUHO (p = 0.03) compared to MHO. Adiponectin levels were lower in MUHO compared to MHNW (p = 0.002). In this Mexican-American population, the results showed that leptin levels were influenced by obesity and not by overall metabolic health status. These findings confirm Hypothesis number 1 and run contrary to Hypothesis number 2. Additionally, resistin levels were significantly higher in metabolically unhealthy patients irrespective of BMI, while both metabolic health and normal weight favored higher adiponectin. Obesity showed a robust association with leptin, metabolic health displayed a strong association with resistin, and both factors influenced adiponectin levels in this population.