Assessment of Aortic Elasticity in Patients with Celiac Disease

BACKGROUND AND OBJECTIVES: Celiac disease (CD) is a chronic autoimmune disorder induced by dietary gluten intake by individuals who are genetically sensitive. Many studies report an increased risk of cardiovascular diseases in such patients. The aim of this study is to assess aortic elasticity properties in patients with CD that may be associated with an increased risk of cardiovascular disease. SUBJECTS AND METHODS: Eighty-one patients diagnosed with CD by antibody test and biopsy and 63 healthy volunteers were included in this prospective study. Electrocardiographic and echocardiographic examinations were performed. RESULTS: The CD group did not have any differences in the conventional echocardiographic parameters compared to the healthy individuals. However, patients in the CD group had an increased aortic stiffness beta index (4.3±2.3 vs. 3.6±1.6, p=0.010), increased pressure strain elastic modulus (33.6±17.0 kPa vs. 28.5±16.7 kPa, p=0.037), decreased aortic distensibility (7.0±3.0×10(-6) cm2/dyn vs. 8.2±3.6×10(-6) cm2/dyn, p=0.037), and similar aortic strain (17.9±7.7 vs. 16.0±5.5, p=0.070) compared to the control group. Patients with CD were found to have an elevated neutrophil/lymphocyte ratio compared to the control group (2.54±0.63 vs. 2.24±0.63, p=0.012). However, gluten-free diet and neutrophil/lymphocyte ratio were not found to be associated with aortic elasticity. CONCLUSION: Patients with CD had increased aortic stiffness and decreased aortic distensibility. Gluten-free diet enabled the patients with CD to have a reduction in the inflammatory parameters whereas the absence of a significant difference in the elastic properties of the aorta may suggest that the risk of cardiovascular disease persists in this patient group despite a gluten-free diet.

Agnogenic myeloid metaplasia: a rare cause of ascites

A 65-year-old woman diagnosed with agnogenic myeloid metaplasia [AMM] was referred to our hospital due to complaints of ascites that developed two months after a splenectomy. The patient had massive ascites with a serumascites albumin gradient of 1.5. The ascites was transudative, assumed to have developed from peritoneal hematopoiesis during the course of portal hypertension that itself developed after splenectomy. To the best of our knowledge, no report in the literature has described a case diagnosed as AMM with ascites after splenectomy. Thus this report is the first case of AMM with ascites that developed two months after splenectomy