• Title/Summary/Keyword: Protein-losing enteropathies

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Disseminated Cytomegalovirus Infection and Protein Losing Enteropathy as Presenting Feature of Pediatric Patient with Crohn's Disease

  • Cakir, Murat;Ersoz, Safak;Akbulut, Ulas Emre
    • Pediatric Gastroenterology, Hepatology & Nutrition
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    • v.18 no.1
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    • pp.60-65
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    • 2015
  • We report a pediatric patient admitted with abdominal pain, diffuse lower extremity edema and watery diarrhea for two months. Laboratory findings including complete blood count, serum albumin, lipid and immunoglobulin levels were compatible with protein losing enteropathy. Colonoscopic examination revealed diffuse ulcers with smooth raised edge (like "punched out holes") in the colon and terminal ileum. Histopathological examination showed active colitis, ulcerations and inclusion bodies. Immunostaining for cytomegalovirus was positive. Despite supportive management, antiviral therapy, the clinical condition of the patient worsened and developed disseminated cytomegalovirus infection and the patient died. Protein losing enteropathy and disseminated cytomegalovirus infection a presenting of feature in steroid-naive patient with inflammatory bowel disease is very rare. Hypogammaglobulinemia associated with protein losing enteropathy in Crohn's disease may predispose the cytomegalovirus infection in previously healthy children.

Resolution of Protein-Losing Enteropathy after Congenital Heart Disease Repair by Selective Lymphatic Embolization

  • Kylat, Ranjit I;Witte, Marlys H;Barber, Brent J;Dori, Yoav;Ghishan, Fayez K
    • Pediatric Gastroenterology, Hepatology & Nutrition
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    • v.22 no.6
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    • pp.594-600
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    • 2019
  • With improving survival of children with complex congenital heart disease (CCHD), postoperative complications, like protein-losing enteropathy (PLE) are increasingly encountered. A 3-year-old girl with surgically corrected CCHD (ventricular inversion/L-transposition of the great arteries, ventricular septal defect, pulmonary atresia, postdouble switch procedure [Rastelli and Glenn]) developed chylothoraces. She was treated with pleurodesis, thoracic duct ligation and subsequently developed chylous ascites and PLE (serum albumin ${\leq}0.9g/dL$) and was malnourished, despite nutritional rehabilitation. Lymphangioscintigraphy/single-photon emission computed tomography showed lymphatic obstruction at the cisterna chyli level. A segmental chyle leak and chylous lymphangiectasia were confirmed by gastrointestinal endoscopy, magnetic resonance (MR) enterography, and MR lymphangiography. Selective glue embolization of leaking intestinal lymphatic trunks led to prompt reversal of PLE. Serum albumin level and weight gain markedly improved and have been maintained for over 3 years. Selective interventional embolization reversed this devastating lymphatic complication of surgically corrected CCHD.

The Changes in Intestinal Damage and Bacterial Translocation with Time after Administration of Diclofenac (Diclofenac 투여 후 시간경과에 따른 장손상과 장내세균전위의 변화)

  • Kim, Eun-Jeong;Kim, Jeong-Wook
    • YAKHAK HOEJI
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    • v.52 no.4
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    • pp.293-298
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    • 2008
  • Non-steroidal anti-inflammatory drug (NSAID)-induced gut damage and bacterial translocation (BT) have not been studies well, especially from the perspective of time after administration of NSAIDs. We therefore examined these changes in animals. The study was performed on 5 groups of rat; a control group (group A) and diclofenac groups (groups B, C, E, and F). Rats in the diclofenac groups were orally administered diclofenac sodium before intestinal permeability (IP) measurement (group B, 1 h before measurement; group C, 10 h before; group D, 22 h before; and group E, 52 h before). The IP, stool pellet number, serum biochemical profile, enteric bacterial number, and BT in the mesenteric lymph nodes (MLNs), liver, spleen, kidney and heart were measured. The administration of diclofenac resulted in significantly increased IP, caused intestinal protein loss, decreased stool pellet number, caused enteric bacterial overgrowth and increased BT in multiple organs in groups A, B, C, and D. IF, intestinal protein loss, and the BT in the liver and the spleen in group E were decreased than those in group D. There were no differences in the other parameters between group D and E. In the recovery phase of the diclofenac-induced gut damage, enteric bacterial overgrowth and BT in the kidneys and the heart did not change while the BT in the reticuloendothelial systems such as in the MLNs and liver was decreased.

A case of cytomegalovirus-negative M$\acute{e}$n$\acute{e}$trier's disease with eosinophilia in a child

  • Son, Keun-Hyung;Kwak, Jeong-Ja;Park, Jae-Ock
    • Clinical and Experimental Pediatrics
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    • v.55 no.8
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    • pp.293-296
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    • 2012
  • M$\acute{e}$n$\acute{e}$trier's disease is a rare form of acquired gastropathy characterized by giant rugal folds in the stomach and protein-losing gastropathy. Children with M$\acute{e}$n$\acute{e}$trier's disease tend to follow a benign self-limited course with symptoms typically completely resolving within 2 to 10 weeks in contrast to the chronic course in adults. A 9-year-old girl presented with a history of gradually worsening abdominal distension, increasing body weight, and abdominal pain for 2 weeks. Physical examination on admission indicated periorbital swelling, pitting edema in both the legs, and abdominal distension with mild diffuse tenderness and shifting dullness. Laboratory tests on admission showed hypoalbuminemia, hypoproteinemia, and peripheral eosinophilia. The test result for anti-cytomegalovirus immunoglobulin M was negative. Increased fecal alpha 1 anti-trypsin excretion was observed. Radiological findings showed massive ascites and pleural effusion in both the lungs. On gastroscopy, large gastric folds, erythema, erosion, and exudation were noted in the body and fundus of the stomach. Microscopic findings showed infiltration of eosinophils and neutrophils in the gastric mucosa. Her symptoms improved with conservative treatment from day 7 of hospitalization and resolved completely.

Evaluation of Hemostatic Function with Thromboelastography in Dogs with Hypercoagulable Diseases

  • Kim, Ja-Won;Nam, Aryung;Lee, Kyu-Pil;Song, Kun-Ho;Youn, Hwa-Young;Seo, Kyoung-Won
    • Journal of Veterinary Clinics
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    • v.34 no.2
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    • pp.65-69
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    • 2017
  • Thromboembolic complications are increasing in veterinary medicine. Thromboelastography (TEG) is a more comprehensive method for assessing the clotting process than standard plasma-based coagulation tests. This study compared the ability of TEG and standard coagulation tests to analyze the overall hemostatic state of dogs. The study involved 40 dogs with underlying diseases that predispose to hypercoagulability, including neoplasia, hyperadrenocorticism, immune-mediated diseases, gastrointestinal diseases, and protein-losing nephropathies and enteropathies, and 20 healthy dogs. Their overall hemostatic functional state was evaluated by TEG and routine coagulation assays, including activated partial thromboplastin time, prothrombin time, platelet count, and D-dimer concentration. TEG analysis showed significant differences in clot formation time, ${\alpha}$ angle, and maximum amplitude (MA) between diseased and control dogs (P < 0.001 each). Increased MA was the most frequent abnormality on TEG and was indicative of hypercoagulability. TEG was useful in detecting hemostatic dysfunction in dogs with diseases associated with hypercoagulability. Dogs with TEG tracings indicative of hypercoagulability are likely to be in procoagulant states. Future prospective studies are needed to evaluate whether TEG tracings indicative of hypercoagulability are predictive of thrombosis in dogs.