Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0162316 (iron deficiency anemia)
 3,806 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Intestinal mucosal biopsy immunoglobulin content in a patient with eosinophilia, allergic gastroenteropathy (atopy, food sensitivities, protein-losing enteropathy, iron deficiency anemia, and growth retardation), and hyperimmunoglobulinemia E (68,000 units) was compared with that of a control group and a group with eosinophilic gastroenteritis who had no atopic features. The patient had no evidence of cellular or humoral immunodeficiency but was severely hypersensitive to multiple inhalant and dietary allergens. In contrast to the findings in patients with nonallergic eosinophilic gastroenteritis, whose intestinal immunoglobulin content was similar to that of controls, tissue immunoglobulin IgE and IgG was markedly increased in the allergic patient. These results support an intestinal reaginic mechanism in the etiology of the allergic form of eosinophilic gastroenteritis.
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PMID:Eosinophilic gastroenteritis in extreme allergy. Immunopathological comparison with nonallergic gastrointestinal disease. 45 50

Four children who underwent extensive small-bowel resection in infancy developed recurrent iron deficiency anemia due to gastrointestinal bleeding between 4 and 12 years later. The initial resections were required for multiple ileal atresia (n = 2) and gastroschisis (n = 2). Three patients have had melena and one had persistently guaiac-positive stools. Three patients had protein-losing enteropathy, and in one there was persistent hypoalbuminemia. Colonoscopy identified circumferential ulcerative lesions at the surgical anastomosis (n = 2) and at laparotomy another patient had well-defined linear ulcers close to the surgical anastomosis. Histology demonstrated focal ulceration with chronic inflammation, but did not show granulomata, crypt abscesses, or malignancy. Multiple imaging procedures and gastroduodenoscopy failed to identify an alternative bleeding source. Medical therapy including iron, antacids, sucralfate, H2 antagonists, and cholestyramine was ineffective. Two patients have undergone anastomotic resection. One experienced symptomatic recurrence 4 months after surgery. Repeat colonoscopy found ulceration at the new anastomosis with similar histology. The other patient remains asymptomatic 7 months postsurgery. Recurrent gastrointestinal hemorrhage due to anastomotic ulceration, of unknown etiology, appears to be a late complication of small-bowel resection in infancy.
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PMID:Late gastrointestinal bleeding and protein loss after distal small-bowel resection in infancy. 253 7

We studied 12 children with peripheral eosinophilia, iron deficiency anemia secondary to blood loss in the stools, protein-losing enteropathy, and eosinophilic infiltration of the stomach and small intestine. On the basis of immunologic features and responses to therapy, these patients could be divided into two groups. In the first group the disease was transient, presented in the first year of life, remitted on withdrawal of milk from the diet, and was not associated with IgE-mediated immediate hypersensitivity (milk-sensitive enteropathy). In contrast, the second group, which we termed eosinophilic gastroenteropathy, represented patients with a chronic disease that had its onset later in childhood, did not respond to dietary manipulations, was associated with atopy and IgE-mediated immediate hypersensitivity reactions to food, and required corticosteroid therapy to establish remission and control. The mechanism by which food causes gastrointestinal damage appears to be different in these two groups even though the clinical syndromes are similar.
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PMID:Milk-sensitive and eosinophilic gastroenteropathy: similar clinical features with contrasting mechanisms and clinical course. 654 62

A patient initially treated for iron deficiency anemia was later found to have myelofibrosis. She developed increasing splenomegaly and then a mass in the right iliac fossa for which a right hemicolectomy was performed. Histopathology demonstrated extramedullary hemopoiesis in the spleen and cecum. The patient subsequently developed a protein-losing enteropathy and she deteriorated and died 14 mths later. Autopsy was not performed.
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PMID:Extramedullary hemopoiesis arising in the gut mimicking carcinoma of the cecum. 816 30

We describe a 23-year-old man with protein-losing enteropathy, iron deficiency anemia, and recurrent gastrointestinal bleeding. The patient eventually developed disseminated intravascular coagulation, portal vein thrombosis, and extensive small bowel infarction. The autopsy showed multiple telangiectases in the intestines, mesentery, liver, gallbladder, renal pelves, and diaphragm. In addition, lymphangiectases were found in the retroperitoneal space, intestines, and liver. These lesions appeared to have been the cause of the gastrointestinal bleeding and the protein-losing enteropathy. The case most likely represents Osler-Weber-Rendu disease without the usual manifestations in the skin and oral-nasal cavities.
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PMID:Multiple abdominal telangiectases and lymphangiectases. A limited form of Osler-Weber-Rendu disease? 858 83

Ileal dysgenesis is an uncommon condition of unknown etiology occurring in the distal ileum in the region of the vitelline duct. The CT appearance of this lesion, although not previously described to our knowledge, is characteristic. We report a patient with ileal dysgenesis who had an abdominal CT scan to evaluate chronic iron deficiency anemia and protein-losing enteropathy. Recognition of this lesion by pediatric radiologists is important; so that surgical treatment, which is simple and effective, can be initiated quickly.
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PMID:CT manifestations of ileal dysgenesis. 1711 13

A joint study group on cow's milk allergy was convened by the Emilia-Romagna Working Group for Paediatric Allergy and by the Emilia-Romagna Working Group for Paediatric Gastroenterology to focus best practice for diagnosis, management and follow-up of cow's milk allergy in children and to offer a common approach for allergologists, gastroenterologists, general paediatricians and primary care physicians.The report prepared by the study group was discussed by members of Working Groups who met three times in Italy. This guide is the result of a consensus reached in the following areas. Cow's milk allergy should be suspected in children who have immediate symptoms such as acute urticaria/angioedema, wheezing, rhinitis, dry cough, vomiting, laryngeal edema, acute asthma with severe respiratory distress, anaphylaxis. Late reactions due to cow's milk allergy are atopic dermatitis, chronic diarrhoea, blood in the stools, iron deficiency anaemia, gastroesophageal reflux disease, constipation, chronic vomiting, colic, poor growth (food refusal), enterocolitis syndrome, protein-losing enteropathy with hypoalbuminemia, eosinophilic oesophagogastroenteropathy. An overview of acceptable means for diagnosis is included. According to symptoms and infant diet, three different algorithms for diagnosis and follow-up have been suggested.
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PMID:Cow's milk protein allergy in children: a practical guide. 2020 81

Intestinal lymphangiectasia in the adult may be characterized as a disorder with dilated intestinal lacteals causing loss of lymph into the lumen of the small intestine and resultant hypoproteinemia, hypogammaglobulinemia, hypoalbuminemia and reduced number of circulating lymphocytes or lymphopenia. Most often, intestinal lymphangiectasia has been recorded in children, often in neonates, usually with other congenital abnormalities but initial definition in adults including the elderly has become increasingly more common. Shared clinical features with the pediatric population such as bilateral lower limb edema, sometimes with lymphedema, pleural effusion and chylous ascites may occur but these reflect the severe end of the clinical spectrum. In some, diarrhea occurs with steatorrhea along with increased fecal loss of protein, reflected in increased fecal alpha-1-antitrypsin levels, while others may present with iron deficiency anemia, sometimes associated with occult small intestinal bleeding. Most lymphangiectasia in adults detected in recent years, however, appears to have few or no clinical features of malabsorption. Diagnosis remains dependent on endoscopic changes confirmed by small bowel biopsy showing histological evidence of intestinal lymphangiectasia. In some, video capsule endoscopy and enteroscopy have revealed more extensive changes along the length of the small intestine. A critical diagnostic element in adults with lymphangiectasia is the exclusion of entities (e.g. malignancies including lymphoma) that might lead to obstruction of the lymphatic system and "secondary" changes in the small bowel biopsy. In addition, occult infectious (e.g. Whipple's disease from Tropheryma whipplei) or inflammatory disorders (e.g. Crohn's disease) may also present with profound changes in intestinal permeability and protein-losing enteropathy that also require exclusion. Conversely, rare B-cell type lymphomas have also been described even decades following initial diagnosis of intestinal lymphangiectasia. Treatment has been historically defined to include a low fat diet with medium-chain triglyceride supplementation that leads to portal venous rather than lacteal uptake. A number of other pharmacological measures have been reported or proposed but these are largely anecdotal. Finally, rare reports of localized surgical resection of involved areas of small intestine have been described but follow-up in these cases is often limited.
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PMID:Intestinal lymphangiectasia in adults. 2136 42

We describe the case of an adult who developed protein-losing enteropathy 21 years after having undergone a Fontan procedure. Investigations revealed iron deficiency anemia which was treated with intravenous iron sucrose leading to resolution of both the anemia as well as symptoms of protein-losing enteropathy.
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PMID:The role of iron deficiency in protein-losing enteropathy following the Fontan procedure. 2139 62

Two toddlers presented to their primary medical providers with anasarca and severe anemia. Laboratory evaluation revealed iron deficiency along with hypoproteinemia and hypoalbuminemia. Both children were diagnosed with iron deficiency anemia and were suspected to have an associated protein-losing enteropathy. A brief review of the literature is provided, and data supporting the notion of protein-losing enteropathy being a consequence of severe iron deficiency anemia are discussed. The American Academy of Pediatrics recommendations for prevention of iron deficiency anemia are reviewed. These cases illustrate the importance of the primary medical care provider's role in preventive medicine and provide an example of severe complications that may arise from iron deficiency anemia if it is not recognized and treated early.
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PMID:Toddlers with anasarca and severe anemia: a lesson in preventive medicine. 2215 60


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