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)

Factor XII deficiency and impaired prekallikrein activity were diagnosed in a 1-year-old Chinese Shar Pei. The dog experienced repeated episodes of intestinal hemorrhage and diarrhea. Laboratory findings were compatible with blood loss (iron deficiency anemia and hypoproteinemia). Necropsy findings suggested mild infiltrative bowel disease that could have been responsible for the dog's diarrhea, but no explanation for the severe recurrent gastrointestinal hemorrhage could be found. Factor XII deficiency is uncommon in the dog and is not associated with hemorrhagic tendencies. The factor XII deficiency in this case may have contributed to the gastrointestinal hemorrhage.
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PMID:Factor XII and partial prekallikrein deficiencies in a dog with recurrent gastrointestinal hemorrhage. 199 70

Iron absorption is under delicate control and the level of absorption is adjusted to comply with the body's need for iron. To measure the intestinal setting for iron absorption, and thereby indirectly assess body iron requirements, cobaltous chloride labelled with (57)Co or (60)Co was given by mouth and the percentage of the test dose excreted in the urine in 24 hours was measured in a gamma counter. Seventeen control subjects with normal iron stores excreted 18% (9-23%) of the dose. Increased excretion, 31% (23-42%), was found in 10 patients with iron deficiency anemia and in 15 patients with depleted iron stores in the absence of anemia. In contrast, 12 patients with anemia due to causes other than iron deficiency excreted amounts of radiocobalt within the normal control range. In patients with iron deficiency, replenishment of iron stores by either oral or parenteral iron caused the previously high results to return to normal.Excretion of the test dose was normal in portal cirrhosis with normal iron stores but it was markedly increased in patients with cirrhosis complicated by either iron deficiency or endogenous iron overload. It was also raised in primary hemochromatosis. Excretion of the dose was reduced in gluten-sensitive enteropathy. Gastrointestinal surgery and inflammatory disease of the lower small intestine had no effect on the results except that some patients with steatorrhea had diminished excretion.The cobalt excretion test provides the clinician with a tool for the assessment of iron absorption, the detection of a reduction in body iron stores below the level that is normal for the subject in question, the differentiation of iron deficiency anemia from anemia due to other causes, and the investigation of patients with iron-loading disorders.
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PMID:Cobalt excretion test for the assessment of body iron stores. 557 25

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 45-year-old woman reported the development of thigh pain followed within a year by proximal muscle weakness. Clinical findings included short stature, prominent kyphoscoliosis, proximal weakness, and brisk reflexes. Recognition of an increased level of serum alkaline phosphatase and hypophosphatemia led to the diagnosis of osteomalacia. Identification of iron deficiency anemia and hypocholesterolemia implicated previously unrecognized gluten-sensitive enteropathy with associated vitamin D malabsorption as the cause of the osteomalacia. Adherence to a gluten-free diet and treatment with vitamin D2 resulted in weight gain, resolution of pain, and improvement in strength within 3 months. Painful proximal weakness and hyperreflexia may be the initial and primary manifestations of osteomalacia, a readily treatable cause of muscle and bone disease.
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PMID:Osteomalacic myopathy. 787 Jan 21

Coeliac disease is associated with an increased risk of certain gastrointestinal malignancies, especially of the small bowel. Metachronous malignancies are well established in the colon, where adenocarcinoma is common, but are exceptional in the small intestine. We describe a young woman with a long history of malabsorption who was shown to have coeliac disease complicated by a small-bowel adenocarcinoma. The cancer was resected, and the coeliac disease went into complete remission on a strict gluten-free diet. Fifteen years later she developed iron deficiency anaemia. Investigations showed a metachronous small-bowel adenocarcinoma but continuing remission of the coeliac disease. The case provides strong evidence against a causative role for the enteropathy of active coeliac disease in small-bowel adenocarcinoma and against a protective effect of a gluten-free diet in tumour development. Predisposition to adenocarcinoma in coeliac disease is probably genetic.
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PMID:Metachronous small-bowel adenocarcinoma in coeliac disease: gluten-free diet is not protective. 951 36

A 17 year old male suffered from iron deficiency of undetermined cause for 2 years. Iron substitution was able to correct it for short periods. With the exception of fatigue and recurring abdominal pain attributed to oral iron therapy no further symptoms were present. The physical status on admission was unremarkable. The laboratory detected intestinal disorders, an anemia of the chronic type without evidence for malignancy or renal failure suggested an inflammatory gastro-intestinal disorder. In spite of a twice negative noninvasive test for gluten-intolerance the clinician favored in his differential diagnosis non tropical sprue over inflammatory bowel disease (IBD, Crohn's disease, Whipple's disease). Histopathology of small bowel specimens did not indicate sprue. An ileo-colonoscopy revealed severe ulcerating ileitis and mild chronic colitis. The histologic specimen revealed a severe ileal inflammation with cosinophilia and the colon specimens epitheloid microgranuloma. These findings are highly compatible with the diagnosis of Crohn's disease. Iron deficiency anemia is common in Crohn's disease. In the current case it is due to disturbed iron uptake. Iron deficiency anemia as sole symptom of Crohn's disease is extremely rare.
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PMID:[Severe chronic iron deficiency in a 17-year-old student]. 962 33

Vascular lesions of the gastrointestinal (GI) tract include arterio-venous malformations as angiodysplasia and Dieulafoy's lesion, venous ectasias (multiple phlebectasias and haemorroids), teleangiectasias which can be associated with hereditary hemorrhagic teleangiectasia (HHT), Turner's syndrome and systemic sclerosis, haemangioma's, angiosarcoma's and disorders of connective tissue affecting blood vessels as pseudoxanthoma elasticum and Ehlers-Danlos's disease. As a group, they are relatively rare lesions that however may be a major source of upper and lower gastrointestinal bleeding. Clinical presentation is variable, ranging from asymptomatic cases over iron deficiency anaemia to acute or recurrent bleeding that may be life-threatening. Furthermore, patients may present with other symptoms, e.g. pain, dysphagia, odynophagia, the presence of a palpable mass, intussusception, obstruction, haemodynamic problems resulting from high cardiac output, lymphatic abnormalities with protein loosing enteropathy and ascites, or dermatological and somatic features in syndromal cases. Diagnosis can usually be made using endoscopy, sometimes with additional biopsy. Barium radiography, angiography, intraoperative enteroscopy, tagged red blood cell scan, CT-scan and MRI-scan may offer additional information. Treatment can be symptomatic, including iron supplements and transfusion therapy or causal, including therapeutic endoscopy (laser, electrocautery, heater probe or injection sclerotherapy), therapeutic angiography and surgery. The mode of treatment is of course depending on the mode of presentation and other factors such as associated disorders. If endoscopic or angiographic therapy is impossible and surgical intervention not indicated, pharmacological therapy may be warranted. Good results have been reported with different drugs, albeit most of them have not been tested in large trials.
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PMID:Vascular lesions of the gastrointestinal tract. 1261 28

Coeliac disease and hereditary haemochromatosis are genetic disorders paradoxically associated with altered intestinal absorption of iron. Hereditary haemochromatosis is the most common autosomal recessive disease in the Caucasian population and is characterised by an iron overload state. Coeliac disease, or gluten sensitive enteropathy, on the other hand is frequently associated with iron deficiency anaemia. We report the cases of two patients who developed both coeliac disease and hereditary haemochromatosis. We review the literature of this rare association and examine how the clinical presentation is modified by their co-existence and the potential genetic linkage of these two disorders.
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PMID:Coeliac disease and hereditary haemochromatosis: association and implications. 1507 2

Celiac disease is an immune-mediated enteropathy caused by a permanent sensitivity to gluten in genetically susceptible individuals. It occurs in children and adolescents with gastrointestinal symptoms, dermatitis herpetiformis, dental enamel defects, osteoporosis, short stature, delayed puberty and persistent iron deficiency anemia and in asymptomatic individuals with type 1 diabetes, Down syndrome, Turner syndrome, Williams syndrome, selective immunoglobulin (Ig)A deficiency and first degree relatives of individuals with celiac disease. The Celiac Disease Guideline Committee of the North American Society for Pediatric Gastroenterology, Hepatology and Nutrition has formulated a clinical practice guideline for the diagnosis and treatment of pediatric celiac disease based on an integration of a systematic review of the medical literature combined with expert opinion. The Committee examined the indications for testing, the value of serological tests, human leukocyte antigen (HLA) typing and histopathology and the treatment and monitoring of children with celiac disease. It is recommended that children and adolescents with symptoms of celiac disease or an increased risk for celiac disease have a blood test for antibody to tissue transglutaminase (TTG), that those with an elevated TTG be referred to a pediatric gastroenterologist for an intestinal biopsy and that those with the characteristics of celiac disease on intestinal histopathology be treated with a strict gluten-free diet. This document represents the official recommendations of the North American Society for Pediatric Gastroenterology, Hepatology and Nutrition on the diagnosis and treatment of celiac disease in children and adolescents.
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PMID:Guideline for the diagnosis and treatment of celiac disease in children: recommendations of the North American Society for Pediatric Gastroenterology, Hepatology and Nutrition. 1562 18

Various factors have been shown to be involved in the pathophysiology of NSAID-induced small intestinal damage. Recent advances in diagnostic methods including video capsule endoscopy and double-balloon endoscopy have enabled us to examine the entire small intestine, and we now recognize that prevalence of small intestinal damage in patients taking NSAIDs is high. NSAIDs cause intestinal damage including redness, erosions, and ulcers in both jejunum and ileum. Most of patients with intestinal pathology are asymptomatic, although a few patients present with iron deficiency anemia and/or hypoalbuminaemia. The risk factors for NSAID-induced enteropathy are unknown. Experimental and clinical studies would unravel the mechanism by which NSAIDs injure intestinal mucosa.
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PMID:[Clinical features of NSAID-induced small intestinal damage]. 1792 37


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