Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0240066 (iron deficiency)
 7,156 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A series of 130 consecutive outpatients with recurrent aphthous stomatitis were screened at the oral medicine department, Glasgow Dental Hospital, for deficienciesin vitamin b12, folic acid, and iron. In 23 patients (17.7%) such deficiencies werefound; five were deficient in vitamin B12, seven in folic acid, and 15 in iron. Four had more than one deficiency. Out of 130 controls matched for age and sex 11 (8.5%) were found to have deficiencies. The 23 deficient patients with recurrent aphthaewere treated with specific replacement therapy, and all 130 patients were followed up for at least one year. Of the 23 patients on replacement therapy 15 showed complete remission of ulceration and eight definite improvement. Of the 107 patientswith no deficiency receiving local symptomatic treatment only 33 had a remission or wereimproved. This difference was significant (P less than 0.001). Most patients withproved vitamin B12 or folic acid deficiency improved rapidly on replacement therapy;those with iron deficiency showed a less dramatic response. The 23 deficient patientswere further investigated to determine the cause of their deficiencies and detect the presence of any associated conditions. Four were found to have Addisonian perniciousanaemia. Seven had a malabsorption syndrome, which in five proved to be a gluten-induced enteropathy. In addition, there were single patients with idiopathic proctocolitis, diverticular disease of the colon, regional enterocolitis, and adenocarcinoma of thecaecum. We suggest that the high incidence of deficiencies found in this series andthe good response to replacement therapy shows the need for haematological screening of such patients.
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PMID:Recurrent aphthae: treatment with vitamin B12, folic acid, and iron. 114 67

In a group of nine children with postenteritis enteropathy (i.e., persisting small-intestinal mucosal damage and failure-to-thrive after an acute episode of gastroenteritis), absorption capacities for vitamin B12 and folic acid were studied and compared with hematological status in peripheral blood. The fractional absorptions of vitamin B12 (FAB12) and folic acid (FAFol) were determined by means of a double-isotope technique employing a single-stool-sample test. The children were examined when growth retardation was maximal, and examinations were repeated during the late recovery period. In spite of considerable small-intestinal mucosal damage, only the absorption of vitamin B12 was markedly affected, while that of folic acid was almost intact. When growth retardation was maximal, FAB12 was below the normal age-correlated range in half of the children. FAB12 was also severely reduced in all longitudinally observed children when compared with the results obtained during the late recovery period (p less than 0.005). FAFol was below the normal range in one fourth of the children, but the reduction was modest and insignificant when compared with the results of repeated examinations during the late recovery period. A moderate iron deficiency was detected in half the children. High levels of plasma vitamin B12, folic acid, and erythrocyte folate were detected at both early and later examinations, indicating that these parameters were not affected by the reduced absorption capacities. However, if malabsorption and chronic diarrhea are combined with low dietary intake of vitamin B12, as is the case for many children in the Third World, depletion of vitamin B12 stores may result.
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PMID:Vitamin B12 and folic acid absorption and hematological status in children with postenteritis enteropathy. 224 17

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

Peroral jejunal biopsies were performed in 63 adult patients from a population of 40,000. Twenty-two patients had definite pathologic biopsy findings; 20 of these had gluten-induced enteropathy. With the 15 previously known patients in the region, this makes a minimum prevalence of 1 per 1,143. Subtotal villous atrophy was found in 8 patients, whereas partial villous atrophy was found in 12 patients. The clinical picture varied considerably, borborygmia, diarrhoea, abdominal pain, and psychiatric symptoms being the most commonly encountered symptoms. Steatorrhoea was found in only two patients with subtotal villous atrophy. In all the remaining patients, including six with subtotal villous atrophy, the faecal fat excretion was normal. A low whole blood folic acid concentration was the most consistent laboratory finding, although some patients had values slightly above the lower normal limit. Anaemia was not pronounced. Iron deficiency, as measured by the erythrocyte protoporphyrin IX concentration, was not common. A high degree of clinical awareness and broad indications for jejunal biopsy-taking is recommended.
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PMID:Prevalence and clinical picture of adult gluten-induced enteropathy in a Norwegian population. 743 1

We review the adverse effect of non-steroidal anti-inflammatory drugs (NSAIDs) on the small and large intestine. NSAIDs cause small intestinal inflammation in 65% of patients receiving the drugs long-term. The clinical implications of NSAID-induced enteropathy are that patients bleed and lose protein from the inflammatory site, contributing to iron deficiency and hypoalbuminemia, respectively. Some patients develop intestinal strictures, which may require surgery, and the occasional one may develop discrete ulcers with perforations. There are a number of therapeutic options available to treat the enteropathy and the attendant complications, including antibiotics, sulphasalazine and misoprostol. The colon, by comparison, is only rarely affected by NSAIDs, but colitis is well recognized and NSAIDs may be an important factor in diverticular complications and the relapse of inflammatory bowel disease. There is an association between NSAID intake and appendicitis in the elderly.
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PMID:Intestinal toxicity of non-steroidal anti-inflammatory drugs. 799 40

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

Young Aboriginal children in remote regions of tropical and desert Australia are at risk of developing urate stones in their upper urinary tract from an early age. These radiolucent calculi were only recognized with the availability of ultrasound diagnosis and are not associated with anatomic anomalies or abnormal uric acid production/metabolism. Although these stones appear to resolve spontaneously after the weaning period, some result in ureteric obstruction and infection which may lead to renal damage. This pattern of urolithiasis differs from the usual global urolithiasis pattern of either endemic bladder stones in young children in developing countries or predominantly calcium-based stones in upper tracts of older children and adults in affluent industrialized countries, where upper tract urate stones account for only a minority of childhood urinary tract stones. Risk factors for urate stones are low urine output and acidic urine. An association between urolithiasis and carbohydrate intolerance leading to chronic acidosis has been suggested for Aboriginal children, but existing limited evidence does not support this as a major aetiological factor. Although further studies on the epidemiology, natural history and management of these urate stones are needed, we believe the focus should be on improving the known social and environmental risk factors of remote Aboriginal children during the weaning period which contribute to the unacceptably high prevalence of failure to thrive, diarrhoeal disease, environmental enteropathy, iron deficiency and urolithiasis.
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PMID:Unique pattern of urinary tract calculi in Australian Aboriginal children. 1288 59

We report the case of a patient with a severe chronic radiation enteropathy. She had been dependent on red cell transfusions for many years. On admission, she displayed anemia (8.6 g/dL) resulting from both inadequate EPO production and a functional iron deficiency. A 3-wk IV iron sucrose treatment (200 mg once weekly) resulted in an increased reticulocyte count, but did not raise the hemoglobin (Hb) level. The adjunction of epoetin alpha (10,000 IU three times a week) made it possible to reach the normal range (12.9 g/dL) after a 17-wk treatment. As the anti-anemic treatment discontinued, the Hb level decreased to 11.1 g/dL within 2 wk. Giving EPO again (10,000 IU twice a week) failed to maintain the Hb level, which dropped under basal values (7.8 g/dL). In contrast, a second combination EPO/iron sucrose did restore a normal Hb level and maintained it. This case report supports the combination of EPO and IV iron supplementation in patients with anemia of chronic disease and either an impaired iron absorption or intolerance to oral iron.
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PMID:Epoetin alfa and intravenous iron sucrose to treat severe anemia in a patient with chronic radiation enteropathy: a case report. 1451 81

Chronic use of non-salicylate NSAIDs causes in most individuals an asymptomatic enteropathy involving the small bowel, particularly its distal part. This enteropathy is characterised by an increase in intestinal permeability and a mild mucosal inflammation. Hypoalbuminemia and iron deficiency may occur. In addition, non-salicylate NSAIDs may cause focal lesions of the small intestine. Ulcerations and ulcers, that can be accidentally discovered during an ileoscopy, may cause acute or chronic bleeding. Deep ulcers may provoke sudden peritonitis. Small bowel diaphragms are rare fibrotic lesions, specifically associated with the use of non-salicylate NSAIDs or salicylates (duodenal diaphragms only). NSAID use is not associated with a constant toxicity on colonic mucosa. NSAID-induced colonic ulcers and diaphragms are rare. In patients with colonic diverticulosis, NSAID intake is a risk factor for severe attacks of diverticulitis. Acute or chronic use of non-salicylate NSAIDs increases the risk for ischemic colitis and flare-ups of inflammatory bowel disease. De novo colitis caused by non-salicylate NSAIDs are rare. The definite diagnosis of this entity relies on the absence of recurrence of colitis in the 2-3 following years. Such a recurrence would lead to the post-hoc diagnosis of first attack of inflammatory bowel disease triggered by NSAID use. Experimental data suggest that selective COX-2 inhibitors do not alter constantly mucosa of the small intestine. Pilot epidemiological works suggest that severe intestinal lesions are less frequent in association with COX-2 inhibitor use than in association with conventional NSAIDs. However, COX-2 appears as playing a beneficial role in mucosal healing, and it seems that COX-2 inhibitors, like conventional NSAIDs, may trigger flare-ups of inflammatory bowel disease.
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PMID:[Gastrointestinal complications related to NSAIDs]. 1536 76

Celiac disease is an immune-mediated enteropathy affecting 0.5% to 1% of children and is induced by dietary gluten in susceptible individuals carrying the human leukocyte antigen DQ2 or DQ8 heterodimer. If serological screening is positive or if a patient displays suggestive symptoms, an endoscopic biopsy of the distal duodenum is required to confirm the diagnosis. Symptoms of celiac disease are often mild or absent. Overt malabsorption occurs in only 2% to 10% of children. Individuals with a higher risk of developing celiac disease, including first-degree relatives of affected patients and children with type I diabetes, Turner syndrome, Williams syndrome or Down syndrome, should be offered screening for celiac disease along with a discussion of the implications. If serological testing is negative, a high index of suspicion should remain if malabsorption, iron deficiency or osteopenia is present. Also, immunoglobulin A deficiency should be excluded. At-risk individuals should undergo serial serological screening. Lifelong adherence to a gluten-free diet is the only treatment. If left untreated, symptomatic children with celiac disease carry an increased risk of developing osteoporosis and have a greater lifetime risk of cancer. The long-term outcome of undiagnosed or untreated asymptomatic individuals is less clear.
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PMID:Practical considerations for the identification and follow-up of children with celiac disease. 1968 81


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