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Query: UMLS:C0240066 (iron deficiency)
7,156 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In a patient with celiac disease, folate and iron deficiency, and epilepsy, CT over a 4-month period showed parietoocipital calcifications in the corticomedullary junctions. The calcification was progressive, but it and the seizures stabilized after institution of a gluten-free diet and iron and folic acid supplements.
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PMID:Bilateral occipital calcification associated with celiac disease, folate deficiency, and epilepsy. 748 40

Neuroimaging and management advances require review of indications for excluding cerebral venous sinus (sinovenous) thrombosis (CSVT) in children. Our goals were to examine (i) clinical presentations of CSVT, (ii) prothrombotic risk factors and other predisposing events, (iii) clinical and radiological features of brain lesions in CSVT compared with arterial stroke, and (iv) predictors of outcome. We studied 42 children with CSVT from five European paediatric neurology stroke registries. Patients aged from 3 weeks to 13 (median 5.75) years (27 boys; 64%) presented with lethargy, anorexia, headache, vomiting, seizures, focal signs or coma and with CSVT on neuroimaging. Seventeen had prior chronic conditions; of the 25 previously well patients, 23 had recent infections, eight became dehydrated and six had both. Two children had a history compatible with prior CSVT. Anaemia and/or microcytosis (21 probable iron deficiency, five haemolytic, including two with sickle cell disease and one with beta-thalassaemia) was as common (62%) as prothrombotic disorder (13/21 screened). High factor VIII and homozygosity for the thermolabile methylene tetrahydrofolate reductase polymorphism were the commonest prothrombotic disorders. The superficial venous system was involved in 32 patients, the deep in six, and both in four. Data on the 13 children with bland infarction and the 12 with haemorrhage in the context of CSVT were compared with those from 88 children with ischaemic (AIS) and 24 with haemorrhagic (AHS) arterial stroke. In multiple logistic regression, iron deficiency, parietal infarction and lack of caudate involvement independently predicted CSVT rather than arterial disease. Five patients died, three acutely, one after recurrence and one after 6 months being quadriparetic and blind. Follow-up ranged from 0.5 to 10 (median 1) years. Twenty-six patients (62%) had sequelae: pseudotumour cerebri in 12 and cognitive and/or behavioural disabilities in 14, associated with epilepsy in three, hemiparesis in two and visual problems in two. Eighteen patients, including six with haemorrhage, were anticoagulated. Older age [odds ratio (OR) 1.54, 95% confidence limits (CI) 1.12, 2.13, P = 0.008], lack of parenchymal abnormality (OR 0.17, 95% CI 0.02, 1.56, P = 0.1), anticoagulation (OR 24.2, 95% CI 1.96, 299) and lateral and/or sigmoid sinus involvement (OR 16.2, 95% CI 1.62, 161, P = 0.02) were independent predictors of good cognitive outcome, although the last predicted pseudotumour cerebri. Death was associated with coma at presentation. Of 19 patients with follow-up magnetic resonance (MR) venography, three had persistent occlusion, associated with anaemia and longer prodrome. A low threshold for CT or MR venography in children with acute neurological symptoms is essential. Nutritional deficiencies may be modifiable risk factors. A paediatric anticoagulation trial may be required, after the natural history has been further established from registries of cases with and without treatment.
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PMID:Cerebral venous sinus thrombosis in children: risk factors, presentation, diagnosis and outcome. 1569 61

The symptoms of celiac disease are diverse, and the disease is often asymptomatic. Without active serologic screening, most cases probably remain undiagnosed. Recent serologic screening assays allow mass screening for the disease. However, there is no evidence as yet to suggest that symptom-free celiac disease patients run an increased risk of small intestinal lymphoma or other complications. The prevention of osteoporosis seems to be the strongest indicator for widespread screening today. Screening asymptomatic individuals for celiac disease may be even harmful. A lifelong gluten-free diet is not easy to maintain, and the subject's quality of life may deteriorate. It is also debatable whether patients found by active screening adhere to a gluten-free diet similarly to symptomatic ones. The cost-effectiveness of population screening is dubious. Serologic screening should be applied in individuals with even subtle symptoms indicative of celiac disease, such as subclinical-isolated iron deficiency. In various autoimmune conditions, the risk of celiac disease is approximately 5% and, in individuals with affected first-degree relatives, 15%. Infertility, neurologic symptoms such as polyneuropathy, ataxia, epilepsy with posterior cerebral calcification, and osteoporosis are conditions in which celiac disease should be kept in mind. Elevated aminotransferases and liver failure can lead to a diagnosis of celiac disease. Evidence today does not support mass screening of celiac disease. Instead, increased alertness should be observed in patients at risk of the condition.
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PMID:Should adults be screened for celiac disease? What are the benefits and harms of screening? 1582 17

Attention-deficit/hyperactivity disorder is a neurobiological syndrome with an estimated prevalence among children and adolescents of 5%. It is a highly heritable disorder, but acquired factors in etiology are sometimes uncovered that may be amenable to preventive measures or specific therapy. Early reports have described symptoms similar to attention-deficit/hyperactivity disorder that followed brain trauma or viral encephalitis, and recent MRI studies have demonstrated brain volumetric changes that may be involved in the pathophysiology of the syndrome. The American Psychiatric Association's Diagnostic Statistical Manual, introduced in 1968, emphasizes symptomatic criteria in diagnosis. Here, an overview of environmental factors in the etiology of attention-deficit/hyperactivity disorder is presented to encourage more emphasis and research on organic causal factors, preventive intervention, and specific therapies. An organic theory and the genetic and biochemical basis of attention-deficit/hyperactivity disorder are briefly reviewed, and an etiologic classification is suggested. Environmental factors are prenatal, perinatal, and postnatal in origin. Pregnancy- and birth-related risk factors include maternal smoking and alcohol ingestion, prematurity, hypoxic-ischemic encephalopathy, and thyroid deficiency. Childhood illnesses associated with attention-deficit/hyperactivity disorder include virus infections, meningitis, encephalitis, head injury, epilepsy, toxins, and drugs. More controversial factors discussed are diet-related sensitivities and iron deficiency. Early prenatal recognition, prevention, and treatment of environmental etiologies of attention-deficit/hyperactivity disorder may reduce physician reliance on symptomatic modification with medication, a frequent reason for parental concern.
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PMID:Etiologic classification of attention-deficit/hyperactivity disorder. 1824 8