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

Cerebral infarction in children is often caused by intracranial vascular disorder, cardiac disease, head injury, or infection, and is rarely induced by blood disease. In this paper, we describe an infantile case of cerebral infarction associated with thrombocytosis. A female infant of eight months of age developed left hemiparesis after a slight head injury. Her CT and MRI demonstrated a cerebral infarction located from the right internal capsule to the right corona radiata. Laboratory findings revealed iron-deficiency anemia and thrombocytosis with a platelet count 107.5 x 10(4)/mm3. Although she had no disorder that had caused iron deficiency, serum Fe value of the patient was low with a count of 18 micrograms/dl. Her bone marrow was normal except for a slight increase in the number of megakaryocytes. One month later, her anemia was improved by means of oral iron replacement. However, her platelet count remained at more than 100 x 10(4)/mm3 as it had been before. Her condition of left-sided hemiparesis gradually improved by a program of rehabilitation, and did not recur after aspirin administration. Although the main cause of her thrombocytosis that led to a transient cerebrovascular accident is obscure, it is postulated that her iron deficiency anemia induced secondary thrombocytosis, or else the patient had essential thrombocytosis.
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PMID:[An infantile case of cerebral infarction associated with thrombocytosis]. 159 Oct 25

Iron deficiency is an important nutritional problem in third world countries because it diminishes work performance. In meat-eating countries, iron excess may be more important than iron deficiency. Heme iron is more efficiently absorbed from the diet than inorganic iron, and iron excess can produce cellular oxidation in association with superoxide dismutase. Metal ion catalysis is linked to aging, coronary artery disease, stroke, carcinogenesis, neurodegenerative disorders, and inflammatory disorders. Prudence is advised in the excessive consumption of meat and iron supplementation of the diet until this process is more thoroughly investigated.
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PMID:Ironic catastrophes: one's food--another's poison. 819 51

Iron deficiency is a common pediatric problem affecting 20%-25% of the world's infants. Most commonly causing anemia, iron deficiency is also implicated in such neurologic sequelae as irritability, lethargy, headaches, developmental delay, and infrequently papilledema, pseudotumor cerebri, and cranial nerve abnormalities. Rarely has iron deficiency been recognized as a significant cause of stroke in the adult or pediatric populations. We report a series of 6 children, 6 to 18 months of age, who presented with an ischemic stroke or venous thrombosis after a viral prodrome. All patients had iron deficiency as a consistent finding among the group, and other known etiologies of childhood stroke were excluded. These patients provide evidence of a strong association between iron deficiency and ischemic events in children between 6 and 18 months of age.
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PMID:Iron deficiency: a cause of stroke in infants and children. 904 2

In Eisenmenger's syndrome a central left-to-right shunt in the heart, a congenital anomaly, leads to pulmonary hypertension which subsequently causes the shunt to be reversed. The hypoxaemia resulting from a right-to-left shunt is compensated by an increase of the haemoglobin concentration due to a rise of the haematocrit. In adult patients not operated (adequately), the symptoms are the consequence of the erythrocytaemia and an increased haemorrhagic diathesis. In the long run heart failure develops. Phlebotomy is indicated for patients with haematocrits higher than 0.65 with signs of hyperviscosity and is also advised before non-cardiac surgery to improve coagulation parameters. Phlebotomy should be performed slowly (500 ml in 30-45 min) with simultaneous volume replacement. Excessive phlebotomy causes iron deficiency and spherocytosis which increase viscosity as well as the risk of CVA. Treatment consists of iron supplementation. Anticoagulation is indicated only in case of atrial fibrillation or mechanical valves. The use of acetylsalicylacid or NSAIDs is relatively contraindicated, because of abnormal haemostasis in these patients. During treatment with ACE inhibitors and other vasodilators, hypovolaemia should be avoided, because at a lower systemic blood pressure the right-to-left shunt increases and a potentially fatal cyanosis may occur.
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PMID:[Eisenmenger syndrome in adults]. 1032 Dec 57

Myocardial infarction remains the No. 1 killer of American men and women, with a death rate of 225,000 per year, and stroke, the third leading cause of death in the United States, afflicts about 600,000 per year. The combined financial burden of these diseases is approximately $134 billion per year. Therefore, interventions that reduce mortality and suffering will have a significant impact on the health care system. This article summarizes research conducted during the last 2 decades that addresses the idea that stored iron plays a role in the pathogenesis of atherosclerosis and that iron reduction through phlebotomy may play a role in the treatment or prevention of atherosclerosis. Body iron stores rise after adolescence in men and menopause in women. This rise has been linked to the pathogenesis of atherosclerosis through iron-induced oxidation of low-density lipids and foam cell formation. However, the available evidence on the iron hypothesis remains circumstantial. Reduction of body iron stores in the setting of a controlled, prospective intervention trial is necessary to determine whether the amount of stored iron is related to clinically meaningful vascular disease. Such a study is feasible because reduction in iron stores can be achieved safely and predictably without induction of iron deficiency by graded phlebotomy. The Iron and Atherosclerosis Study (FeAST), a Veteran's Administration Cooperative Study, is under way to test this concept.
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PMID:Role of stored iron in atherosclerosis. 1199 91

Iron deficiency is a common disorder in pediatric patients. Although the most common manifestation is that of anemia, iron deficiency is frequently the source of a host of neurologic disorders presenting to general pediatric neurologic practices. These disorders include developmental delay, stroke, breath-holding episodes, pseudotumor cerebri, and cranial nerve palsies. Although frequent, the identification of iron deficiency as part of the differential diagnosis in these disorders is uncommon and frequently goes untreated. The purpose of the current review is to highlight what is understood regarding iron deficiency and it's underlying pathophysiology as it relates to the brain, and the association of iron deficiency with common neurologic pediatric disease.
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PMID:Neurologic manifestations of iron deficiency in childhood. 1221 7

The Philadelphia chromosome-negative chronic myeloproliferative disorders (CMPD), polycythemia vera (PV), essential thrombocythemia (ET) and chronic idiopathic myelofibrosis (IMF), have overlapping clinical features but exhibit different natural histories and different therapeutic requirements. Phenotypic mimicry amongst these disorders and between them and nonclonal hematopoietic disorders, lack of clonal diagnostic markers, lack of understanding of their molecular basis and paucity of controlled, prospective therapeutic trials have made the diagnosis and management of PV, ET and IMF difficult. In Section I, Dr. Jerry Spivak introduces current clinical controversies involving the CMPD, in particular the diagnostic challenges. Two new molecular assays may prove useful in the diagnosis and classification of CMPD. In 2000, the overexpression in PV granulocytes of the mRNA for the neutrophil antigen NBI/CD177, a member of the uPAR/Ly6/CD59 family of plasma membrane proteins, was documented. Overexpression of PRV-1 mRNA appeared to be specific for PV since it was not observed in secondary erythrocytosis. At this time, it appears that overexpression of granulocyte PRV-1 in the presence of an elevated red cell mass supports a diagnosis of PV; absence of PRV-1 expression, however, should not be grounds for excluding PV as a diagnostic possibility. Impaired expression of Mpl, the receptor for thrombopoietin, in platelets and megakaryocytes has been first described in PV, but it has also been observed in some patients with ET and IMF. The biologic basis appears to be either alternative splicing of Mpl mRNA or a single nucleotide polymorphism, both of which involve Mpl exon 2 and both of which lead to impaired posttranslational glycosylation and a dominant negative effect on normal Mpl expression. To date, no Mpl DNA structural abnormality or mutation has been identified in PV, ET or IMF. In Section II, Dr. Tiziano Barbui reviews the best clinical evidence for treatment strategy design in PV and ET. Current recommendations for cytoreductive therapy in PV are still largely similar to those at the end of the PVSG era. Phlebotomy to reduce the red cell mass and keep it at a safe level (hematocrit < 45%) remains the cornerstone of treatment. Venesection is an effective and safe therapy and previous concerns about potential side effects, including severe iron deficiency and an increased tendency to thrombosis or myelofibrosis, were erroneous. Many patients require no other therapy for many years. For others, however, poor compliance to phlebotomy or progressive myeloproliferation, as indicated by increasing splenomegaly or very high leukocyte or platelet counts, may call for the introduction of cytoreductive drugs. In ET, the therapeutic trade-off between reducing thrombotic events and increasing the risk of leukemia with the use of cytoreductive drugs should be approached by patient risk stratification. Thrombotic deaths seem very rare in low-risk ET subjects and there are no data indicating that fatalities can be prevented by starting cytoreductive drugs early. Therefore, withholding chemotherapy might be justifiable in young, asymptomatic ET patients with a platelet count below 1500000/mm(3) and with no additional risk factors for thrombosis. If cardiovascular risk factors together with ET are identified (smoking, obesity, hypertension, hyperlipidemia) it is wise to consider platelet-lowering agents on an individual basis. In Section III, Dr. Gianni Tognoni discusses the role of aspirin therapy in PV based on the recently completed European Collaboration on Low-dose Aspirin in Polycythemia Vera (ECLAP) Study, a multi-country, multicenter project aimed at describing the natural history of PV as well as the efficacy of low-dose aspirin. Aspirin treatment lowered the risk of cardiovascular death, non-fatal myocardial infarction, and non-fatal stroke (relative risk 0.41 [95% CI 0.15-1.15], P =.0912). Total and cardiovascular mortality were also reduced by 46% and 59%, respectively. Major bleedings were slightly increased nonsignificnsignificantly by aspirin (relative risk 1.62, 95% CI 0.27-9.71). In Section IV, Dr. Giovanni Barosi reviews our current understanding of the pathophysiology of IMF and, in particular, the contributions of anomalous megakaryocyte proliferation, neoangiogenesis and abnormal CD34(+) stem cell trafficking to disease pathogenesis. The role of newer therapies, such as low-conditioning stem cell transplantation and thalidomide, is discussed in the context of a general treatment strategy for IMF. The results of a Phase II trial of low-dose thalidomide as a single agent in 63 patients with myelofibrosis with meloid metaplasia (MMM) using a dose-escalation design and an overall low dose of the drug (The European Collaboration on MMM) will be presented. Considering only patients who completed 4 weeks of treatment, 31% had a response: this was mostly due to a beneficial effect of thalidomide on patients with transfusion dependent anemia, 39% of whom abolished transfusions, patients with moderate to severe thrombocytopenia, 28% of whom increased their platelet count by more than 50 x 10(9)/L, and patients with the largest splenomegalies, 42% of whom reduced spleen size of more than 2 cm.
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PMID:Chronic myeloproliferative disorders. 1463 83

Stroke affects up to 13 of 100,000 children, is more common in boys and African Americans, and is associated with considerable cognitive and psychiatric morbidity, as well as motor disability. Around half are hemorrhagic and half are ischemic. Underlying conditions include sickle cell disease, cardiac abnormalities, chromosomal abnormalities (eg, Down syndrome), and neurocutaneous conditions (eg, neurofibromatosis), but up to half the patients with ischemic stroke have no previously diagnosed condition. Although there is almost certainly an important genetic component to stroke risk, head trauma, infections, drugs and radiation appear to play an etiological role in some patients. The majority of the patients with infarction in an arterial distribution have associated cerebrovascular disease. Vascular pathologies include carotid or vertebrobasilar dissection, intracranial vasculopathy affecting the middle and anterior cerebral arteries, which is often transient, and moyamoya. Intermediate risk factors may include hypertension, hypoxia, and poor nutrition leading, for example, to iron deficiency and hyperhomocysteinemia. Some chronic conditions may directly influence the child's behavior and stroke recurrence risk, although large cohorts and randomized controlled trials will be needed before strategies for modification can be evidence-based.
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PMID:Risk factors for arterial ischemic stroke in childhood. 1516 88

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

A relationship is described between H. pylori infection and diseases localized beyond the gastrointestinal tract, for example: atherosclerosis, stenocardia, cerebral stroke, chronic urticaria, rosacea, hemicrania and in, children with height deficit or anaemia, caused by iron deficiency. Two cases of sideropenic anaemia in children resistant to oral iron are presented. Gastrointestinal tract symptoms were not observed and most probably the reason for anaemia was H. pylori infection. The first 14 years old patient with normal menstrual periods had been treated for four months by oral iron, without any effect (Hgb 10.2 g%, Fe 36.8%, ferritin < 10.8 mg%). On endoscopy of upper gastrointestinal tract there were macroscopic typical changes of H. pylori infection in antrum part of the stomach. On histological examination of biopsy segments inflammation of stomach mucosa in average intensification and H. pylori infection was confirmed. Recovery caused normalization of iron in the organism and of erythrocyte morphology. There was no recurrence of anaemia in long-term observation of the girl. A 14 years old boy treated without success for severe sideropenic anaemia (Hgb 7.1 g%), with positive family history (father has gastric ulcer). In spite of lack of gastrointestinal tract symptoms, on endoscopy there were features of chronic active hemorrhagic inflammation of stomach mucosa with H. pylori infection. Oral iron and effective eradication (proton pump inhibitor, amoxycillin, clarithromycin), achieved normalization of morphological changes. Recurrence of anaemia has not been observed.
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PMID:[Helicobacter pylori infection as a cause of sideropenic anaemia resistant to treatment - own observation]. 1682 22


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