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 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Blood lead levels and parallel ambient lead exposure levels were studied in selected Israeli population groups. The studies were prompted by newly emerging findings on subtle renal, hematologic and neurobehavioral effects of low levels of exposure to lead in both children and adults. There was a high correlation (r = 0.89) between individual blood lead levels in the groups studied and free erythroprotoporphyrin, a measure of the toxic effect of lead on hemoglobin synthesis. Hemoglobin depression was weakly associated (r = 0.66) with rises in blood lead levels. Blood lead and free erythroprotoporphyrin determinations can be jointly used in screening for lead toxicity and iron deficiency. Our data suggest that the Jerusalem population at large is experiencing lead exposure in the range of rural USA levels, but that in Israel there are several foci of medically significant exposure requiring a comprehensive approach to control of occupational and environmental hazards. Furthermore, children of workers from high-exposure locations may face an additional risk.
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PMID:Lead exposure: effects in Israel. 736 71

Male Fischer rats were maintained for a period of 17 weeks on an iron-deficient diet along with suitable controls. The effect of long term deprivation of iron on xenobiotic metabolism was studied by the activities of various drug metabolising enzymes in both liver as well as extra-hepatic tissues like lungs, kidneys and intestinal mucosa (I.M.). The results show that among the Phase I (activating) enzymes, the hepatic activities of benzo(a)pyrene hydroxylase (AHH) and microsomal epoxide hydrolase (mEH) are significantly reduced in iron deficiency. The other parameters of the activating system, namely cytochrome P450, aminopyrene demethylase (ADM) and aniline hydroxylase (AH), are not altered. Of the two Phase II (conjugating) enzymes studied, only uridine diphospho glucuronyl transferase (UDPGT) is found to be depressed, but not glutathione S-transferase (GST) in liver in iron deficiency. Activities of Phase I enzymes are markedly lowered in extra-hepatic tissues compared to liver; such depression is not observed in conjugating enzymes. Iron deficiency does not seem to make much impact on the enzyme activities of extra-hepatic tissues. Overall, the hepatic results suggest a defect in detoxification mechanisms in iron deficiency. Such impairment may very well predispose an iron-deficient host to an increased risk of carcinogenesis.
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PMID:Effect of long term iron deficiency on the activities of hepatic and extra-hepatic drug metabolising enzymes in Fischer rats. 785 40

Exposure of rats to high dietary levels of sodium saccharin (NaSac) started in utero produce physiological effects at 30 days post-birth that are similar to those found in pups of iron-deficient dams. These similarities suggest that some of the changes due to NaSac are secondary to iron deficiency. The present experiment investigated whether the effects of 7.5% dietary NaSac in the newborn rat could be prevented by dietary iron and/or folate supplementation. The NaSac-related effects prevented by iron supplementation included anaemia, decreased serum iron and folate, increased serum cholesterol and triglyceride and increased serum vitamin E. Folate supplementation prevented NaSac-induced depression of serum folate and increase in serum vitamin E. Although bladder hyperplasia was increased by dietary iron and/or folate supplementation, the majority of the urinary chemistry changes associated with NaSac treatment were not affected. The results show that some physiological changes associated with NaSac treatment in the newborn rat may occur as a consequence of iron deficiency rather than a direct effect of NaSac treatment. These changes may be independent of the urinary and bladder effects, which are not reversed by iron supplementation.
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PMID:Effects of dietary iron and folate supplementation on the physiological changes produced in weanling rats by sodium saccharin exposure. 822 26

Rats (Wistar, female, 4 weeks old) were fed iron-deficient (Fe-; 2.2 micrograms Fe/g) or manganese- and copper-deficient (Mn.Cu-; 0.3 microgram Mn/g, 0.4 microgram Cu/g) diets for 8 weeks to determine the oxidative damage of DNA by element deficiency. After feeding of the diets, 2-nitropropane (2-NP, 80 mg/kg body weight) was administered i.p. as an inducer of 8-hydroxy-2'-deoxyguanosine (8-OH-dG) to the element-deficient rats. The hemoglobin concentration of rats in the Fe- group showed an induction of severe anemia (8.4 g/100 ml whole blood). In the Mn.Cu- group, Mn-superoxide dismutase (SOD) activities of plasma and Cu.Zn-SOD activities were significantly lower than that of the normal diet group. However, total SOD activities of plasma were not depressed severely in contrast to that of the liver in the Mn.Cu- group. Background (spontaneous) levels of 8-OH-dG in normal diet group were 0.96 +/- 0.37/10(5) deoxyguanosine (dG), however, significantly higher levels were detected in the Fe- group (1.56 +/- 0.19, P < 0.01). Conversely, a lower (but not significant) level of 8-OH-dG than the normal diet group were detected in the Mn.Cu- group (0.78 +/- 0.08). Six hours after 2-NP treatment, 8-OH-dG levels in liver DNA were significantly induced to 1.44 +/- 0.24 in the normal diet fed group 1.89 +/- 0.22 in the Fe- and 1.08 +/- 0.12 in the Mn.Cu- groups. Compared to the normal diet group, these induced levels of 8-OH-dG in the Fe- group were significantly higher (P < 0.05), and that in Mn.Cu- group were significantly lower (P < 0.05). The high level of 8-OH-dG in severe iron deficiency might be the results of: (i) an increase of hydroxyl radical generation by accumulated copper in hepatocytes; or (ii), a depression of enzymatic activity for removing 8-hydroxy-2'-deoxyguanosine in DNA, which is dependent on divalent cations. On the other hand, the low level of 8-OH-dG in manganese and copper deficiency might be the result of a decrease of lipid peroxidation which has been suggested to be an intermediator from active oxygen species to hydroxyl radical.
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PMID:Spontaneous and 2-nitropropane induced levels of 8-hydroxy-2'-deoxyguanosine in liver DNA of rats fed iron-deficient or manganese- and copper-deficient diets. 838 15

Severe anemia in a weanling kitten resulted in volume overload hypertrophy of the heart and signs of congestive heart failure. A 6-week-old moribund kitten was admitted to the hospital with a PCV of 3%. The anemia was determined to have resulted from severe flea infestation and iron deficiency. Supportive therapy consisted of flea removal, blood transfusions, and oral nutritional support. On day 3 of hospitalization, the kitten had signs of depression and became tachypneic. Auscultation revealed a systolic murmur, gallop rhythm, and crackles over the ventral lung fields. Thoracic radiography revealed pulmonary edema and massive cardiomegaly. Echocardiographic evaluation revealed dilatation of all cardiac chambers. The addition of furosemide to the kitten's treatment protocol resulted in resolution of the pulmonary edema. On follow-up examination 1 month later, the kitten had mild residual cardiomegaly and the anemia had resolved. Anemia is a well-known sequela to severe flea infestation in young animals. A less commonly reported, but potentially life-threatening, sequela to anemia may include the development of volume overload hypertrophy of the heart and congestive heart failure.
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PMID:Severe cardiomegaly secondary to anemia in a kitten. 846 24

It is the aim of this article to provide an overview of difficulties in children with poor growth enrolled in an intensive community intervention trial for failure to thrive (FTT). Children were assessed for developmental delay (Bayley test), inadequate diet, iron deficiency, eating and other behavioural problems, and maternal anxiety and depression (HAD Scales). Sixty-three children aged 6 months to 2 1/2 years were studied. The majority of children were from families living in poverty with many from divorced, separated or single families. On developmental testing (Bayley Developmental Scales) 55% were delayed, 27% severely. Seventy-seven per cent had caloric intakes below the expected average requirement (EAR) with 19% reported at less than 50% of requirements. Iron intakes were similarly low and one-third had iron deficiency anaemia on testing. Sixty per cent of children were reported to have eating difficulties, principally in terms of responding negatively to food. Eating difficulties had commonly presented within the first weeks of life. Other behavioural and sleeping difficulties were also common. Children identified as failing to thrive in the community are likely to have associated developmental, dietary and behavioural problems which may not be immediately evident and to an extent which may require intensive multidisciplinary involvement.
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PMID:What do we know about children who fail to thrive? 881 27

The cause of taste abnormality was investigated in 25 patients with decreased taste sensation (hypogeusia group) and 14 patients with abnormal taste sensation (dysgeusia group) by examining taste threshold, salivary flow rate, Candida cell culture, and laboratory examination of peripheral blood. The cause of hypogeusia was identified as iron deficiency in 7 patients, oral candidiasis in 6, hyposalivation (xerostomia) in 6, and psychiatric distress in 3, and could not be determined in 3 (idiopathic). Dysgeusia was associated with psychiatric distress in 8 patients, oral candidiasis in 3, drug medication in 2, and hyposalivation in 1. In the hypogeusia group, the decreased taste sensation generally corresponded with elevated taste thresholds, which decreased along with improvement of the decreased taste sensation in all except the 3 patients with psychiatric etiology and 2 of the 3 patients with idiopathic etiology. In contrast, no elevation or depression of taste thresholds were observed in the dysgeusia group, and the abnormal taste sensation did not disappear in most cases; however, drug-induced dysgeusia improved completely within 2 months after cessation of the drug administration. The serum copper and zinc levels were not decreased in any patient, but a decreased serum iron level was observed in 7 patients. Based on these results, it is concluded that abnormal taste sensation may be induced by many oral and systemic disturbances and that hypogeusia, which may be induced by deficiency of iron but not of zinc or copper, is usually accompanied by elevation of taste thresholds, while dysgeusia is not.
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PMID:Clinical and physiological investigations in patients with taste abnormality. 885 Mar 56

Previous studies of dopamine metabolism in iron-deficient rats demonstrated an elevation in extraneuronal levels of dopamine and a depression in the number of dopamine D2 receptors; however, the importance of anemia per se and the reversibility of these observations are not completely resolved. The purpose of this study was to determine if in vivo reuptake of caudate dopamine is altered by iron deficiency anemia, if it is reversible with iron therapy, and if anemia per se produced the same effects on dopamine metabolism. Male Sprague-Dawley rats (21-d old) were fed an iron-deficient diet (4 mg Fe/kg diet) and then iron repleted (5 mg iron dextran), or were fed an iron adequate diet (35 mg Fe/kg diet) and then given phenylhydrazine to induce hemolytic anemia. In vivo microdialysis was performed in steady-state conditions both before and after iron or no therapy and was followed by an intraperitoneal injection of a dopamine reuptake blocker (cocaine-HCl 30 mg/kg). Thirty percent higher extracellular dopamine levels in the caudate-putamen were observed in iron-deficient rats compared with control rats, but no differences were observed in tissue levels. Hemolytic anemic and iron-repleted rats had normal extracellular dopamine levels. The response to dopamine reuptake blockade was significantly attenuated in iron-deficient rats compared with control, iron-repleted, or hemolytic anemic rats. These experiments provide evidence that iron deficiency blunts the dopamine reuptake mechanism, that this is a reversible process in postweaning rats, and that anemia per se does not cause the increased extracellular dopamine levels.
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PMID:In vivo dopamine metabolism is altered in iron-deficient anemic rats. 940 75

Serum visceral protein and hematological indices and their behavioral and clinical correlates were determined in women with bulimia nervosa and depressed controls. One hundred and fifty-two women who met DSM-IV criteria for bulimia nervosa and 68 women with DSM-IV major depression completed a structured clinical interview and had blood samples drawn prior to admission to outpatient treatment programs. Albumin and prealbumin concentrations were lower in the depressed women, possibly due to recent weight loss. Elevated transferrin values suggested mild iron deficiency in nearly one-fifth of women with bulimia nervosa. Of women with bulimia nervosa, the 10.7% who had hemoglobin and 5.1% who had vitamin B12 levels below the normal range were not distinguishable on measures of body mass index, binge eating, vomiting, or restriction frequency. The 4.3% with low prealbumin levels experienced significantly more episodes of binge eating and vomiting in the prior fortnight than those with normal values. Frequency of vomiting was also inversely associated with albumin concentration. Hamilton Depression Rating Scale scores were inversely and linearly related to serum vitamin B12. Lower B12 levels in those with alcohol abuse/dependence did not explain the association between B12 and HDRS scores. No hematological indices were related to body mass index, binge eating or restriction frequency, or restriction intensity. In summary, women with bulimia nervosa do not appear to be at greater risk of visceral protein or hematological abnormalities than psychiatric controls. It is suggested that a high frequency of vomiting and alcohol abuse/dependence, increases the risk of subclinical malnutrition in women with bulimia nervosa, and that poor vitamin B12 nutriture may interfere with the functioning of the serotonergic or catecholaminergic systems and contribute to depressive symptoms in bulimia nervosa.
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PMID:Visceral protein and hematological status of women with bulimia nervosa and depressed controls. 1022 89

Restless legs syndrome (RLS) is common in the elderly, with an estimated prevalence of 10 to 35% in individuals over 65 years of age. RLS is characterised by paraesthesias and dysaesthesias of the legs, typically occurring in the evening. The symptoms occur at rest and result in motor restlessness; movement often temporarily relieves the symptoms. Patients with poorly controlled RLS may develop related problems including insomnia (due to sleep-onset restlessness or periodic limb movements or related sleep fragmentation) and depression. RLS can be a primary disorder that develops in the young and includes familial cases. Secondary RLS occurs in association with iron-deficiency anaemia, uraemia and polyneuropathies. Typically, RLS is misdiagnosed or undiagnosed for years. In the elderly, both primary and secondary types of the disorder are common. It is thought that RLS represents lower CNS levels of, or reduced responsiveness to, dopamine. The symptoms improve with dopaminergic therapy. Ergotamine dopamine-receptor agonists such as pergolide, and the non-ergotamine dopamine-receptor agonists pramipexole and ropinirole, are becoming more commonly used to treat RLS. The dopamine precursor levodopa, in combination with carbidopa, is another effective therapeutic agent. An advantage of levodopa is lower cost than non-ergotamine and ergotamine dopamine-receptor agonists. However, the adverse effect of symptom augmentation appears to develop more frequently with levodopa than dopamine-receptor agonists; therefore, levodopa may currently be used somewhat less often as first-line therapy. Patients with painful symptoms may respond favourably to the anticonvulsants gabapentin and carbamazepine. Opioids and hypnosedatives are helpful in selected patients; however, these agents may have troubling adverse effects in the elderly. Correction of iron deficiency improves symptoms in patients with low ferritin levels. Lifestyle modification may also be helpful. Therapy is directed at symptoms, and most symptomatic patients benefit from treatment. It is important to consider RLS in the differential diagnosis of any patient with paraesthesias of the limbs.
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PMID:Restless legs syndrome in the older adult: diagnosis and management. 1239 51


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