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)

Platelet monoamine oxidase (MAO) activity was found to be significantly reduced in human alcoholics as compared to matched controls. A probable transitory increase in activity was observed during the abstinence phase. The low platelet MAO activity was not due to iron deficiency or to the presence of acetaldehyde. Since we have previously found a lowered MAO activity in the brains of suicide victims, especially in those with a previous history of alcohol abuse, we suggest that low platelet MAO activity reflects a primarily "weak" monoaminergic system in the CNS which causes an increased vulnerability to alcohol abuse and suicidal behaviour.
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PMID:Low platelet monoamine oxidase activity in human alcoholics. 89 16

45 consecutive patients with chronic alcohol abuse up to the day before admission were examined to determine to what extent the bone marrow smear can be used to detect alcohol abuse and to monitor abstinence. Bone marrow aspiration was performed within the first three days of admission and repeated an average of two weeks later in 35 patients. Using Prussian Blue staining, disturbances of iron utilization presented the most striking hematologic finding and were detected in 91% (41/45) of subjects. By contrast, both abnormal vacuolization of red and/or white cell precursors (in 38%) and megaloblastic marrow (in 27%) of patients respectively occurred significantly less often (p less than 0.005). However, if iron stores were fully depleted no sideroblasts were detectable. Obviously, iron deficiency limited the development both of normal and pathological sideroblasts. Sideroachrestic disturbances were divided into four degrees of severity according to frequency and types of sideroblasts. 3 pathological types of sideroblasts were differentiated: two forms of abnormal intermediate sideroblasts and ring sideroblasts, representing an increasing degree of sideroachrestic disturbance. The intermediate types were much more common than the ringed forms and therefore claim full attention. Abstinence from alcohol caused a highly significant decrease in sideroachrestic signs, as shown by the sideroblast score (p less than 0.005), which largely returned to normal in the period of examination. On the other hand, no significant decrease in the control value of the sideroblast score was observed in the patients which did not abstain from alcohol.
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PMID:[Cytomorphologic diagnosis of iron utilization disturbance in chronic alcohol abuse]. 376 16

Alcohol abuse is known to increase erythrocyte mean cell volume mainly as a consequence of direct toxic effect on the developing red cell. The influence of alcohol on other red cell parameters is unclear. The objective of this cross-sectional survey was to examine the consequences of different alcohol amounts on red cell parameters among women. We compared red cell parameters between female alcoholics, heavy drinkers, and controls. Controls (n = 138) and heavy drinkers (n = 65) consisted of consecutive 40- and 45-year-old women participating in the health screening, and alcoholics (n = 73) of consecutive women coming to a detoxification clinic. Alcoholics had significantly smaller erythrocyte counts (p < 0.01), and higher erythrocyte mean cell volume values (p < 0.001), reticulocyte counts (p < 0.01), and red cell distribution width values (p < 0.001) than controls. No difference between these groups was found, however, in hemoglobin distribution width value. The only red cell difference between controls and heavy drinkers was erythrocyte mean cell volume, which was significantly higher among heavy drinkers (p < 0.001). In alcoholics, red cell distribution width values were even more often increased (in 44%) than erythrocyte mean cell volume values (in 34%). This increase in red cell distribution width was not solely explained by iron deficiency or liver disease. Chronic alcohol abuse not only affects erythrocyte mean cell volume values, but also leads to anisocytosis seen in blood count as an increased red cell distribution width value.
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PMID:Women, alcohol, and red cells. 784 1

Although serum iron determinations play an important role in the diagnostic process, the accuracy of routine methods is suspect. The poor performance of currently used methods is well documented in the quarterly College of American Pathologists survey reports. Compared with the 1990 method of the International Committee for Standardization in Haematology (ICSH), the 1978 ICSH Reference Method shows a +3.4% bias and the standard method of the National Committee for Clinical Laboratory Standards shows a -17.8% bias for iron results. All routine methods checked--DuPont aca, Abbott TDx, Kodak Ektachem (except one lot), BM/Hitachi 717, and Synermed--show a negative bias over the entire analytical range, a significant negative intercept, and extremely poor correlation with the 1990 ICSH method for iron values < 750 micrograms/L. Individual discrepancies of several hundred percent were observed. Imprecision of the methods is not the reason for these discrepancies. We question whether most routine methods measuring low iron concentrations provide results sufficiently reliable for confirmation of iron deficiency.
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PMID:When is a serum iron really a serum iron? The status of serum iron measurements. 814

Despite a number of investigations suggesting the value of carbohydrate-deficient transferrin (CDT) as a marker of alcohol abuse, a variety of issues on the applicability of CDT measurements in clinical settings have remained unexplored. Earlier studies in this field have focused on the relationship of CDT and the amount of alcohol consumption or presence of liver disease, whereas the influence of alterations in serum transferrin concentrations on CDT has received less attention. In this study, we compared two different methods for measuring CDT (CDTect and %CDT) and total transferrin concentrations in a sample of 83 alcohol abusers (20 patients with alcoholic liver disease and 63 heavy drinkers who were devoid of liver disease, despite excessive alcohol consumption) and 89 controls, who were social drinkers or abstainers. The control population included 53 hospitalized patients with expected abnormalities in serum transferrin concentrations caused by conditions such as negative iron balance, pregnancy, or nonalcoholic liver disease. Both methods gave significantly higher values in alcohol abusers than in controls (p < 0.01), but the overall sensitivity for detecting alcohol abuse was clearly higher for CDTect (59%) than for %CDT (34%). The correlation between the results obtained by the two methods (r = 0.629) significantly improved, when the CDTect values were replaced by the ratio of CDTect/total transferrin (r = 0.770) (p < 0.05). There was a positive correlation between the CDTect and serum transferrin (r = 0.201, p < 0.01), which was significant both in the alcoholics (r = 0.240, p < 0.05), and especially in the controls (r = 0.727, p < 0.001). A significant inverse correlation emerged between %CDT and total transferrin (r = -0.302, p < 0.01). The sensitivities of CDTect and %CDT for correctly classifying alcohol abusers in the subgroup of alcoholic liver disease patients were 90% and 70% and in the subgroup of heavy drinkers without liver disease (49% and 22%), respectively. Specificities for CDTect and %CDT in this sample were 81% and 100%, respectively. However, in the subgroup of hospitalized control patients with abnormal serum transferrin, the specificity of CDTect was only 48%. According to present data, CDTect seems to be more sensitive than %CDT for detecting alcohol abuse. However, any alteration in serum total transferrin concentration markedly decreases the assay specificity. This should be considered when interpreting the assay results in patients with elevated serum transferrin, such as iron deficiency, pregnancy, or liver diseases.
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PMID:Sensitivity and specificity of carbohydrate-deficient transferrin as a marker of alcohol abuse are significantly influenced by alterations in serum transferrin: comparison of two methods. 872 36

Carbohydrate-deficient transferrin (CDT), a microheterogeneous form of serum transferrin (Tf), has been proposed as the most reliable marker of chronic alcohol consumption, although unexplained false-positive and -negative results have been reported. We investigated whether body iron influenced CDT serum levels by studying alcohol abusers with or without iron overload and nonabusers with iron deficiency or iron overload caused by genetic hemochromatosis (GH). In alcohol abusers, CDT was significantly lower in the presence of iron overload than in the absence (24.6 +/- 16.5 U/L vs. 33.3 +/- 11.7 U/L; P <.01), with false-negative results almost exclusively in patients with iron overload. Similarly, in nonabusers with GH, CDT was lower than in normal controls (9.6 +/- 2. 2 U/L vs. 15.7 +/- 3.3 U/L; P <.0001), whereas, patients with iron deficiency anemia had significantly higher levels than controls (28. 1 +/- 5.8 U/L vs. 15.7 +/- 3.3 U/L; P <.0001). In nonabusers, iron supplementation therapy significantly decreased CDT levels in patients with iron deficiency anemia (33.7 +/- 6.6 U/L vs. 21.7 +/- 5.2 U/L; P =.0007), while iron-depletion treatment significantly increased CDT levels in patients with GH (9.7 +/- 2.0 U/L vs. 14.7 +/- 4.0 U/L; P =.001). Alcohol abusers had a significant relationship between liver iron concentration (LIC) and the reciprocal of CDT (r =.65; P <.0001), while in nonabusers, there was a significant correlation between Tf and CDT (r =.72; P <.0001). In conclusion, CDT serum levels are markedly affected by the patient's iron status, with iron overload reducing its sensitivity in alcohol abusers and iron deficiency its specificity in nonabusers. CDT can be considered a reliable marker of alcohol abuse only when iron stores are normal.
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PMID:Carbohydrate-deficient transferrin, a sensitive marker of chronic alcohol abuse, is highly influenced by body iron. 1005 65

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

Fetal alcohol spectrum disorders (FASD) are the leading non-genetic cause of neurodevelopmental disability in children. Although alcohol is clearly teratogenic, environmental factors such as gravidity and socioeconomic status significantly modify individual FASD risk despite equivalent alcohol intake. An explanation for this variability could inform FASD prevention. Here we show that the most common nutritional deficiency of pregnancy, iron deficiency without anemia (ID), is a potent and synergistic modifier of FASD risk. Using an established rat model of third trimester-equivalent binge drinking, we show that ID significantly interacts with alcohol to impair postnatal somatic growth, associative learning, and white matter formation, as compared with either insult separately. For the associative learning and myelination deficits, the ID-alcohol interaction was synergistic and the deficits persisted even after the offsprings' iron status had normalized. Importantly, the observed deficits in the ID-alcohol animals comprise key diagnostic criteria of FASD. Other neurobehaviors were normal, showing the ID-alcohol interaction was selective and did not reflect a generalized malnutrition. Importantly ID worsened FASD outcome even though the mothers lacked overt anemia; thus diagnostics that emphasize hematological markers will not identify pregnancies at-risk. This is the first direct demonstration that, as suggested by clinical studies, maternal iron status has a unique influence upon FASD outcome. While alcohol is unquestionably teratogenic, this ID-alcohol interaction likely represents a significant portion of FASD diagnoses because ID is more common in alcohol-abusing pregnancies than generally appreciated. Iron status may also underlie the associations between FASD and parity or socioeconomic status. We propose that increased attention to normalizing maternal iron status will substantially improve FASD outcome, even if maternal alcohol abuse continues. These findings offer novel insights into how alcohol damages the developing brain.
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PMID:Adequacy of maternal iron status protects against behavioral, neuroanatomical, and growth deficits in fetal alcohol spectrum disorders. 2309 56