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 and plasma amine oxidase activity was determined in a group of 99 healthy male (active duty military) alcoholics referred for hospital treatment who had been abstinent from alcohol for 2-10 days, and compared with that of a control military group. Platelet MAO activity was slightly but significantly lower in the alcoholic group. Both groups were significantly lower in MAO activity compared to a group of 42 non-military controls. In the alcoholic group there was no correlation between platelet MAO and severity or chronicity of drinking, nor was there evidence of iron deficiency to account for the lowered MAO activity. When the alcoholic and military control groups were split at the median, the first degree relatives of both the 'low' MAO alcoholics and the 'low' MAO military controls had a higher incidence of alcoholism than did the relatives of both 'high' MAO subgroups. No personal or family history data of alcohol-related problems were available on the non-military control group.
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PMID:Platelet and plasma amine oxidase activity in alcoholic individuals. 65 22

We examined the relationship of serum ferritin to bone marrow iron stores in 73 anemic male medical inpatients with liver disease, alcoholism, chronic inflammatory disease, and malignancies. A correlation of r = 0.75 (P less than .00005) was found between serum ferritin and bone marrow iron stores (BMIS) for the entire group. Liver disease as manifested clinically or by increased levels of serum glutamic-oxaloacetic transaminase did not appear to significantly affect this relationship. Patients with folic acid deficiency did tend to have a disproportionate increase in ferritin in relation to BMIS, but this did not seem to destroy the usefulness of ferritin levels. A useful clinical rule seems to be that serum ferritin of greater than 100 ng/ml tends to exclude iron deficiency, and a level of less than 30 ng/ml tends to confirm decreased iron stores.
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PMID:Ferritin as an index of bone marrow iron stores. 72 24

A dual isotope vitamin B12 absorption test in which vitamin B12 is given both in aqueous solution and bound to protein (chicken serum), was evaluated in 26 controls and 68 patients with subnormal serum vitamin B12 concentrations (19 with pernicious anaemia, 13 with iron deficiency, seven after partial gastrectomy, seven with malabsorptive states, five with folate deficiency, four with chronic alcoholism and 13 in whom no cause was apparent). In control patients protein bound absorption decreased with age; isotope excretion was 1.0% or over in those aged under 60 and 0.5% or over in those aged 60 and above. Malabsorption of protein bound vitamin B12 with normal aqueous absorption occurred in five patients with iron deficiency, three with alcoholism, two after partial gastrectomy, two with folate deficiency and in one with a malabsorptive state. In alcoholics abstinence produced an improvement in protein bound absorption. All patients in the group for whom no cause could be found for the subnormal serum vitamin B12 concentration had normal aqueous absorption but four had malabsorption of protein bound vitamin. Although the dual isotope test gave reproducible results and was consistent with the standard Schilling test some anomalies were detected; nine patients had reduced aqueous absorption with normal protein bound absorption. Despite this the dual test may prove useful in determining the importance of a subnormal vitamin B12 concentration where the cause is not clinically apparent. Further development is needed before it can be considered for routine use.
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PMID:Experiences with dual protein bound aqueous vitamin B12 absorption test in subjects with low serum vitamin B12 concentrations. 361 94

Twenty-seven alcoholic patients were studied for folate status. Twenty-two (81%) had neutrophil hypersegmentation and were detected as folate deficient by also having low serum folate, erythrocyte folate, lymphocyte folate and/or an abnormal peripheral blood lymphocyte deoxyuridine suppression test. Seventeen (63%) had an abnormal lymphocyte deoxyuridine suppression test and all 17 were corrected by the addition of methyltetrahydrofolate or pteroylglutamate. Comparison of these 63% abnormal (corrected by folate) results using the peripheral blood lymphocyte deoxyuridine suppression test with the lower percent abnormal (corrected by folate) bone marrow deoxyuridine suppression tests found in folate-deficient alcoholics by others suggests that the peripheral blood deoxyuridine suppression test may be more useful than the bone marrow deoxyuridine suppression test for laboratory diagnosis of folate deficiency responsive to folate therapy in alcoholism. Hidden iron deficiency is common in alcoholism, and in the concomitant presence of deficiencies of hemoglobin synthesis and of folate, the serum and erythrocyte folate and deoxyuridine suppression test in bone marrow are frequently normal, despite the suppression test being abnormal in lymphocytes and corrected by folate.
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PMID:Detection of folate deficiency in alcoholism using the peripheral blood lymphocyte deoxyuridine suppression test. 376 Oct 48

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 addiction can cause an infinite variety of pathologies but anaemia is one of the commonest clinical phenomena. Megaloblastic, sideroblastic and iron deficiency anaemias are certainly the commonest and best known causes of erythrocyte deficiency. However other rarer conditions also help to reduce the blood mass and should be borne in mind since their diagnosis and treatment can cause problems.
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PMID:[Causes of anemia in alcoholism]. 406 19

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

Effective management of early anaemia in the course of chronic renal insufficiency requires the following: (i) implementing an efficient diagnostic strategy to exclude common contributing factors; (ii) initiating epoetin therapy for the majority of patients; for and (iii) ensuring adequate iron supply erythropoiesis. Diagnostic inquiry is warranted whenever the haemoglobin concentration is below the normal range adjusted for age and gender. The most efficient diagnostic approach is to assume erythropoietin deficiency, exclude iron deficiency, and pursue further diagnostic tests only when red-cell indices are abnormal or when leukopenia or thrombocytopenia are also present. Macrocytosis should prompt an inquiry into alcoholism, B12 deficiency, or folate deficiency. Microcytosis suggests iron deficiency or thalassaemia. Associated cytopenias raise the possibility of alcohol toxicity, pernicious anaemia, malignancy, or myelodysplastic syndrome. Epoetin therapy is warranted whenever the haemoglobin concentration has fallen below 10.0 g/dl. To initiate therapy prior to dialysis, epoetin should be administered at an average dose of 100 IU/kg/week (80-120 IU/kg/week, 50-150 IU/kg/ week) by subcutaneous injection. Haemoglobin concentration should be monitored every 2 weeks and the epoetin dose adjusted by increments or decrements of 25% to maintain a rate of rise of haemoglobin concentration of 0.2-0.6 g/dl (0.3 0.6 g/dl/week, 0.2-0.5 g/dl/week). When the target range is achieved, the dose of epoetin should be continually adjusted to maintain a stable haemoglobin concentration. Transferrin saturation and ferritin concentration should be monitored monthly, and sufficient iron provided to maintain transferrin saturation above 20%. The lower the haemoglobin concentration, the greater the likelihood that future intravenous iron will be required. Oral iron supplements should be avoided, since they are costly, ineffective, and troublesome to patients. Finally, a blunted therapeutic response to epoetin therapy provides important diagnostic information and gnostic inquiry.
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PMID:Management of early renal anaemia: diagnostic work-up, iron therapy, epoetin therapy. 1103 56

Psychiatric manifestations are frequently associated with pernicious anemia including depression, mania, psychosis, dementia. We report a case of a patient with vitamin B12 deficiency, who has presented severe depression with delusion and Capgras' syndrome, delusion with lability of mood and hypomania successively, during a period of two Months. Case report - Mme V., a 64-Year-old woman, was admitted to the hospital because of confusion. She had no history of psychiatric problems. She had history of diabetes, hypertension and femoral prosthesis. The red blood count revealed a normocytosis with anemia (hemoglobin=11,4 g/dl). At admission she was uncooperative, disoriented in time and presented memory and attention impairment and sleep disorders. She seemed sad and older than her real age. Facial expression and spontaneous movements were reduced, her speech and movements were very slow. She had depressed mood, guilt complex, incurability and devaluation impressions. She had a Capgras' syndrome and delusion of persecution. Her neurologic examination, cerebral scanner and EEG were postponed because of uncooperation. Further investigations confirmed anemia (hemoglobin=11,4 g/dl) and revealed vitamin B12 deficiency (52 pmol/l) and normal folate level. Antibodies to parietal cells were positive in the serum and antibodies to intrinsic factor were negative. An iron deficiency was associated (serum iron=7 micromol/l; serum ferritin concentration=24 mg/l; serum transferrin concentration=3,16 g/l). This association explained normocytocis anemia. Thyroid function, hepatic and renal tests, glycemia, TP, TCA, VS, VDRL-TPHA were normal. Vitamin B12 replacement therapy was started with hydroxycobalamin 1 000 ng/day im for 10 days and iron replacement therapy. Her mental state improved dramatically within a few days. After one week of treatment the only remaining symptoms were lability of mood, delusion of persecution, Capgras' syndrome but disappeared totally 9 days after the beginning of the treatment. A neurologic examination was possible because of cooperation. All the tendon reflexes of inferior members were absent. The plantars were in flexion and there was a left inferior member hypoesthesia. The cerebral scan and EEG were normal. Fundic biopsy, realized by fibroscopy, revealed fundic atrophia and intestinal metaplasia compatible with Biermers' disease. The iron deficiency exploration concluded diet deficiency. Mme V. appeared euphoric, her speech was very rapid with play on words and overactivity. This hypomania state totally disappeared 3 days after. Six Months after her hospitalisation, she presented an hypothyroidism (TSH=3,780; T3=1,35; T4=1,08). A thyroid hormones replacement was started and she continued to receive Monthly B12 replacement. Discussion - This case report illustrates psychiatric manifestations of Biermers' disease. The clinical arguments in favour are: white woman, more than 60 Years old, no history of psychiatric problems, atypical symptoms (confusional state with psychiatric symptoms), fluctuation of symptoms (severe depression with confusional state, delusion of persecution and Capgras' syndrome; delusion with lability of mood and hypomania), dramatic improvement after 9 days of vitamin B12 replacement therapy. The biological arguments are: anemia, vitamin B12 deficiency, normal folate level, atrophia and fundic metaplasia, positive antibodies to parietal cells in the serum, association between Biermers' disease and autoimmune disease (Haschimoto thyroidite). Psychiatric manifestations can occur in the presence of low serum B12 levels but in the absence of the other well recognized neurological and haematological abnormalities of pernicious anemia. Mental or psychological changes may precede haematological signs by Months or Years. They can be the initial symptoms or the only ones. Verbank et al. described the case of a patient with vitamin B12 deficiency in whom hypomania, paranoia and depression had been successively presented during a period of 5 Years before anemia have been developed. The case of Mme V. is similar in the succession of severe depression with delusion of persecution and Capgras' syndrome, delusion with lability of mood and hypomania, during a period of two Months. This report seems to be the first one of a sequence of several psychiatric states with pernicious anemia during a period of two Months with normocytosis anemia. To illustrate this illness we reviewed the literature regarding psychopathology associated with B12 deficiency. The most common psychiatric symptoms were depression, mania, psychotic symptoms, cognitive impairment and obsessive compulsive disorder. The neuropsychiatric severity by vitamin B12 deficiency and the therapeutic efficacy depends on the duration of signs and symptoms. Conclusion - We recommend consideration of B12 deficiency and serum B12 determinations in all the patients with organic mental disorders, atypical psychiatric symptoms and fluctuation of symptomatology. B12 levels should be evaluated with treatment resistant depressive disorders, dementia, psychosis or risk factors for malnutrition such as alcoholism or advancing age associated with neurological symptoms, anemia, malabsorption, gastrointestinal surgery, parasite infestation or strict vegetarian diet. In first intention, B12 deficiency should be researched by serum B12 determination (normal 200-950 pg/ml). Studies of methylmalonic acid and homocysteine showed that they are very sensitive functional indicators of cobalamin status especially when other evidence of cobalamin (B12) deficiency was equivocal. Measurement of methylmalonic acid (normal 73-271 nmol/l) and homocysteine (normal 5,4-13,9 micromol/l) should not replace the measurement of serum cobalamin.
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PMID:[Psychiatric manifestations of vitamin B12 deficiency: a case report]. 1502 91

Delusional parasitosis (DP) is a psychotic condition in which a person has the unshakeable and mistaken belief (delusion) and/or aberrant perception (hallucination) of being infested with parasites. The disorder will be usually classified in a primary DP-group without a detectable cause (so-called pure forms), while secondary DP-groups are associated with general organic conditions, psychiatric illnesses and drugs (substance induced). Etiology and pathophysiology of DP remain however unknown. In the present paper we hypothesize for the first time a decreased striatal dopamine transporter (DAT)-functioning (corresponding with an increased extracellular dopamine-level) as etiologic condition for DP (primary and secondary groups). The DAT as key regulator of the dopamine-reuptake in the human brain is well known (regulation of the extracellular dopamine concentration). It is a presynaptic plasma membrane protein highly dense represented in the striatum. The hypothesis of a decreased DAT-functioning as etiologic condition by DP is revealed in case reports which show that DAT-inhibitors, such as cocaine, pemoline, methylphenidate and other amphetamine-derivatives can induce the clinical expression of DP. Several other associated causes of secondary DP-groups (medications, parkinson, chorea huntington, multiple system atrophy, diabetes, cerebrovascular diseases, alcoholism, traumatic brain injury, hyperuricemia, human immunodeficiency virus, iron deficiency, schizophrenia, depression) suggest that the clinical expression of DP may be related to a decreased striatal DAT-functioning (blocking, reduced ligand binding, reduced density, reduced activity). Our examined DP-cases (2-females) show means of magnetic resonance imaging a structurally damaged striatum. Furthermore, we presume that by the primary DP-group, the physiologically age-related decline of the DAT-density is pathologically elevated. Based on this hypothesis we show in the present paper the relation between DP and decreased striatal DAT-functioning, trying to give a new insight into the pathophysiologically mechanism involved. The hypothesis provides supporting evidence that increased levels of extracellular dopamine in the striatum of DP-patients is likely to be the result of decreased DAT-functioning and not increased rates of release. The hypothesis can be investigated simply by dopamine transporter imaging in patients with DP.
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PMID:Delusional parasitosis and the dopamine transporter. A new insight of etiology? 1713 47


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