Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:1.16.3.1 (ceruloplasmin)
 5,074 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A summary of the effects of contraceptive pills on vitamins in the b lood is presented. The significant increase of Vitamin-A in the plasma of contraceptive users is believed to be a result of the increase of bet alipoprotein, which binds chiefly to Vitamin-A. Although high concentrations of Vitamin-A have caused teratogenicity in test animals, the increase found in humans using contraceptive pills is not high enough to cause risk. A lowering of Vitamin-B6 (pyridoxin) levels has occurred with the use of contraceptive pills. This can cause alteration in the metabolism of tryptophan, which could cause depression in pill users. The lack of pyridoxine can also increase the production of xanthuric acid which binds with insulin, resulting in a decreased glucose tolerance. A decrease in folic acid in pill users has also been observed, caused by some effect of the pill on the folate deconjugate. The Vitamin-B12 level is also lowered for unascertainable reasons related to the decrease in folic acid. No anemia occurs in spite of the lowered Vitamin-B complex levels in the blood. A lack in Vitamin-C in users of pills containing estrogens is possibly effected by a corresponding increase between estrogens and ceruloplasmin, a protein active in the oxidation of ascorbic acid. This lack of Vitamin-C has had no clinical significance thus far.
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PMID:[P-pills and vitamins]. 114 66

Dementia--a syndrome of acquired intellectual deterioration--is an etiologically non-specific condition which is permanent, progressive, or reversible. In the evaluation of demented patients, a careful exposure history will determine the possible role of drugs, metals, or toxins. The physical examination may reveal focal deficits in cases of intracranial mass lesions and spasticity or ataxia of the lower limbs if hydrocephalus is present. Coexistance of dementia and peripheral neuropathy usually indicates a toxic or metabolic disorder. Asterixis, myoclonus, and postural tremor are common in toxic-metabolic dementias, while resting tremor, choreoathetosis, and rigidity occur in progressive extrapyramidal disorders. EEG is focally abnormal in cases of cerebral mass lesions and exhibits generalized slowing in toxic-metabolic encephalopathies. CT will aid in the identification of hydrocephalus, subdural hematomas, and intracranial mass lesions. A thorough laboratory evaluation including complete blood count, erythrocyte sedimentation rate, electrolytes, blood urea nitrogen and blood sugar, liver and thyroid tests, calcium and phosphorus levels, B12 and folate levels, serum copper and ceruloplasmin, VDRL, chest X-ray, electrocardiogram, and lumbar puncture may demonstrate treatable disorders that are adversely affecting intellectual function. Elderly individuals are particularly susceptible to the effects of toxic or metabolic disorders, and a mild dementia might be exaggerated by relatively minor fluctuations in metabolic status. Treatable causes of dementia should be considered in all demented patients.
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PMID:[Treatable dementia syndromes]. 358 48

Six of eight patients with Addisonian pernicious anemia were found to have diminished corticosteroid-binding globulin (CBG) concentrations, which returned within 2 weeks to normal after the im administration of cobalamin. T4-binding globulin was found to be completely normal before and after cobalamin replacement. Other estrogen-responsive proteins, i.e. ceruloplasmin, alpha 1-trypsin inhibitor, haptoglobin, transferrin, and alpha 2-macroglobulin, also did not follow CBG concentration in a parallel fashion. The immunoglobulins similarly did not follow a course parallel to that of CBG. The CBG concentration in two untreated patients had a normal increase in response to estrogen administration, similar to that described in CBG deficiency from other causes. No clue was found regarding the mechanism by which B12 influences the putative hepatic control of CBG concentration. It is speculated that at least two control points may be necessary for a normal CBG concentration. Patients with a genetic deficiency of CBG may also have to have cobalamin deficiency in order for them to reach a concentration approaching zero.
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PMID:Vitamin B-12 (cobalamin) deficiency: a heretofore undescribed control mechanism for plasma corticosteroid-binding globulin concentration in man. 617 43

Dementia, a syndrome of acquired intellectual deterioration, is an etiologically nonspecific condition that can be permanent or reversible. When evaluating demented patients, a careful exposure history will determine the possible role of drugs, metals, or toxins. Physical examination may reveal focal deficits in cases of intracranial mass lesions and spasticity or ataxia of the lower limbs if hydrocephalus is present. Coexistence of dementia and a peripheral neuropathy usually indicates the existence of a toxic or metabolic disorder. Depressed mood, sleep disturbance, anorexia, impotence, constipation, and psychomotor retardation indicate the presence of a depressive syndrome. Asterixis, myoclonus, and postural tremor are common in toxic-metabolic dementias, whereas resting tremor, choreoathetosis, or rigidity occur in progressive extrapyramidal disorder. EEG is focally abnormal in cases of cerebral mass lesions and shows generalized slowing in toxic-metabolic encephalopathies. CT will aid in the identification of hydrocephalus, subdural hematomas, and intracranial mass lesions. A thorough laboratory evaluation including complete blood count, erythrocyte sedimentation rate, electrolytes, blood urea nitrogen and blood sugar, liver and thyroid function tests, serum calcium and phosphorus levels, B12 and folate levels, serum copper and ceruloplasmin, VDRL, chest X-ray, electrocardiogram, and lumbar puncture may demonstrate treatable disorders that are adversely affecting intellectual function. Elderly individuals are particularly susceptible to the effects of toxic or metabolic disorders, and a mild dementia may be exaggerated by relatively minor fluctuations in metabolic status. Treatable causes of dementia should be sought in all demented patients.
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PMID:Treatable dementias. 635 58

A 68-year-old man was hospitalized on 24 June, 1998 because of visual and gait disturbance. A month before admission, he had been aware of blurred or double vision while watching TV. A few days later, he developed dysphagia and clumsiness in the fingers. His gait became unstable and he exhibited restless finger movements. His shoulders and trunk showed torsion while walking. On admission, he became disoriented and showed rigidity in the legs and athetosis in the bilateral fingers. Routine laboratory findings, thyroid function data, and the serum levels of vitamin B1, B12, Cu, and ceruloplasmin were within the normal ranges. Periodic synchronous discharges (PSD) were observed on electroencephalography. MRI showed T2-high intensity and atrophy of the bilateral caudate nucleus and putamen in addition to the cerebral cortex. 99mTc-ECD-SPECT showed a decrease of local blood flow in the bilateral frontal, right temporal, and bilateral parietal lobes and bilateral thalami. Athetosis became exacerbated and was observed for a month, overlapping with myoclonus. We diagnosed the patient as having CJD because of progressive dementia, myoclonus and PSD. Analysis of the prion protein revealed that codon 129 was Met/Met and codon 219 Glu/Glu by DNA sequences. The patient developed akinetic mutism and rigid contracture, and died of pneumonia on 5 September, 1998. Because athetosis is thought to involve the bilateral caudate nucleus, putamen and thalamus, the findings of diagnostic imaging in this patient might be relative to the clinical symptoms.
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PMID:[A case of Creutzfeldt-Jakob disease exhibiting athetosis in the early stage]. 1055 90

Iron is one of the most important essential metal ions of which significance is well known for ages. This element is a key moiety of several enzymes in iron containing heme or nonheme form and transfer and storage protein, hemoglobin and myoglobin. Several membrane carriers of iron have already been identified. The redox state of iron is determined by xanthine oxidase, cytochromes and Hp or ceruloplasmin and ferroxidase activity of apo-ferritin, respectively. Some vitamins (C, B2-, B3-, B6-, B12) play also a role in the metabolism of iron. The iron content of cells of the organs is well regulated by the iron homeostasis. Iron has a significant role in the immune system by producing oxygen containing free radicals. Anaemia induced by iron deficiency may cause a challenge concerns for pregnant women, babies and adolescent, primarily.
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PMID:[Physiologic and pathologic role of iron in the human body. Iron deficiency anemia in newborn babies]. 1550 4

A 19-year-old man who developed extensive oesophageal lye (Alkali) stricture and received long-term enteral nutrition (eight months) with a jejunostomy tube developed macrocytic anaemia (Hb: 41 g/L) with leucopenia (white blood cell [WBC]: 3.0 x 10(9)/L). The patient's serum vitamin B12, folate, iron and liver function tests were normal. Bone marrow examination revealed gross erythroid hyperplasia and cytoplasmic vacuolization of erythroid and myeloid elements. Further investigations revealed low serum copper (0.3 micromol/L) and ceruloplasmin concentrations (<30 mg/L) with marginally low normal serum concentration of red cell peroxidase (13 U/gHb), establishing the diagnosis of copper deficiency anaemia. The anaemia and leucopenia responded intermittently to intravenous copper therapy, but the serum copper concentration dropped when intravenous copper therapy was withdrawn. Enteral jejunostomy copper supplementation failed to maintain adequate serum copper concentrations. After stabilizing the general condition of the patient, a pharyngo-gastric anastamosis was performed and normal oral diet commenced, which restored normal serum copper concentration. This case report suggests that copper supplements in the form of copper sulphate are not adequately absorbed when administered through a jejunostomy tube.
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PMID:Acquired copper deficiency following prolonged jejunostomy feeds. 1594 60

Smoking is associated with oxidative stress and increased risks of many chronic diseases that both shorten life and impair its quality. Low concentrations of several micronutrients, especially the antioxidants vitamin C and beta-carotene, are also associated with smoking, and there has been much interest in determining whether deficiencies in micronutrients are involved etiologically in smoking-related diseases. The objective of this review was to bring together reports on dietary intakes, biochemical indicators of micronutrient status, and results of some intervention studies on micronutrients where authors had compared outcomes in smokers and non-smokers. The micronutrients discussed are vitamins A, E, and C; the carotenoids; some of the B-vitamin group; and the minerals selenium, zinc, copper, and iron. The data were then examined to determine whether effects on the biochemical markers of micronutrient status were due to differences in dietary intakes between smokers and non-smokers or to the consequences of inflammatory changes caused by the oxidative stress of smoking. It was concluded that although smoking is associated with reduced dietary intake of vitamin C and carotenoid-containing foods, inflammatory changes increase turnover of these micronutrients so that blood concentrations are still lower in smokers than non-smokers even when there is control for dietary differences. In the case of vitamin E, there is some evidence for increased turnover of this nutrient in smokers, but this has little to no influence on blood concentrations, and there are no differences in dietary intake of vitamin E between smokers and non-smokers. Serum concentrations of vitamin A, folate, and vitamin B12 and B6 markers do not appear to be influenced by smoking, although there is some influence of dietary intake on concentrations of these nutrients in the body. In the case of the minerals examined, the main effects on biochemical markers of mineral status were attributed to inflammation and were therefore greater in heavy or long-term smokers. Serum concentrations of selenium and erythrocyte GPx activity were lower in smokers. Erythrocyte CuZn-SOD activity and serum ceruloplasmin concentrations were elevated, while serum zinc concentrations were depressed only in heavy smokers. Lastly, smoking appears to affect iron homeostasis mainly by changing hemoglobin concentrations, which were in general increased. Serum iron, TfR, and ferritin were mostly unaffected by smoking, except in pregnancy where there is evidence of increased erythropoiesis causing lower saturation of plasma transferrin and some evidence of lowering of iron stores.
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PMID:Monitoring micronutrients in cigarette smokers. 1704 81

A 48-year-old man was referred to our hospital in December, 2005 because of general fatigue, gait disturbance and bradycardia. He had a history of polysurgery due to recurrent ileus and had been treated with home total parenteral nutrition for the short-bowel syndrome since 2003. Clinical findings on admission included marked emaciation and severe weakness of the extremities. Pancytopenia was noted in the peripheral blood. The serum levels of copper and ceruloplasmin were 3 microg/dl and 3 mg/dl, respectively, while Vit. B12 and folate were within the normal range. The bone marrow demonstrated cytoplasmic vacuolation in the myeloid and megakaryocytic series, and sideroblastic changes. No evidence of hematologic malignancies was presented. The diagnosis was copper deficiency and the patient was treated with copper supplementation. Four weeks after copper therapy, the serum level of copper rose to 50 microg/dl and ceruloplasmin to 14 mg/dl. Significant improvements in the hematologic profile, ECG findings and weakness of extremities were noted. Although bicytopenia (anemia and neutropenia) is considered to be a feature of hematologic disorders caused by copper deficiency, the present case showed pancytopenia. The exact mechanism of the unusual association of thrombocytopenia and other abnormalities with copper deficiency remains to be elucidated.
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PMID:[Copper deficiency with pancytopenia, bradycardia and neurologic symptoms]. 1744 78

One of the hallmarks of both sickle cell disease (SCD) and thalassemia major (TM) is accelerated oxidative damage. Decreased antioxidant levels and increased oxidant stress biomarkers are found in both diseases. Although isolated vitamin deficiencies have been reported in TM and nontransfused SCD patients, a comprehensive evaluation of vitamin and trace mineral levels has never been performed in chronically transfused SCD or TM patients. As vitamins and trace minerals may be consumed as a result of chronic oxidative stress; we hypothesized that levels of these compounds would correlate with surrogates of iron overload, hemolysis, and inflammation in chronically transfused patients. Using a convenience sample of our group of chronically transfused patients we studied 43 patients with SCD (17 male, 26 female) and 24 patients with TM (13 male and 11 female). The age range for our patients varied from 1.5 to 31.4 years. Levels of vitamins A, thiamin, B6, B12, C, D, E as well as selenium, zinc, copper, and ceruloplasmin were measured. We found that 40-75% of the patients were deficient in A, C, D and selenium and 28-38% of the patients had low levels of B vitamins and folate. There was little association with iron overload, hemolysis, or inflammation. Although the precise mechanism of these deficiencies is unclear, they may contribute to the morbidity of chronically transfused hemoglobinopathy patients.
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PMID:Nutritional deficiencies in iron overloaded patients with hemoglobinopathies. 1941 22


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