Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0002871 (anemia)
 52,094 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The term ''iatrogenic disease'' means disease caused by therapy prescribed by doctors. Most such diseases are drug induced. Adverse effects of drugs have been more common in seriously ill patients who have received many drugs. Drug interaction has often been the cause. Most have been dose-related from cumulative pharmacologic effects. Reported data have been incomplete. Individual variability due to a genetic basis has been a factor. Environmental influences, such as smoking, atmospheric pollution, and hardness of the water supply may be involved. Sometimes the patient's metabolism has been impaired by concomitant liver or kidney malfunction. In such cases the drug, or its metabolites, may build up to a toxic level. A lowered threshold to the normal action of a drug is frequent among the very old and the very young. Geriatric patients have a considerable reduction in the reserve capacity of many organs. Hypersensitivity to a drug may be present. Skin rashes and eruptions are most common in this type of allergic reaction although jaundice and hemolytic anemia have followed. Polypharmacy increases the risk. Some patients make errors in taking prescribed drugs. Also, additional self-medication is common. Drug-food interactions may occur. Needed vitamins may be absorbed and eliminated by the use of liquid paraffin as a laxative. Intestinal flora-destroying antibiotics permit other organisms to grow. Alcohol is an additional hazard. Oral contraceptive use may be followed by anemia, and may react with other drugs. A list of such known reactions is given. Delayed iatrogenic neoplasia is being considered. Effects on the progeny have been shown with several drugs. Forewarning creates awareness and caution.
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PMID:Iatrogenic disease: a hazard of multiple drug therapy. 79 37

Present investigation was undertaken to elucidate the significance of changes in erythrocyte zinc levels in anemia. A preliminary study for the determination of erythrocyte zinc by atomic absorption spectrophotometry was done. The simple dilution method, in which zinc was determined directly from a sample of erythrocyte lysed and diluted with deionized water, appeared satisfactory in view of its rapidity, simplicity and accuracy. Of importance is that the temperature of sample and standard solution had to be matched. By using the above method, the mode of changes in erythrocyte zinc levels was investigated in healthy individuals and it was found that erythrocyte zinc expressed per gram of hemoglobin was inversely correlated to mean corpuscular hemoglobin concentration (MCHC). This relationship was also shown in patients with iron deficiency anemia and phlebotomy-induced anemia in rabbits. However, erythrocyte zinc expressed per milliliter of packed red cells was generally increased in these cases. The difference of erythrocyte zinc levels between 9:00 a.m. and 3:00 p.m. was not statistically significant. In addition, the levels of the B and of the C type erythrocyte carbonic anhydrases were assayed immunochemically. It was ascertained that there was a significant correlation between erythrocyte zinc levels and those of total carbonic anhydrase. This, the clinical importance of changes in erythrocyte zinc levels in anemia was discussed in relation to the role of this zinc - metalloenzyme.
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PMID:[Determination of erythrocyte zinc by atomic absorption spectrophotometry: Its significance in iron deficiency anemia (author's transl)]. 82 Jun 20

Weanling male rats were fed a Torula yeast diet supplemented with selenium, vitamin E, or both for 3 months. Of rats fed each diet, one group received 250 ppm lead in the drinking water and another group did not. In rats not poisoned with lead, neither vitamin E nor selenium deficiency affected spleen weight, hematocrit value, or erythrocyte mechanical fragility. Vitamin E deficiency increased the splenomegaly, anemia, and mechanical fragility of red cells of lead-poisoned rats, whereas selenium deficiency did not. Addition of 0.5 ppm selenium to the vitamin E-supplemented diet increased slightly the splenomegaly and anemia in lead-poisoned rats. Excess levels of selenium (2.5 and 5 ppm) in the vitamin E-deficient diet had little or no effect on spleen size or hematocrit of rats not receiving lead, but partially prevented the splenomegaly and anemia of red cells from either non-poisoned or lead-oisoned vitamin E-deficient rats, but not as effectively as vitamin E. These results show that vitamin E status of rats is more important that selenium status in determining response to toxic levels of lead. Excess dietary selenium did protect partially against lead poisoning in vitamin E-deficient rats, but the levels of selenium used were toxic in themselves.
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PMID:Comparative effects of selenium and vitamin E in lead-poisoned rats. 84 75

The role of vitamin E in human nutrition was studied by investigation of patients with cystic fibrosis (CF) and associated pancreatic insufficiency. Vitamin E status was assessed by measurement of the plasma concentration of the principal circulating isomer, alpha-tocopherol. Results of such determinations in 52 CF patients with pancreatogenic steatorrhea revealed that all were deficient in the vitamin. The extent of decreased plasma tocopherol varied markedly but correlated with indices of intestinal malabsorption, such as the serum carotene concentration and percentage of dietary fat absorbed. Supplementation with 5-10 times the recommended daily allowance of vitamin E in a water-miscible form increased the plasma alpha-tocopherol concentrations to normal in all 19 CF patients so evaluated. Studies on the effects of vitamin E deficiency focused on possible hematologic alterations. An improved technique was developed to measure erythrocyte hemolysis in vitro in the presence of hydrogen peroxide. While erythrocyte suspensions from control subjects demonstrated resistance to hemolysis during a 3-h incubation, all samples from tocopherol-deficient CF patients showed abnormal oxidant susceptibility, evidenced by greater than 5% hemoglobin release. The degree of peroxide-induced hemolysis was related to the plasma alpha-tocopherol concentration in an inverse, sigmoidal manner. The possibility of in vivo hemolysis was assessed by measuring the survival of (51)Cr-labeled erythrocytes in 19 vitamin-E deficient patients. A moderate but statistically significant decrease in the mean (51)Cr erythrocyte half-life value was found in this group. Measurement of erythrocyte survival before and after supplementation of 6 patients with vitamin E demonstrated that the shortened erythrocyte lifespan could be corrected to normal with this treatment. Other hematologic indices in deficient subjects, however, were normal and did not change upon supplementation with vitamin E. It is concluded that CF is invariably associated with vitamin E deficiency, provided that the patient in question has pancreatic achylia and is not taking supplementary doses of tocopherol. Concomitant hematologic effects consistent with mild hemolysis, but not anemia, occur and may be reversed with vitamin E therapy. Patients with CF should be given daily doses of a water-miscible form of vitamin E to correct the deficiency.
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PMID:The occurrence and effects of human vitamin E deficiency. A study in patients with cystic fibrosis. 87 86

A number of total colectomies with end-to-end ileo-rectal anastomosis was performed in the inbred Lister rat. The following data were studied: survival rate, body weight curves, variations of appetite, thirst and diuresis, daily weight and electrolytes content of feces, intestinal transit time, histology of terminal ileum, rectum, liver and kidney. After an initial lose of body weight, rats gained their original weight at about two months after colectomy; at this time a syndrome was observed caracterized by anemia, leucocitosis with neutrophilia, ipoproteinemia, remarkable increase of thirst (up to 400%) and of water and sodium content of feces; appetite and diuresis were normal; intestinal transit tice was slightly reduced. Histologically there was a "coloni" transformation of the terminal ileum and vacuolization of the proximal renal tubules.
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PMID:[Total colectomy in the rat : its metabolic and functional consequences]. 89 Aug 71

Either simultaneous or separate dietary deficiencies of vitamin E and selenium in Atlantic salmon during first 4 weeks of feeding caused twice the mortality shown in fish fed both supplemental vitamin E (0.5 IU/g dry diet) and selenium (0.1 mug/g). Subsequent dietary repletion with both vitamin E and selenium significantly reduced mortality during the following 2 weeks. Larger salmon (0.9 g initial mean weight), with vitamin E deficiency with or without selenium resulted in the following deficiency signs: extreme anemia, pale gills, anisocytosis, poikilocytosis, elevated plasma protein, exudative diathesis, dermal depigmentation, in vitro ascorbic acid-stimulated peroxidation in hepatic microsomes, yellow-orange liver color, yellow-brown intestinal contents, enlarged gall bladder distended with dark green bile, low vitamin E in carcass and hepatic tissue, muscular dystrophy, increased carcass fat and water, and a response to handling characterized by a transitory fainting with interruption in swimming. A deficiency of dietary selenium suppressed plasma glutathione peroxidase activity. Supplemental selenium with vitamin E significantly increased tocopherol activity in hepatic, but not carcass tissues. Supplements of both vitamin E and selenium were necessary to prevent muscular dystrophy.
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PMID:Vitamin E and selenium interrelations in the diet of Atlantic salmon (Salmo salar): gross, histological and biochemical deficiency signs. 93 27

The management of patients with chronic renal failure is complicated and demanding for both physician and patient, but is frequently rewarding. When specific treatment of the underlying cause is not possible, therapy is aimed at making the maximum use of existing nephrons and preventing further loss of nephrons through hypertension and infection. Careful attention to salt and water balance is necessary, and all patients and all drugs prescribed must be considered with care. Special problems exist with regard to anaemia, bone disease, pericarditis and hyperkalaemia. An important aspect of care at this time is the education of patients about the next major phase of management, dialysis and transplantation.
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PMID:The conservative management of chronic renal failure. 93 26

Failing kidneys can play havoc with other parts of the body. Specific treatment of these associated problems may help ward off uremia and preserve whatever renal function remains. Sodium levels may drop if too much water is mistakenly given to counteract kidney failure. Hyperkalemia can lead to cardiac arrest if potassium levels aren't reduced without delay. Acidosis also may reach life-threatening proportions, especially if diarrhea occurs. Almost all patients with chronic renal failure have a bleeding tendency and anemia, with the hematocrit dipping as low as 20 percent. Over half have decreased tolerance to carbohydrares, although severe hyperglycemia is rare. Disorders of calcium metabolism also are common, ranging from asymptomatic hypocalcemia to osteomalacia. The kidneys' impaired filtration ability should be kept in mind when drugs are prescribed. Dosages may need to be cut to avoid an adverse reaction.
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PMID:Conservative management of chronic renal failure. 95 17

An unclassified case of haemolytic anaemia with voluminous splenomegaly is reported. This anaemia was normocytic without any specific morphologic aspect of red blood cells (RBC); Coombs test was negative; the osmotic fragility was normal; the increased autohaemolysis was not affected by the presence of glucose; Hb studies were normal; no RBC enzyme deficiency was found; RBC lipids and membrane proteins were normal; there was a marked reduction in RBC survival with exclusive splenic uptake of erythrocytes. Before splenectomy, RBC cations and water content were abnormal: 1) the RBC water was decreased moderately; 2) the RBC sodium was about twice the normal mean with an increased 22Na turn-over; 3) the RBC potassium was markedly reduced and 42K influx was twice the normal mean; 4) the RBC calcium content was increased. Splenectomy was followed by rapid disappearance of haemolysis and RBC water and cation disturbances. Because of this extremely rapid disappearance after splenectomy the authors suggest this case of haemolytic anaemia could be a primary disease of the spleen.
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PMID:Unclassified haemolytic anaemia with splenomegaly and erythrocyte cation abnormalities--a disease of the spleen? 96 54

The activities of 2Cu,2Zn-superoxide dismutase, ferroxidase (ceruloplasmin), catalase and glutathione peroxidase were measured in the blood of rats during copper depletion. Two control groups of animals were used; one received the regular diet containing all essential components including copper and the other group was maintained on a diet, containing 1% the amount of copper in normal diet, copper being supplied as Cu(Leu)2 in the drinking water. Both groups showed no detectable differences, either in the copper content of blood or in the measured four enzymic activities. Excessive copper (injected intraperitoneally) caused only an insignificant rise in the enzymic activities (0-10%) compared to either control. After starting copper depletion ferroxidase activity decreases to 15% on the 15th day, while the 2Cu,2Zn-superoxide dismutase activity decreases to 40% on the 45th day. Ferroxidase activity shows rapid but transient changes immediately after perturbation in plasma copper levels. By contrast, the 2Cu,2Zn-superoxide dismutase activity more closely parallels the overall copper deficiency. Dietary repletion with copper raises the 2Cu,2Zn-superoxide dismutase activity to 94% and the ferroxidase activity to 80% of the control values within 36 h. Apart from the copper-dependent anemia catalase activity was decreased. However, 15 days after the start of the copper depletion catalase activity rises again and reaches the control value on the 40th day and a 30% stimulation was even seen on the 58th day. Upon copper repletion catalase activity reaches 166% of the control within 14 days. No copper-dependent differences of glutathione peroxidase activity were seen regardless whatever copper level was present in the rats.
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PMID:Copper deficiency and erythrocuprein (2Cu, 2Zn-superoxide dismutase). 97 14


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