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 therapeutic effect of most immunosuppressive agents is unspecific and therefore often limited by an increased risk of infection by viral, bacterial or fungal organisms as well as by an increased incidence of malignant neoplasms. This short review includes the most commonly used immunosuppressants such as corticosteroids, azathioprine, methotrexate, cyclophosphamide and cyclosporine. The most common risks of long-term corticosteroid treatment are Cushing-like changes, decreased glucose tolerance and the usually benign steroid diabetes. Also clinically important is osteoporosis, since it can be prevented by physical training, calcium supplementation and treatment with vitamin D if necessary. Although there is still no proof of a significantly increased risk of peptic ulcer during steroid therapy, patients may develop gastrointestinal hemorrhage and even perforation without producing pain while being treated with corticosteroids. Mineralocorticoid effects, such as salt and water retention, are seen only with hydrocortisone and prednisone, whereas with synthetic steroids such as dexamethasone, sodium retention is absent despite their strong antiphlogistic activity. The most important side effect of the cytotoxic agents azathioprine, methotrexate and cyclophosphamide is marrow suppression. Due to the high turnover of neutrophils, patients most frequently suffer neutropenia rather than thrombocytopenia or anemia. Neutropenia, as well as impaired humoral and cellular immune mechanisms, are responsible for increased susceptibility to bacterial, viral or parasitic diseases during immunosuppressive therapy. Hepatotoxicity has been reported among patients receiving azathioprine (cholestatic hepatitis) and methotrexate (elevated AST levels and, rarely, liver fibrosis or cirrhosis). Cyclophosphamide causes hemorrhagic cystitis in a substantial proportion of patients, as well as an increased incidence of urothelial neoplasms. Both these side effects may be prevented by Mesna. The most important side effects of cyclosporine are acute and chronic nephrotoxicity usually associated with significantly elevated plasma levels of the drug. It must be borne in mind that severe nephrotoxicity may occur in patients receiving cyclosporine and ketoconazole together, since the latter may inappropriately increase the plasma cyclosporine level.
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PMID:[Immunosuppression--a tightrope walk between iatrogenic harm and therapy]. 892 65

Eighty-two children with the toxic dystrophic syndrome coursing in the presence of acute enteric infection were examined. A number of pathogenetically significant disorders were revealed: salt-deficient exsicosis, exsication, hypopotassemia, anemia, hypoproteinemia, stable metabolic acidosis, protein and energy insufficiency. Among the causes of protein and energy insufficiency associated with progressive weight loss the principal were impaired cavitary digestion, decrease of the absorption capacity of the intestine for proteins, fats, and carbohydrates, and long inadequate nutrition because of protracted diarrhea. Newly developed three-staged intensive care protocol with correction of homeostasis, provision with energy and nutrients, and repair of cavitary digestion and absorption capacity of the intestine helped reduce the mortality in this patient population from 13.4 to 4.8%.
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PMID:[Pathogenesis and intensive care of infants with toxic-dystrophic syndrome]. 904 71

Cardiomyopathy in chronic uremia results from pressure and volume overload. The former causes concentric left ventricular [LV] hypertrophy, results from hypertension and aortic stenosis, and is also associated with diabetes mellitus and anemia. Volume overload causes LV dilatation, results from arteriovenous shunting, salt and water overload, and anemia, and is also associated with ischemic heart disease, hypertension, and hypoalbuminemia. Decreased major arterial compliance and an early return of arterial wave reflections are also associated with the extent of LV hypertrophy. Cardiomyopathy predisposes to diastolic and systolic dysfunction. The latter results from myocyte death, and predisposing factors include ischemic heart disease and the uremic environment. Ischemic heart disease may be atherosclerotic or nonatherosclerotic in origin. Multiple factors contribute to the vascular pathology of chronic uremia, including injury to the vessel wall, dyslipidemia, prothrombotic factors, increased oxidant stress, and hyperhomocysteinemia. Ischemic risk factors include hypertension, LV hypertrophy, hypoalbuminemia, and perhaps hyperparathyroidism. The clinical consequences of cardiomyopathy include heart failure, ischemic heart disease, dialysis hypotension, and arrhythmias. The adverse impact of ischemic heart disease is probably mediated through the development of cardiac failure.
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PMID:Cardiac disease in chronic uremia: pathogenesis. 923 25

Therapy with human recombinant erythropoietin (EPO) has been accepted as effective for renal anemia in dialysis patients. However, studies in rats have shown that correcting anemia with EPO may affect the progression of renal dysfunction. In humans, however, the effect of EPO on residual renal function is a matter of controversy. We, therefore, investigated whether the long-term administration of EPO to predialysis patients influences residual renal function. Anemic patients at the predialysis stage with a serum creatinine (Cr) concentration ranging from 2 to 4 (average 2.9) mg/dl and a hematocrit (Ht) of less than 30% were randomly assigned to two groups which consisted of anemic patients not treated with EPO (group I, untreated anemic controls, n = 31) and anemic patients treated with EPO (group II, treated anemics, n = 42). Patients with nonsevere or moderate anemia (Ht > 30%) with a Cr ranging from 2 to 4 (average 2.6) mg/dl were also recruited as nonanemic controls (group III, untreated nonanemic controls, n = 35). Blood pressure was controlled to the same degree among the three groups by combined treatment with calcium antagonists and angiotensin-converting enzyme inhibitors. All patients were kept strictly on a low-protein (0.6 g/kg/day) and a low-salt (7 g/day) diet. The degree of control of dietary protein and blood pressure and the frequency of angiotensin-converting enzyme inhibitor administration were comparable among the three groups. The primary end point for each patient was a doubling of the baseline Cr which yielded cumulative renal survival rates which were plotted against time. Ht rose significantly from 27.0+/-2.3 to 32.1+/-3.2% in group II (n = 42, p < 0.001) with a rate of increase of 0.4+/-0.06%/week. However, it declined from 27.9+/-1.8 to 25.3+/-1.9% in group I (n = 31, p < 0.001) and from 35.9+/-3.5 to 32.2+/-3.9% in group III (n = 35, p < 0.001). Cr doubled in 26 patients (84%) in group I as compared with 22 (52%) in group II and 21 (60%) in group III. The cumulative renal survival rates in groups II and III were significantly better than that in group I: p = 0.0003 (group I vs. group II) and p = 0.0024 (group I vs. group III). However, there was no difference in the renal survival rate between groups II and III (p = 0.3111). The better survival rate obtained in group II was attributable to the better survival rate for the nondiabetic patients in this group. The present study suggests that anemia, per se, is a factor in the progression of end-stage renal failure and that reversal of anemia by EPO can retard the progression of renal failure, especially in nondiabetic patients, provided that blood pressure control, rate of increase in Ht, and dietary protein restriction are appropriate.
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PMID:Reversal of anemia by erythropoietin therapy retards the progression of chronic renal failure, especially in nondiabetic patients. 934 84

Diarrhea and malabsorption are common findings in patients with the acquired immunodeficiency syndrome (AIDS). The pathogenesis and consequences of malabsorption in human immunodeficiency virus (HIV) infection are similar to those found in non-HIV-related conditions, and are related to both direct intestinal damage and alterations in the coordination of the body's response to feeding. The pathogenesis of malabsorption is multifactorial and includes primary enterocyte injury with partial villus atrophy and crypt hyperplasia, ileal dysfunction with bile salt wasting and fat malabsorption, and exudative enteropathy. Clinical studies show that intestinal cryptosporidiosis leads to excess fecal losses of about 20% for protein and fat. The consequences of malabsorption include decreased appetite; "enterogastrone" effects including dry mouth, decreased gastric acid secretion, decreased rate of gastric emptying, and slowed intestinal transit; anemia resulting from iron, folate, or vitamin B12 malabsorption; and metabolic effects including osteomalacia, gallstones, renal stones, and hypocholesterolemia. Few studies of nutritional therapy have been applied specifically to AIDS patients with malabsorption. Total parenteral nutrition promotes weight gain, although the response to this therapy depends on the underlying clinical problem, with body cell mass repletion noted in patients with malabsorption but predominantly fat gain in patients with systemic infections. Nutritional stabilization also was noted in response to oral administration of a semielemental diet.
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PMID:Human immunodeficiency virus-related wasting: malabsorption syndromes. 962 87

To improve the health and nutritional status of school children in an area of iodine deficiency disorders (IDD) by means of different iodine fortifications in salt, fish sauce and drinking water, anthropometric assessment for nutritional measurement, including hematological status, were performed. There was a significant difference in the weight and height of the children from the four schools investigated, before and after supplementation in each school. The prevalence of anemia (as indicated by hematological measurement) and iodine deficiency (as indicated by urinary iodine concentration in the children from the four schools) were assessed and compared before and after iodine supplementation; a decrease in prevalence was found in all school children, however, serum ferritin did not change before and after supplementation.
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PMID:Nutritional status of school children in an endemic area of iodine deficiency disorders (IDD) after one year of iodine supplementation. 974 Feb 68

Severe deficiencies of iron (Fe) and iodine (I) affect more than one third of the world's population. A table salt, fortified with I and Fe, would be useful in areas in which anemia and goiter coexist. However, interactions between the two minerals have prevented their simultaneous use as fortificants. A method has been developed to coat I with dextran such that after spraying onto table salt, Fe and I do not interact. Our objective was to determine the absorption of Fe and the urinary excretion of I from table salt when provided in meals designed to significantly inhibit or enhance Fe absorption. Subjects (n = 16) ingested Fe-enhancing and Fe-inhibiting meals containing 5 g of table salt with 0.39 micromol dextran-coated I as potassium iodide and 1 mg of Fe (ferrous fumarate labeled with 59Fe) per gram of salt. Subjects also received a reference dose of 3 mg of ferrous fumarate labeled with 59Fe to "correct" for interindividual variation in iron absorption at a later date. Measured by whole-body counting, Fe-absorption from the Fe-enhancing meal (36.2 +/- 12.0%, corrected; 13.5 +/- 13.8% uncorrected) was significantly higher than that from the Fe-inhibiting meal (7.4 +/- 11.3%, corrected; 4.0 +/- 8.4%, uncorrected) (P < 0.0001). Urinary excretion of iodine at baseline and postingestion were not significantly different (0.89 +/- 0.5 vs. 1.06 +/- 0.39 micromol/L, P < 0.47) and were within the normal range. We conclude that Fe was well absorbed but influenced by the composition of the meal and that urinary excretion of iodine was maintained in the normal range with dextran-coated iodine.
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PMID:Iron is well absorbed by healthy adults after ingestion of double-fortified (iron and dextran-coated iodine) table salt and urinary iodine excretion is unaffected. 991 86

Micronutrient malnutrition cannot be eradicated, but the elimination and control of iron, vitamin A and iodine deficiencies and their health-related consequences as public health problems are currently the targets of global programmes. Remarkable progress is occurring in the control of goitre and xerophthalmia, but iron-deficiency anaemia (IDA) has been less responsive to prevention and control efforts. Subclinical consequences of micronutrient deficiencies, i.e. "hidden hunger", include compromised immune functions that increase the risk of morbidity and mortality, impaired cognitive development and growth, and reduced reproductive and work capacity and performance. The implications are obvious for human health and national and global economic and social development. Mixes of affordable interventions are available which, when appropriately adapted to resource availability and context, are proven to be effective. These include both food-based interventions, particularly fortification programmes, such as salt iodization, and use of concentrated micronutrient supplements. A mix of accompanying programmes for infection control, community participation, including education, communication and information exchange, and private sector involvement are lessons learned for overcoming deterrents and sustaining progress towards elimination.
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PMID:Perspectives from micronutrient malnutrition elimination/eradication programmes. 1006 71

We report a case of a 23-year-old Japanese woman who had severe hyperparathyroidism associated with chronic renal failure before the start of dialysis treatment. Her chief complaints were swelling and pain in both shoulders. Laboratory examination revealed renal failure (BUN 134 mg/dl, serum Cr 7.3 mg/dl), severe normocytic normochromic anemia (hemoglobin 4.3 g/dl), hypercalcemia (11.8 mg/dl), and hyperphosphatemia (9.7 mg/dl). Serum PTH levels were extremely increased (intact PTH >1,000 pg/ml: normal range 10-50 pg/ml). X-ray examination of the skull and shoulders showed a salt and pepper appearance, and cauliflower-like deformity of the distal end of both clavicles, respectively. Accelerated ectopic calcification was observed in the costal cartilages, internal carotid arteries, and splenic arteries. Ultrasonographic examination revealed enlargement of the four parathyroid glands. Thallium-technetium subtraction scintigraphy of the parathyroid glands showed increased uptake into the upper two. Renal needle biopsy revealed severe impairment of the interstitium and tubules with much milder changes in glomeruli. The etiology of the renal failure could not be identified. Hemodialysis, total parathyroidectomy and auto-transplantation into the forearm were immediately performed. The pathological diagnosis was chief cell hyperplasia of the parathyroid glands. Based on the presence of chronic renal failure, remarkable hyperphosphatemia with mild hypercalcemia, an unusually high level of serum PTH, and accelerated ectopic calcification, the patient was diagnosed to have severe secondary hyperparathyroidism caused by chronic renal failure with major impairment of the renal interstitium and tubules.
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PMID:Severe hyperparathyroidism with hypercalcemia associated with chronic renal failure at pre-dialysis stage. 1042 82

Gastroenteric angiodysplasia is an important cause of haemorrhage in chronic renal failure patients. This paper reports on 2 patients on maintenance haemodialysis with upper gastrointestinal bleeding due to different manifestations of angiodysplasic lesions (sudden appearance of haematemesis and melaena in one case, progressive anaemia with apparent resistance to erythropoietin in the other case). Exploratory endoscope examination of the first digestive tract showed in both cases the presence of bleeding angiodysplasic lesions. Both patients were there and then submitted to surgical endoscopy, during which the bleeding angiodysplasic lesion was sclerosed with physiological salt solution plus adrenaline 1/10000 and 1% polydocanol. In one patient, bleeding occurred again ten days later, making renewed surgical endoscopy necessary. In the course of this an elastic ligature was made to the superangular angiodysplasia. A year later in both cases there were no direct or indirect signs of further bleeding; an endoscopic check-up showed the treated lesions to be sclerosed. Endoscopy offers the unique possibility of being used for both diagnostic and therapeutic purposes in a single session. In expert hands, endoscope therapy is effective and markedly reduces the risk of side effects.
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PMID:Endoscopy as a tool for diagnosing and treating gastrointestinal angiodysplasia in haemodialysis patients. 1049 56


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