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)

We often encounter diabetic patients with anemia in whom the causes of anemia were not clearly identified despite differential hematologic studies. We therefore studied the clinical and biochemical characteristics of diabetic patients with anemia of uncertain cause and measured erythropoietin (Epo) concentrations in 35 diabetic subjects without significant diabetic renal disease. Among 62 medical records of diabetic patients with anemia, showing no evidence of advanced diabetic nephropathy (creatinine clearance > or = 30 mg/kg/1.73 m2), the causes of the anemia were not able to be identified in 28 cases (45.2%). In addition, we enrolled 35 diabetic patients with uncertain causes of anemia in order to evaluate the serum Epo responsiveness to anemia, and compared levels to a group of non-diabetic subjects also with anemia. The serum Epo concentrations of diabetic patients (17.6 +/- 8.1 mIU/ml) were significantly lower than those of non-diabetic patients with similar degree of decrease in hemoglobin concentrations (144.9 +/- 108.0 mIU/ml, P<0.001). The hemoglobin concentrations of diabetic patients correlated with creatinine clearance (r = 0.34, P = 0.03), serum creatinine (r = -0.49, P = 0.003) and albumin excretion rate (r = -0.44, P = 0.009), but showed no relation to age, duration of diabetes, glycated hemoglobin, presence of retinopathy or neuropathy. We concluded that reduced Epo responsiveness to anemia could explain the anemia present in diabetic patient but without advanced diabetic nephropathy. This may reflect early renal interstitial damage.
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PMID:Reduced erythropoietin responsiveness to anemia in diabetic patients before advanced diabetic nephropathy. 1062 88

Tumor necrosis factor alpha (TNF alpha) is usually excreted by the kidney. In dialysis patients, it accumulates. TNF alpha has been implicated in the pathogenesis of malnutrition, diabetic neuropathy, and erythropoietin resistance. We studied TNF alpha plasma levels in 49 stable peritoneal dialysis (PD) patients, with the aim of correlating those levels with the presence and severity of peripheral neuropathy, hypertrophic cardiomyopathy, and anemia. Kt/Vurea' residual renal creatinine clearance (CrC), nutritional markers, and general biochemistry were also determined. The average plasma level of TNF alpha was 67 +/- 32 pg/mL (range: 18.1-156.3 pg/mL; normal value 3-20 pg/mL). No correlation was observed between TNF alpha and KT/Vurea' but a negative correlation with CrC was seen (r: -0.37, p < 0.05). TNF alpha levels were higher in patients with neuropathy as compared to patients with normal results (72.5 +/- 32 pg/mL vs 44 +/- 22 pg/mL, p < 0.05). Patients with neuropathy also showed a lower CrC value (1.5 +/- 1.7 mL/min vs 3.9 +/- 2.6 mL/min, p < 0.01). TNF alpha levels were higher in patients with left ventricular hypertrophy (LVH) with respect to normal individuals (70.4 +/- 32 pg/mL vs 38.5 +/- 20.8 pg/mL, p < 0.05). Patients with severe LVH showed the lowest CrC value. A direct, significant relationship was found between TNF alpha levels and weekly erythropoietin dose (r: 0.41, p < 0.05). Patients with hypertriglyceridemia or taking lipid-lowering agents showed a positive linear correlation between TNF alpha and triglycerides (r = 0.7, n = 14, p < 0.05). These data suggest that accumulation of TNF alpha may contribute to the development or maintenance of some neurologic, hematologic, and cardiac complications of uremic syndrome. Loss of residual renal function conditions an increment in TNF alpha levels. These data continue to add support to the idea that TNF alpha may be considered a uremic toxin.
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PMID:Tumor necrosis factor alpha as a uremic toxin: correlation with neuropathy, left ventricular hypertrophy, anemia, and hypertriglyceridemia in peritoneal dialysis patients. 1068 77

A large randomized clinical trial in advanced, previously untreated, non-small cell lung cancer (NSCLC) patients revealed better response rates and better tolerance for paclitaxel+cisplatin (TAXCIS) compared to teniposide+cisplatin (TENCIS). Since economic evidence is receiving increasing attention in health care, we conducted an economic evaluation based on the trial results in The Netherlands, Belgium, France and Spain. The evaluation was based on (i) differences in drug costs, (ii) differences in chemotherapy administration and (iii) the economic consequences of significantly different clinical outcomes in the trial: anemia, thrombocytopenia, neutropenia, neuropathy and arthralgia/myalgia. Data regarding medical resource utilization were obtained from clinician interviews using a Delphi technique and validated by patient charts analysis. Differences in medical management occurred across countries, but TAXCIS was cost-additive in all countries, i.e. the extra cost of chemotherapy was only partially compensated by savings in medical resource use, resulting in a net cost per patient of US$2311. In the trial, TAXCIS therapy produced a 37% response rate compared to 26% for TENCIS. The cost per extra responder for TAXCIS is on average US$21011, which is comparable to the cost per responder obtained with TENCIS (US$27266). Thus, the cost-effectiveness of TAXCIS, expressed in cost per responder, is similar to the cost-effectiveness obtained with TENCIS.
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PMID:The cost-effectiveness of paclitaxel (Taxol) + cisplatin is similar to that of teniposide + cisplatin in advanced non-small cell lung cancer: a multicountry analysis. 1088 9

Nucleoside analogues represent the cornerstones of antiretroviral regimens. A range of drug- or tissue-specific toxicities, such as peripheral neuropathy, myopathy, pancreatitis and lactic acidosis with hepatic steatosis, has been documented with these agents. The fat atrophy seen on long term antiretroviral therapy may also be related to nucleoside analogues. The mechanisms by which nucleoside analogues cause toxicity are not clearly established. In vitro, the triphosphates of these agents are weak to modest substrates for human DNA polymerases, showing the greatest affinity for mitochondrial DNA polymerase gamma. Short term exposure in vitro to some nucleoside analogues has been demonstrated to cause increased lactate production or falls in mitochondrial DNA suggestive of mitochondrial toxicity. However, stavudine and to a lesser extent zidovudine are poor substrates for mitochondrial thymidine kinase type 2, the predominant form in cells that are not actively mitotic such as neurons, myocytes and adipocytes. These are the cell types where the proposed mitochondrial toxicities neuropathy, myopathy and lipoatrophy are observed. Thus, active concentrations of phosphorylated products of stavudine and zidovudine may not be present in mitochondria. The familial mitochondrial diseases do not have identical presentations to nucleoside analogue toxicities. These disorders most commonly involve the CNS, typically with seizures or dementia, and occasionally the kidneys. Although nucleoside analogues are known to penetrate the CNS and are commonly renally excreted unchanged, mitochondrial toxicities at these sites have not been documented. Furthermore, toxicity caused by nucleoside or nucleotide analogues does not always appear to arise through the mitochondrial route. Cidofovir appears to cause renal tubular dysfunction via a toxic intracellular metabolite, and zidovudine-related anaemia appears to be related to decreased globin RNA synthesis. In vitro or animal models suggest that zidovudine myopathy, stavudine-related (but not zalcitabine- or didanosine-related) neuropathy and didanosine-related pancreatitis may all be not related, or not exclusively related, to mitochondrial dysfunction. The integration of nucleoside analogues into nuclear DNA, best documented with zidovudine but likely to occur with other agents, represents an alternative but potentially delayed pathway to cytotoxicity and cell apoptosis. This is the mechanism of cell death during therapy with antineoplastic nucleoside analogues, and may have contributed to the multisystem toxicities observed with the anti-hepatitis B drug fialuridine. New research evaluating the effects of long term exposure of cell lines is required to address the possibility that nuclear genotoxicity plays a role in long term nucleoside analogue toxicity.
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PMID:Toxicity of antiretroviral nucleoside and nucleotide analogues: is mitochondrial toxicity the only mechanism? 1114 57

In Africa, a rise in complications of diabetes mellitus has gone in hand with the growing disease prevalence, clearly demonstrating the importance of assessing complications. Diabetes mellitus constitutes a major financial burden in developing countries in Africa with relatively limited resources. Ketoacidosis is observed in 24% of juvenile diabetes and is the inaugural sign in 76% of all cases, progressing to coma in 34%. Even in type 2 diabetes, acidoketosis occurs in 34% of the cases. Infection is particularly frequent and is often fatal in tropical Africa because of the involvement of Staphyococcus and Gram-negative microorganisms. Hyperleukocytosis and anemia are correlated with ineffective antibiotic therapy. Pulmonary tuberculosis is the ninth most frequent complication of diabetes. Overall mortality is 14.9 per 1000 person-years of diabetes. Mean age at death is 51.6 years for women and 57.6 years for men after a mean 12.5 year disease duration. Thirty percent of all deaths result from acute metabolic complications, infections and stroke. More than half of the patients with insulin-dependent-diabetes have retinopathy. Differences observed in patients with different ethnic origins is linked basically to unfavorable social and economic conditions that worsen the risk of poor blood glucose control. Retinopathy accounts for 32% of all ocular complications, similar to other African data and more generally in ophthalmology centers. The rate of neuropathy is high, reaching 70% in patients with microangiopathy. Impotence concerns 48.7% of the diabetic population with a mean age of 41.4+/-15.5 years. Coronary artery disease had a recognized influence on hemoglobin diseases, particularly when the coronarography is normal. Lower limb arteriopathy is observed in 18% of the diabetic patients.
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PMID:[Main complications of diabetes mellitus in Africa]. 1117 5

Optic neuropathy in uremia is rare. Although the consequences of optic neuropathy-blindness or substantial loss of vision-are devastating, only a few cases have been reported by way of single case reports and case series studies. The reported patients are heterogeneous with regard to the cause of neuropathy. We report the case of a patient with uremic optic neuropathy and summarize the other cases reported in the literature so far. Based on the data available from these reports, we propose a classification system, which includes nonischemic neurotoxic uremic optic neuropathy; ischemic optic neuropathy, more specifically anterior ischemic optic neuropathy; and optic neuropathy as a result of drug side effects, benign intracranial hypertension, and optic neuritis. The immediate institution of dialysis and corticosteroid therapy and correction of anemia and relative hypotension can optimize the chances of visual recovery for these patients. Close collaboration among nephrologists, ophthalmologists, and neurologists is important in this interdisciplinary emergency.
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PMID:Optic neuropathy in uremia: an interdisciplinary emergency. 1122

Disulone (dapsone + ferrous oxalate) is a sulphone marketed in France since 1958 and authorized in P. Carinii prophylaxis in HIV+ cotrimoxazole intolerant patients, bullous dermatosis, leprosy and polychondritis. Between 1983 and 1998, 249 adverse reactions were reported to French pharmacovigilance centres and Aventis, the manufacturer. Every side-effect was reviewed and the causal relationship was assessed on the basis of the French method for causality assessment. Main side-effects were divided as follows: 117 blood dyscrasias (generally neutropenia and agranulocytosis, rarely methaemoglobinaemia, haemolysis, macrocytosis, anaemia, aplastic anaemia, haemochromatosis and sulphaemoglobinaemia); 29 hypersensitivity syndrome; 39 cutaneous reactions, generally rash; 27 liver injuries (cholestatic, cytolytic and mixed hepatitis); 27 neurological and psychiatric side-effects including 7 axonal neuropathy; 10 gastrointestinal effects, generally nausea and vomiting. Five deaths were reported (4 septicaemia including one case not due to dapsone and 1 digestive bleeding due to underlying disease). In the other cases the outcome was favourable. The results were compared with the published references. It would seem to be important to reinforce information to prescribers about the possible serious adverse reactions with dapsone, particularly hypersensitivity syndrome and agranulocytosis, that can cause death if the drug is not stopped in time.
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PMID:[Adverse effects of Disulone; results of the France pharmacovigilance inquiry. Regional Centers of Pharmacovigilance]. 1147 11

Pernicious anaemia is the most common cause of cobalamin deficiency. Nervous disorders associated with cobalamin deficiency are neuropathy, optic atrophy, dementia and myelopathy (subacute combined degeneration). In this case, symptoms are those of posterior and lateral column dysfunction of the spinal cord, with diminished vibratory sensation, ataxia, weakness of limbs, hyperreflexia, extensor plantar response and spasticity. Macrocytosis and anaemia are often lacking. There is an inverse correlation between the degree of anaemia and the extent of nervous impairment. The most sensitive tool for the diagnosis of cobalamin deficiency is the serum cobalamin level. But a normal cobalamin assay does not fully exclude cobalamin deficiency. Levels of serum methylmalonic acid and total homocysteine are useful as ancillary tests in the diagnosis. Treatment is based on intramuscular injections of vitamin B12.
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PMID:[Pernicious anemia]. 1150 92

Renal replacement treatment options are life-saving treatments for patients with end-stage renal disease (ESRD). However, prolonged survival in patients with ESRD is associated with various functional and morphological disorders from almost all systems. Anaemia, deconditioning, cardiac dysfunction. impairment of cardiac autonomic control and skeletal muscle weakness and fatigue, primarily because of 'uraemic' myopathy and neuropathy, are the main predisposing factors for their poor functional ability. Physical training is being recommended as a complementary therapeutic modality. There are generally 3 methods of exercise training applied in patients with ESRD: (i) the supervised outpatient programme that is held in a rehabilitation centre; (ii) a home exercise rehabilitation programme; and (iii) exercise rehabilitation programme during the first hours of the haemodialysis treatment in the renal unit. All the available training data show that the application of an exercise training programme in patients with ESRD enhances their physical fitness. This improvement is due to central and mainly peripheral adaptations. Exercise training in these patients increases aerobic capacity, causes favourable left ventricular functional adaptations, reduces blood pressure in patients with hypertension, modifies other coronary risk factors, increases the cardiac vagal activity and suppresses the incidence of cardiac arrhythmias. Moreover, exercise training has beneficial effects on muscle structural and functional abnormalities. These central and peripheral adaptations to exercise training cause an increase in their functional capacity and offer them achance of a better quality of life. Moreover, exercise training improves exercisee tolerance of renal post-transplant patients.
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PMID:Central and peripheral adaptations to physical training in patients with end-stage renal disease. 1150 21

Since the adoption of highly active antiretroviral therapy (HAART) in the mid-1990s, certain metabolic toxicities have been increasingly recognized. These include a fat redistribution syndrome (lipohypertrophy, lipoatrophy), hyperlipidaemia, altered glucose metabolism and insulin resistance, mitochondrial toxicity (presenting as anaemia, myopathy, pancreatitis, neuropathy, hepatic steatosis and lactic acidosis), and bone density abnormalities (osteoporosis and osteonecrosis). Metabolic complications are principally reported with protease inhibitors and nucleoside reverse transcriptase inhibitors, but may be seen with all classes of antiretroviral therapy. In this review, we summarize the epidemiology, pathogenesis and management of these various toxicities.
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PMID:The metabolic toxicities of antiretroviral therapy. 1151 63


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