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)

A case of 21 year old male with neuropathy caused by renal insufficiency was present. He had taken bromate (mixed powder of potassium bromate and sodium bromate) for the purpose of suicide and suffered from acute renal insufficiency and hard of hearing. Renal dysfunction improved gradually by peritoneal dialysis and hemodialysis. However, on the 32th day after the onset, burning pain appeared in the bilateral feets. Following this, he began to complain of the disturbances of superficial and deep sensory below the ankle jerks and the weakness of his toes. Considering the clinical features, we supposed that the disturbance of the peripheral nerve was caused by uremia due to taking bromate. N. suralis was biopsied on the 80th day after the onset and examined electron microscopically. Electroscopical findings was as follows. Degeneration of the Schwann cells and irregularity or destruction of the myelin sheaths were observed. The axoplasm of the myelinated nerve fiber were relatively preserved as compared with the changes of the myelin sheaths. In the unmyelinated nerve fibers, cavity formations were observed. The findings of regeneration were not observed. From the electron microscopical findings, we speculate that the changes of the Schwann cells and the myelin sheaths are primary resulting from the disturbance of the metabolism of the Schwann cells. We speculate that anemia and hypoproteinemia caused by bromate disturbed regeneration.
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PMID:[Peripheral nerve disease associated with acute renal failure due to bromate poisoning]. 19 41

Since the introduction of the permanent peritoneal catheter, interest in chronic peritoneal dialysis is increasing. The automatic peritoneal dialysis cycler and the reverse osmosis peritoneal dialysis machine have been other development that made chronic peritoneal possible. Chronic peritoneal dialysis is indicated for the children, the elderly, those without hemodialysis access sites, those living along (for home dialysis) and the diabetics, whose retinopathy seems to progress less on peritoneal dialysis than on hemodialysis. Patients awaiting a kidney transplant can be maintained equally satisfactorily on peritoneal dialysis as on hemodialysis. Because of its simplicity almost any patient can be trained for home peritoneal dialysis, and a high incidence of rehabilitation can be achieved. A flow rate of 4 1/hr with 21 exchanges, 40 hours a week, seem to the ideal dialysis requirements. Complications of chronic peritoneal dialysis include those related to the permanent catheter such as one or two way obstruction and those related the dialysis itself. The latter can be either acute (i.e. peritonitis etc.) or chornic such as neuropathy, renal osteodystrophy, anemia etc. Integrated with hemodialysis and transplantation, peritoneal provides the nephrologists with the ability to treat his patients with the most appropriate treatment.
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PMID:Chronic peritoneal dialysis. 34 70

The unusual occurrence of microcytic anemia with hypochromia, high iron blood levels and excess of sideroblasts in the bone marrow, observed during the treatment of tuberculosis with isoniazid and rifampicine is reported. Three particularities were noted. First, in our experience, the occurrence of this type of anemia has never been noted previously as a result of these two drugs. Secondly, the improvement of the blood abnormalities was obtained by the combined use of vitamin B6 and vitamin C. Thirdly, the anemia was associated with neuropathy, characterized by areflexia and dysesthesia, which improved with vitamin B6 therapy (but not with vitamin C). Some mechanisms are discussed as being possibly the origin of this kind of anemia, particularly a lack of vitamin B6 resulting from a massive urinary loss of pyridoxal induced by isoniazid as well as both a tissue depletion and an overconsumption of this vitamin. The anemia may be the consequence of a deficiency of hemoglobin synthesis involving probably the first step of the biosynthesis of heme.
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PMID:[Anemia with hypersideroblastosis during anti-tuberculosis therapy. Cure with vitamin therapy]. 67 33

Fourteen adults in whom diabetes mellitus and coeliac disease coexist, are described. In no patient was coeliac disease diagnosed (biopsy proven) before the age of 28 years. Diabetes was recognized before coeliac disease in all except one. Diabetic control was very unstable and hypoglycaemia particularly troublesome before treatment with a gluten free diet. Following gluten restriction, insulin requirement increased in six patients, and diabetic control became more stable. Diarrhoea due to coeliac disease in a patient with coexisting diabetes, may be mistakenly diagnosed as 'diabetic diarrhoea'. However, certain clinical and laboratory features should arouse suspicion that the diarrhoea is not of diabetic origin. These included a history of gastrointestinal symptoms preceding the diagnosis of diabetes, the occurrence of repeated hypoglycaemia, absence of neuropathy, anaemia, low serum folate, low serum albumin and a malabsorption pattern on small bowel radiography. A definitive diagnosis of coeliac disease can be made only jejunal biopsy. The opportunity to diagnose coeliac disease in adult diabetics will usually fall to the diabetologist and wider use of jejunal biopsy in diabetics with chronic or recurrent diarrhoea is suggested.
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PMID:Diabetes mellitus and coeliac disease: a clinical study. 67 52

Ten dialysis patients were followed in a prospective study to determine the neurotoxicity of metabolites in the middle molecule (MM) molecular weight (mol wt) range of 500-200 daltons/molecule. In the absence of readily available direct serum measurements of MM concentrations, a theoretically calculated dialysis index, D1(MM), which included the combined effects of dialysis and residual glomerular filtration rate (GFR) on MM removal was used to estimate changes in their predialysis concentrations. The ten patients were dialyzed on protocols which yielded a D1(MM) less than 1.0. Evidence of uremic neuropathy developed in six of these ten patients, and five of these six also developed a progression in their anemia. Two additional patients with no signs of neuropathy developed a progression in their anemia. One patient developed pericarditis with tamponade. A total of eight patients developed complications. One additional patient developed increased weakness, tiredness and general malaise without change in objective findings. When the dialysis therapy to reduce MM concentrations by increasing the D1(MM) above 1.0 was instituted, the complications were reversed. Our data support the findings of others, namely, that there are toxic substances in the MM mol wt range of 500-2000 daltons/molecule. However, a synergism between elevated concentrations of small molecules and MM cannot be ruled out.
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PMID:Uremic neuropathy: evidence of middle molecule toxicity. 68 20

Two cases of lead arsenate polyneuropathy are described in two farmers from the same rural area; the etiology of the neurologic al disorder was ascertained only after repeated hospital admissions. It was a neuropathy of the radial nerve associated with signs of peripheral impairment of the lower limbs with pains and paresthesias. Abdominal colies, arterial hipertension, anaemia and signs of renal impairment were also present. Specific therapy was undertaken which was soon followed by nearly full recovery. Lead and arsenic toxicology are discussed with particular focusing on the necessity emphasis on commun occupational hazards both in terms of diagnostic and therapeutic procedures. The differential diagnosis is considered between the observed clinical picture and other polyneuropathies of different etiology i.e. dysmetabolic (porphyria) or toxic (insecticides, T.O.C.P., etc).
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PMID:[Lead arsenate as an underestimated cause of polyneuropathy in rural environment: description of two cases]. 102 47

Given the high morbi-mortality of foot infections among the diabetics and the poor knowledge of their predictive, clinical and evolutive factors, we have retrospectively studied a group of patients with these characteristics, comparing them with infections among diabetics affecting other locations. We studied 66 infections among diabetics: 34 patients with diabetic's foot and 32 with infections at other locations: 20 pyelonephritis and 12 pneumonias. Medical records were obtained in all cases and all patients underwent a complete physical exploration in order to assess their risk factors. We observed as a significant predictive factor of diabetic's foot, diabetes type I, with an evolution longer than 10 years, neuropathy, vasculopathy or retinopathy. From the clinical point of view and compared with the other infections, these patients showed longer hospitalization, greater initial clinical severity, glucemias higher than 200 mgr/l., anemia and high GSR. Ethiologically, the infection of diabetic's foot was polymicrobian in 42.3% of all cases, being S. aureus the microorganism more frequently isolated. On the contrary, in infections at other locations, monomicrobian flora was more frequent, being E. coli the most frequent in pyelonephritis and S. pneumoniae in pneumonias. The evolution was satisfactory in all cases, with a close medical and surgical combined treatment and the appropriate use of antibiotic combinations, mainly clindamicine + tobramicine in the diabetic's foot and cefuroxime in the other locations.
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PMID:[Infections in the diabetic. Comparative study of infections in the foot and other locations]. 139 75

Forty-five patients with metastatic neuroendocrine tumors were treated with a regimen of etoposide 130 mg/m2/d for 3 days plus cisplatin 45 mg/m2/d on days 2 and 3. Both drugs were given by continuous intravenous infusion. Among 27 patients with well-differentiated carcinoid tumors or islet cell carcinomas, only two partial objective tumor regressions were observed (7%). Among 18 patients prospectively classified as having anaplastic neuroendocrine carcinomas, however, there were nine partial regressions and three complete regressions, an overall regression rate of 67%. For anaplastic disease, the median duration of regression was 8 months (range to 21 months). Tumor response was unrelated to primary site, endocrine hyperfunction, or prior therapy experience. The median survival of all patients with anaplastic tumors was 19 months; this seemed favorable when considering the small experiences with these rare tumors reported in the literature. Toxicity, which was severe for most patients, consisted primarily of vomiting, leukopenia, thrombocytopenia, anemia, alopecia, and neuropathy. The anaplastic neuroendocrine tumor is strongly responsive to therapy with combined etoposide and cisplatin. Patients with undifferentiated carcinomas, originating in typical neuroendocrine tumor sites (small and large bowel, pancreas, and stomach) or of unknown origin, who have consistent histologic findings by light microscopy should be evaluated for this possibility with appropriate immune staining or electron microscopy.
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PMID:Treatment of neuroendocrine carcinomas with combined etoposide and cisplatin. Evidence of major therapeutic activity in the anaplastic variants of these neoplasms. 171 61

We systematically evaluated muscular weakness in a series of patients with systemic lupus erythematosus (SLE) using standardized neurological scoring systems, namely Neuropathy Symptom Score for symptoms, and Neurological Disability Score for signs. Symptoms of weakness were statistically associated with clinical and electrophysiological evidence of nerve and muscle disease. Signs of weakness were statistically associated with malaise, disease activity, anemia, age, and raised erythrocyte sedimentation rate. Various disease associated variables influenced symptoms and signs differently. It is important to define a baseline characterizing muscular weakness in SLE before conclusions are drawn regarding its significance and prevalence.
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PMID:Muscular weakness in systemic lupus erythematosus. 175 38

Cold agglutinin disease (CAD) characteristically presents as anemia and cold-induced rash. We report a man with purpura, anemia, cold agglutinins, and a sensory-autonomic polyneuropathy. Treatment with corticosteroids and plasma exchange resulted in resolution of the anemia and polyneuropathy. We propose that CAD may be associated with a reversible sensory-autonomic neuropathy in the absence of cryoglobulinemia. Although unsupported by pathologic findings, pathogenetic hypotheses for the neuropathy in CAD are similar to those proposed for cryoglobulinemic neuropathy.
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PMID:Peripheral neuropathy in cold agglutinin disease. 185 Dec 46


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