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)

Dapsone proved to be effective treatment in a patient who suffered from erthema elevatum diutinum. Serious neurological side effects, however, appeared. The basic mechanism appeared to be a distal axonal degeneration of the motor neurons. Sensory conduction studies were normal in five consecutive EMG examinations. A diagnosis of anemia pernicosa was also made bu the blood values returned to normal after starting B12-vitamin therapy. Penicous anemia seemed not be an etiological factor in the polyneuropathy of our patient because we were not able toshow any damage to the sensory axons.
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PMID:Dapsone-induced distal axonal degeneration of the motor neurons. 65 72

A 51-year-old man, taking beverage containing inorganic germanium (Ge), (90-100 mg/day, total 70 g) for two years, developed body weight loss, anemia, renal dysfunction, peripheral neuropathy, myopathy, autonomic dysfunctions and multiple cranial nerve palsies. Serum CK, GOT, LDH, BUN, and creatinine levels were elevated. The cerebrospinal fluid showed albumino-cytologic dissociation. Sural nerve biopsy showed axonal degeneration, and peroneal muscle biopsy showed neurogenic changes including type 2 fiber atrophy and ragged red fibers. High level of Ge content was detected from the hair and nail by inductively coupled plasma atomic emission spectrometry. Despite discontinuation of Ge taking, the peripheral neuropathy and autonomic dysfunction progressed. The symptoms remained unchanged even in the treatment with prednisolone. These findings suggest that inorganic Ge has a serious irreversible multiple system toxicity.
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PMID:[A case of inorganic germanium poisoning with peripheral and cranial neuropathy, myopathy and autonomic dysfunction]. 217 40

A 40-year-old woman developed neuropathy and myelopathy with vitamin B12 deficiency without anemia. Motor and sensory nerve conduction velocities were moderately decreased. Sural nerve biopsy showed the coexistence of demyelination and axonal degeneration.
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PMID:Vitamin B12 deficiency neuropathy: sural nerve biopsy study. 357 Jul 38

A 36 year old woman was admitted to the hospital in November 1983 because of her inability to walk. For 3 months prior to admission, she took oral contraceptives (OCs) as a treatment for amenorrhea. 2 months prior to admission, she had general malaise, anorexia, and unsteady gait. 1 month before her admission, tingling and numbness began in the fingertips and spread up to the forearms, a tight feeling around the waist developed, and walking became ataxic. On admission to the hospital, she was thin and pale with greying hair. Her mind was clear and there were no abnormalities of the cranial nerves. Her extremities were hypotonic but not wasted. Slight muscle weakness of the hands and feet was noted. There was myokymia in both legs. Deep tendon reflexes of the extremities were absent. The plantar responses were extensor and lack of coordination in the extremities was noted. There was a definite glove and stocking type of hypesthesia to pinprick and cotton wool. Vibration sense was decreased below T11 and lost in both legs. There was a marked loss of position sense to passive movement in the legs and some impairment in the hands. Laboratory examination revealed mild magaloblastic anemia, elevated LDH, borderline low concentration of vitamin B12 in the serum, increased excretion of methylmalonate in the urine, achylia, positive antiparietal cell antibody and positive anti-intrinsic factor antibody. Cyanocobalamin absorption by the Schilling test was 5.6% after intrinsic factor, 11.3%. The diagnosis of pernicious anemia was made. Upper gastrointestinal studies showed typical carcinoid tumors of the stomach. Cerebrospinal fluid was normal. Peripheral nerve conduction studies demonstrated normal or slightly decreased motor conduction velocities and absent sensory action potential. Sural nerve biopsy was performed. Myelinated fibers were moderately decreased in number to 5554/mm squared and pronounced loss of large myelinated fibers was demonstrated in fiber histogram. Teased method of the single fiber showed mainly axonal degeneration. Anemia and neurologic function improved rapidly with parenteral hydroxocobalamin therapy and 1 month after treatment commenced, she was able to walk without assistance. The clinical significance of peripheral nerve involvement of subacute combined degeneration of the spinal cord was discussed, as the peripheral nerve affection is only poorly understood in contrast to the myelopathy. This was followed by discussion of the possible effect of the OCs and gastric carcinoid to neurological manifestation of pernicious anemia. (author's modified)
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PMID:[Subacute combined degeneration of spinal cord. Significance of peripheral nerve involvement]. 401 64

A neuropathological examination was performed on a patient with parkinsonism induced by prolonged exposure to a mixture of aliphatic hydrocarbons, mainly n-hexane and halogenated compounds. The patient developed a rapid-course disease that progressed even after withdrawal from the toxic exposure. Pathological examination and immunohistochemical analysis of the brain revealed severe and widespread dopaminergic neuronal loss, associated with severe gliosis, in the substantia nigra, and almost complete loss of tyrosine hydroxylase immunostaining in the striatum. No Lewy bodies were detected. Neuronal loss was also observed in the periaqueductal gray matter, locus ceruleus, and pedunculopontine nucleus. These changes, combined with the moderate anemia due to marrow suppression, and the mild axonal neuropathy observed in vivo, are suggestive of a hydrocarbon toxic insult.
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PMID:Clinical and pathological features in hydrocarbon-induced parkinsonism. 900 99

Hearing loss is a common finding in patients with end-stage renal failure. Uremic toxins, ototoxins, and axonal uremic neuropathy appear to be likely pathogenic factors. We analyzed whether an improvement in hearing capacity can be achieved with an improvement of anemia by erythropoietin (EPO) administration. Fifty patients on long-term hemodialysis in a single center were examined audiologically by otoscopy, tympanometry, pure tone audiometry, and the short increment sensitivity index. Twenty-five patients were treated with EPO in a dose of 120 U/kg per week over a period of 5 to 8 months, and the remaining 25 patients were not treated with EPO (controls). Both groups were reexamined audiologically after the study period, and the results were compared. In the group treated with EPO, the hemoglobin level increased from 7 +/- 0.9 to 11 +/- 0.8 g/dL, as against the control group, whose hemoglobin increased from 7.1 +/- 0.9 to 8 +/- g/dL. The audiologic tests were repeated at the end of the study period, and a significant improvement of hearing was found in the patients treated with EPO as compared with the control group (p < .001). Our study suggests that improvement of anemia in patients on long-term hemodialysis by administration of EPO is associated with an improvement in hearing capacity in a significant number of patients. Thus, anemia seems to be an important factor responsible for hearing disorders in patients with end-stage renal failure. Studies with larger numbers of patients are required to confirm this observation.
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PMID:Reversible uremic deafness: is it correlated with the degree of anemia? 915 3

This is a case report of a twenty-five years old man who developed, due to lead intoxication, a severe axonal peripheral predominantly motor neuropathy, after a shotgun injury. The projectile was retained in the right hip. Before this diagnosis had been done he was treated with corticosteroids in immunosuppressive doses and showed an improvement, but he had worsened at each attempt to interrupt the drug. Because he had also other signs of lead intoxication, such as abdominal cramps, severe anemia and seizures it was search for the blood levels of lead that was 101.2 micrograms/dl. The patient was treated with calcium disodium edetate and surgical removal of lead fragments. After that he had a good outcome with no need of corticosteroids. It is emphasized the possible relevance of the immune system on the mechanism of plumbic intoxication and the importance of the withdrawal of the lead material retained in joints.
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PMID:[Possible role of the immune system in lead peripheral polyneuropathy. Case report]. 933 73

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

Folic acid (folate) levels were measured in the serum of patients with various neurological diseases in Japan. Thirty-six patients showed decreased serum folate levels among 343 consecutive neurological patients (10.5%). Folate administration (15 mg/d) to folate-deficient patients improved neurological symptoms in 24 of 36 cases (67%). Serum folate levels were significantly lower in female than in male folate-deficient patients. Folate-deficient patients showed predominantly axonal neuropathy, which responded to folate supplementation more markedly. Male patients more frequently exhibited neuropathy, especially demyelinating and motor-dominant neuropathy, than females. Anemia was correlated with male sex and low serum folate levels. Male patients were more responsive than females to folate treatment. More male patients had taken excess alcohol or received gastrectomies than females. Neurological symptoms were more frequently improved by folate supplementation in patients with neuropathy than exclusive encephalopathy. Serum folate levels were lower in patients with encephalopathy, especially those with dementia, while folate therapy was more effective in neurological patients without dementia. Dysgeusia and anemia improved in all patients after folate administration. Neurological patients with malabsorption or treated with continuous drip infusion were resistant to folate therapy. Since folate-responsive neuroencepahlopathies are not rare among patients with neurological diseases in Japan, the serum folate level would serve as a valuable indicator for folate supplement therapy.
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PMID:Folic acid-responsive neurological diseases in Japan. 1157 72

In this report it is demonstrated for the first time that rabies-G envelope of the rabies virus is sufficient to confer retrograde axonal transport to a heterologous virus/vector. After delivery of rabies-G pseudotyped equine infectious anaemia virus (EIAV) based vectors encoding a marker gene to the rat striatum, neurons in regions distal from but projecting to the injection site, such as the dopaminergic neurons of the substantia nigra pars compacta, become transduced. This retrograde transport to appropriate distal neurons was also demonstrated after delivery to substantia nigra, hippocampus and spinal cord and did not occur when vesicular stomatitis virus glycoprotein (VSV-G) pseudotyped vectors were delivered to these sites. In addition, peripheral administration of rabies-G pseudotyped vectors to the rat gastrocnemius muscle leads to gene transfer in motoneurons of lumbar spinal cord. In contrast the same vector pseudotyped with VSV-G transduced muscle cells surrounding the injection site, but did not result in expression in any cells in the spinal cord. Long-term expression was observed after gene transfer in the nervous system and a minimal immune response which, together with the possibility of non-invasive administration, greatly extends the utility of lentiviral vectors for gene therapy of human neurological disease.
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PMID:Rabies virus glycoprotein pseudotyping of lentiviral vectors enables retrograde axonal transport and access to the nervous system after peripheral delivery. 1159 Jan 28


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