Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0031117 (peripheral neuropathy)
 10,577 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The nitro radiosensitizers, metronidazole and misonidazole, have been shown to react rapidly with the sulphydryl compounds cysteine and cysteamine in the presence of ferrous ions. Similar reactions occur in the presence of copper ions but these are much slower. The initial interactions of the drugs and of oxygen with an iron-cysteine complex are extremely rapid: in the case of oxygen reaction half-lives of 27 ms have been measured. Misonidazole also reacts rapidly with glutathione in the presence of ferrous ions and is subsequently reduced: metronidazole is reduced only slowly if at all. These reactions, which have been found to be inhibited by high concentrations of zince ions, are discussed in the light of the known radiosensitizing and chemotherapeutic efficiencies of the nitro drugs and the side effect of peripheral neuropathy sometimes observed during their clinical use.
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PMID:Metronidazole (Flagyl), misonidazole (Ro 07-0582), iron, zinc and sulphur compounds in cancer therapy. 27 18

Twenty-six uremic patients - serum urea nitrogen (SUN) 110 MG/100 ml plus or minus 22.8 (mean plus or minus SD), serum cretinine (S-Creat) 13.2 mg/100 ml plus or minus 2.27, ratio SUN/S-Creat 8.6 plus or minus 2.26, and endogenous creatinine clearance (Ccr) 3.86 plus or minus 1.41 ml/min - were treated for three months or longer with an unselected protein-poor (16-20 g protein/day) diet with oral supply of the essential amino acids including histidine in high doses as coated tablets. The amino acids were instituted after an initial diet only period (mean 0.4 months). The average treatment time was 8.4 months (range 2.7-33.6). An improvement of the general condition was obtained, persisting for several months. SUN and SUN/S-Creat decreased on the diet alone, continued to decrease after one month, and increased slightly again after three months of treatment, but did not reach the initial levels for several months in spite of an almost doubled nitrogen intake. S-Creat increased after six months indicating a further deterioration of the renal function. In patients with initially low serum total protein (smaller than 6.5 g/100 ml, 9 patients), albumin (smaller than 3.5 g/100 ml, 10 patients), and total iron-binding capacity (smaller than 260 mug/100 ml, 11 patients) the values increased after one month on amino acids and were thereafter stable. No signs of bleeding tendency, progressive muscle atrophy, or progressive peripheral neuropathy were observed. - Five patients died due to cardiovascular maladies. A further 13 patients were withdrawn for medical reasons (overhydration, 4 patients; hypertension, 1 patient; nausea and vomiting, 7 patients; and pericarditis, 1 patient). - The renal function improved in one patient. Four patients received home dialysis training, three a kidney transplant. - The results indicate that it is possible to keep severely uremic patients free from uremic symptoms, counteract protein depletion, and even improve the nutritional status during long-term treatment with an unselected protein-poor diet supplementd with essential amino acids.
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PMID:Treatment of chronic uremic patients with protein-poor diet and oral supply of essential amino acids. II. Clinical results of long-term treatment. 114 44

Magnetic resonance (MR) imaging of a case of Hallervorden-Spatz disease (HSD) using a 1.5 T system is described. The patient showed progressive spastic diplegia with equinovarus deformity of the feet, dystonic postural movements, dysarthria, dysphagia, mental deterioration, optic nerve atrophy, and peripheral neuropathy. These clinical features were compatible with HSD. Symmetrical, decreased signal intensity was seen on both proton density weighted and T2-weighted spin echo images in the globus pallidus as well as in the substantia nigra (Group I). This MR finding suggests an increased iron deposition in these subcortical nuclei, which is characteristic of HSD. The characteristic MR imaging, together with the relevant clinical features, was considered to be useful for establishing the diagnosis of HSD.
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PMID:MR imaging of a group I case of Hallervorden-Spatz disease. 317 Aug 46

Idiopathic hemochromatosis (IHC) is a genetically determined impairment in control of iron absorption that results in excessive parenchymal iron deposition, particularly in the liver. Of patients with IHC, 50% have little or no chemical evidence of liver dysfunction. Cirrhosis may be clinically occult, but still cause a syndrome of chronic hepatocerebral degeneration. Two patients are reported with IHC and a syndrome of ataxia, rigidity, myoclonic jerks, and dementia. Other associated symptoms may include diminished libido, decreased hearing, peripheral neuropathy, and large joint disease. Because symptoms of IHC can be reversed by phlebotomy, appropriate laboratory studies should be considered to exclude IHC in any patient with unexplained dementia, encephalopathy, and gait ataxia.
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PMID:Idiopathic hemochromatosis (IHC): dementia and ataxia as presenting signs. 668 41

We retrospectively studied magnetic resonance (MR) images of the brain in 139 patients (16 cases of Alzheimer's disease, 8 cases of Parkinson's disease, 53 cases of multiple cerebral infarct, 33 cases of other central nervous diseases, and 29 cases of peripheral neuropathy) between the age of 6 and 85 years old with a mean age of 60.6 +/- 18.5 to examine the appearance of T2 low signal intensity areas (T2CLIA) in the cerebral cortex. Motor, occipital, sensory or other cortices were evaluated with long repetition time/echo time (TR/TE) spin-echo sequences and staged into three grades in the motor cortex: none, partial, and whole; and two grades in the others: none or present. In general, T2CLIA was not seen in any cortex in patients less than 50 years old, then after 50 years old T2CLIA increased with age. Over 70 years of age T2CLIA appeared in 50.9% of patients in the whole motor cortex, 88.7% in either whole or partial motor cortex, 47.2% in the occipital cortex, and 20.8% in the sensory cortex. T2CLIA was not observed in other cortices. The incidence of T2CLIA appearance in the motor cortex was significantly higher in all central nervous diseases than in cases of peripheral neuropathy over 70. T2-CLIA showed a correlation with temporal lobe atrophy and white matter lesions in the motor cortex. In the sensory cortex, T2CLIA correlated with white matter lesions. These results suggest that T2-CLIA may correlate with age or accumulation of nonheme iron in the cortex associated with central nervous diseases.
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PMID:[The effect of age and disease on the MR imaging T2 low signal intensity area in the cerebral cortex]. 782 5

Deficiency symptoms of trace elements developed in patients receiving long-term total parenteral nutrition (TPN) are as follows. [Zinc deficiency]: moist eczematoid dermatitis and alopetia are occurred in patients receiving TPN which not containing zinc. Plasma zinc level was very low. The response to intravenous zinc therapy is striking. [Copper deficiency]: anemie and neutropenia caused in patients receiving TPN which not containing copper. These abnormalities disappeared after copper therapy. [Manganese deficiency]: bone changes which thought to be due to manganese deficiency was observed in patient receiving TPN. [Selenium deficiency]: dilated cardiomyopathy resembles to Keshan disease was occurred in patients receiving TPN for long term. [Chromium deficiency]: TPN induced chromium deficiency developed characterized by peripheral neuropathy and glucose intolerance. [Molybudenum deficiency]: Amino acid intolerance due to molybudenum deficiency is occurred in patients receiving TPN. Requirement of trace elements for human adults from TPN estimated as follows. zinc: 3-4 mg/day, copper: 0.02-0.05 mg/day, iron: 1-2 mg/day, manganese: 0.15-0.80 mg/day, selenium: 0.02-0.05 mg/day, chromium: 0.01-0.015 mg/day, molybudenum: 0.075-0.250 mg/day and iodine: 0.070-0.140 mg/day.
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PMID:[Trace elements in long-term total parenteral nutrition]. 858 86

The cerebral cortex of patients with Alzheimer's disease (AD) or amyotrophic lateral sclerosis (ALS) may show low signal intensity on T2-weighted magnetic resonance images (MRI). Since these low intensity areas (LIA) are also often observed in aged patients with other diseases, we suspected that they might be a non-specific finding. We conducted a retrospective study of LIA in 139 patients with various diseases of the central and peripheral nervous systems, and evaluated their relationship to age and other MRI findings. Brain atrophy, ventricular dilatation, white matter lesions, and LIA were visually evaluated on axial images of the spin echo sequences obtained with a 1.5 tesla (T) system. We found that LIA appeared after age 50 and became more common with advancing age. Their presence correlated with brain atrophy and white matter lesions. They were most frequent in the motor cortex, followed by the occipital and sensory cortices. Their incidence in the motor cortex was significantly higher in patients with central nervous system diseases than in those with peripheral neuropathy. We conclude that LIA are common in old patients with various neurological diseases and suggest that the deposition of iron in the cerebral cortices causes their development.
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PMID:Low intensity areas observed on T2-weighted magnetic resonance imaging of the cerebral cortex in various neurological diseases. 884 42

Soft tissue haemorrhage in the foot is a possible precursor of ulceration in patients with diabetic peripheral neuropathy. High resolution 'targetted' magnetic resonance imaging was used to scan the forefoot. Neuropathic patients with and without previous ulceration were matched for degree of neuropathy, mean vibration perception threshold 33.5 +/- 4.2 V (previous ulcer) vs 31.0 +/- 6.9 V (no ulcer), age, sex, and duration of diabetes against non-neuropathic controls. There were nine patients in each category. Paramagnetic materials, e.g. iron compounds, cause a signal void ('drop-out') on gradient-echo images which disappear on spin-echo images. Evidence of haemorrhage was seen in 6 patients with previous ulceration, and none in the other groups (p = 0.009, chi square test). Autologous injection of 20 microliters of blood into the foot of a healthy volunteer produced similar images, a 'drop-out' 1 cm across being visible on magnetic resonance scanning 3 days later. Peak vertical forefoot pressures were not significantly different in the neuropathic groups 0.67 +/- 0.20 vs 0.60 +/- 0.13 Pa but were lower in the non-neuropathic group, 0.43 +/- 0.11 Pa (p = 0.0004, Mann-Whitney), and do not explain the appearance of these haemorrhages. Magnetic resonance imaging provides a sensitive way of detecting micro-haemorrhage and its presence may predict an increased risk of foot ulceration.
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PMID:Magnetic resonance imaging reveals micro-haemorrhage in the feet of diabetic patients with a history of ulceration. 894 56

People with diabetes are prone to develop peripheral vascular and nerve abnormalities which, in extreme cases, can lead to limb amputations. Although numerous theories have been advanced for these complications, no firm explanation is yet available. Recently, evidence has appeared suggesting that these vascular and nerve abnormalities may involve transition metals; administration of chelators such as desferrioxamine has been shown to prevent or actually reverse slowed peripheral nerve conduction and neuronal blood flow, as well as impaired endothelium-dependent arterial relaxation. Here, we argue that (i) the heavily glycated proteins known to accumulate in people with diabetes gain an increased affinity for transition metals such as iron and copper, (ii) as a result, proteins such as elastin and collagen within the arterial wall-which are known to be particularly heavily glycosylated in diabetes-may accumulate bound metal, especially copper, (iii) the bound metal causes the catalytic destruction of endothelium derived relaxing factor (nitric oxide or a derivative thereof), thereby engendering a state of chronic vasoconstriction. The resulting impairment of blood flow to peripheral nerves restricts the delivery of oxygen and nutrients and, in extremis, nerve death eventuates. If this hypothesis is proved correct, there are important implications for the development of novel pharmaceuticals for the treatment of diabetic peripheral neuropathy.
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PMID:Glycochelates and the etiology of diabetic peripheral neuropathy. 1071 47

Restless legs syndrome (RLS) is a perplexing, debilitating, and fairly common condition that can be challenging to manage. Hallmark symptoms include an increase in the severity of sensations during rest and an irresistible urge to move the affected limbs. RLS often occurs concomitantly with periodic limb movement disorder. There are no known causes of RLS, but likely triggers include heredity, iron and vitamin deficiencies, caffeine, and alcohol. Chronic conditions such as diabetes, peripheral neuropathy, and Parkinson's disease can worsen and prolong RLS symptoms. Symptom management begins by establishing proper nutrition intake and improved sleep hygiene. If these fail, conservative pharmacologic treatment is appropriate, with regimens chosen from dopaminergic agents, benzodiazepines, opioids, and anticonvulsants.
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PMID:Restless legs syndrome. How to provide symptom relief with drug and nondrug therapies. 1077 1


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