Acute alcoholic myopathy, rhabdomyolysis and acute renal failure: a case report.
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A case of middle aged male who developed swelling and weakness of muscles in the lower limbs following a heavy binge of alcohol is being reported. He had myoglobinuria and developed acute renal failure for which he was dialyzed. Acute alcoholic myopathy is not a well recognized condition and should be considered in any intoxicated patient who presents with muscle tenderness and weakness. (+info)
Impaired stimulation of intestinal glucose absorption by portal insulin via hepatoenteral nerves in chronically ethanol-intoxicated rats.
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In the isolated, jointly perfused small intestine and liver of rats insulin, infused into the portal vein, induced an increase in intestinal glucose absorption via hepatoenteral cholinergic nerves. The possible loss of function of these nerves due to ethanol-induced neuropathy was investigated with 6 weeks ethanol-fed rats. Portal insulin or arterial carbachol failed to increase intestinal glucose absorption but cAMP still did so. The intact stimulatory effect of cAMP indicated an undisturbed capacity of the enterocytes. The loss of action of portal insulin and of arterial carbachol can be explained by the impairment of the hepatoenteral nerves in line with an ethanol-induced neuropathy. (+info)
Key role for the epsilon isoform of protein kinase C in painful alcoholic neuropathy in the rat.
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Chronic alcohol consumption produces a painful peripheral neuropathy for which there is no reliably successful therapy, attributable to, in great part, a lack of understanding of the underlying mechanisms. We tested the hypothesis that neuropathic pain associated with chronic alcohol consumption is a result of abnormal peripheral nociceptor function. In rats maintained on a diet to simulate chronic alcohol consumption in humans, mechanical hyperalgesia was present by the fourth week and maximal at 10 weeks. Thermal hyperalgesia and mechanical allodynia were also present. Mechanical threshold of C-fibers in ethanol fed rats was lowered, and the number of action potentials during sustained stimulation increased. The hyperalgesia was acutely attenuated by intradermal injection of nonselective protein kinase C (PKC) or selective PKCepsilon inhibitors injected at the site of nociceptive testing. Western immunoblot analysis indicated a higher level of PKCepsilon in dorsal root ganglia from alcohol-fed rats, supporting a role for enhanced PKCepsilon second-messenger signaling in nociceptors contributing to alcohol-induced hyperalgesia. (+info)
Alcoholic polyneuropathy: a clinical and epidemiological study.
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In the present study, we investigated the frequency of polyneuropathy in a sample of 296 alcoholics who were admitted to the 'S. Maugeri' Medical Centre for detoxification from October 1997 to November 1999. Results revealed a high frequency of polyneuropathy in the sample under study. The disorder was often clinically asymptomatic and demonstrable only on electroneurographic investigation. Significant correlations were found between polyneuropathy, the duration of alcoholism, the type of alcoholic beverage consumed (wine) and the presence of liver disease and macrocytosis. (+info)
Current perception threshold and sympathetic skin response in diabetic and alcoholic polyneuropathies.
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OBJECTIVE: Correlation between current perception threshold and sympathetic skin response was investigated in patients with diabetic or alcoholic polyneuropathy. METHODS: Current perception threshold was measured using Neurometer CPT/C, and the sympathetic skin response was measured using Neuropack sigma. PATIENTS: Fourteen patients with diabetic polyneuropathy and 10 patients with alcoholic polyneuropathy were studied. RESULTS: There was a significant negative correlation between the current perception threshold to 5 Hz stimulation and the amplitude of sympathetic skin response. CONCLUSION: Since both current perception threshold to 5 Hz stimulation and sympathetic skin response are related to C fibers, these two are considered to be impaired concurrently in diabetic and alcoholic polyneuropathies. (+info)
Resolution of alcoholic neuropathy following liver transplantation.
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Between 10 and 20% of adult liver transplants are performed for end-stage alcoholic liver disease. Severe extrahepatic end-organ damage from alcoholism (cardiomyopathy, pancreatitis, central nervous system injury, and neuropathy) is widely regarded as an absolute contraindication to liver transplantation, despite a lack of data on the effect of transplantation on these complications. We describe such a patient who presented with decompensated alcoholic liver disease and moderately severe peripheral neuropathy. Both his liver failure and neuropathy progressed despite 9 months abstinence and intensive nutritional support. By 12 months post-transplant, however, this patient had regained almost normal muscle strength, with associated recovery in sensory and motor conduction velocities. Direct alcohol toxicity, nutritional and vitamin deficiencies, and liver failure were all likely etiologic factors in this patient's neuropathy. In conclusion, this case suggests that peripheral neuropathy in a patient with alcoholic cirrhosis may resolve following liver transplantation and should not constitute a contraindication to transplantation, even when it is disabling. (+info)
Lhermitte's sign in alcoholic myelopathy without portosystemic shunting: MRI evaluation.
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We conducted spinal MR imaging on a 35-year-old man with Lhermitte's sign that had manifested over the previous 4 years. He had consumed more than 500 ml of whisky daily for at least 10 years. However, he did not show any evidence of severe liver disease with hepato-systemic blood shunting. Neurologic examination revealed markedly depressed sense of vibration in the feet and mild spasticity in the lower limbs, together with Lhermitte's sign. MR imaging revealed abnormal signal intensity in the posterior column spanning the whole length of the upper cervical cord, which is consistent with Lhermitte's sign. (+info)
Treatment of alcoholic polyneuropathy with vitamin B complex: a randomised controlled trial.
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AIMS: To evaluate the therapeutic efficacy and safety of BEFACT Forte 'new formulation' and BEFACT Forte 'old formulation' in the treatment of sensory symptoms of alcoholic polyneuropathy. METHODS: A multi-centre, randomised, double-blind, placebo-controlled study was conducted on 325 patients with sensory symptoms and signs of alcoholic polyneuropathy. Patients were randomised to the 'old formulation' (i.e. vitamins B1, B2, B6, and B12), 'new formulation' [i.e. identical to the 'old formulation' with additional folic acid (vitamin B9)], or placebo in a 1:1:1 ratio. One tablet of the study medication ('new formulation' or 'old formulation') or placebo was taken orally, three times a day, over a 12-week treatment period. RESULTS: Therapeutic efficacy was assessed in 253 patients by measuring vibration perception threshold (biothesiometry), intensity of pain, sensory function, co-ordination, and reflex responses. Patients treated with the 'new formulation' or 'old formulation' showed significant improvement in the primary efficacy endpoint (vibration perception threshold at the big toe) and secondary efficacy endpoints in comparison to placebo. The active treatment groups were comparable to placebo in terms of safety. CONCLUSIONS: A specific vitamin B complex (with and without folic acid) significantly improved symptoms of alcoholic polyneuropathy over a 12-week treatment period. (+info)