Clinical and electrodiagnostic follow-up of an adolescent poisoned with thallium.

We report a six-year clinical and electrodiagnostic follow-up of an adolescent patient with acute thallium poisoning from attempted suicide. During the acute stage the patient showed gastrointestinal disturbances, alopecia, and clinical and electrodiagnostic signs of severe polyneuropathy. Three years after poisoning, his neurological symptomatology was making progress, and electrophysiologic signs of peripheral neuropathy were mainly confined to lower limbs. Six years after intoxication, he was still complaining of weakness and sensory disturbances at the level of distal lower extremities; his neurologic and electrodiagnostic abnormalities affected mainly the feet. In this case report we underline the importance of early diagnosis and treatment to prevent neurological damage and the role of serial electromyographic and nerve conduction studies in thallium poisoning. These investigations allowed the authors to depict the electrophysiologic course of peripheral nervous system involvement over six years following poisoning.

Peripheral neuropathy in chronic alcoholism: a retrospective cross-sectional study in 76 subjects.

A consecutive sample of 76 chronic alcoholic patients was studied clinically, biochemically and electrophysiologically to assess clinical and/or subclinical signs of alcohol-related neuropathy as well as the most important and disputed risk factors for neuropathy such as age, parental history of alcoholism, nutritional status, alcoholic disease duration and total lifetime dose of ethanol (TLDE). The results show that alcohol-related neuropathy, especially when subclinical, seems to be frequent and mostly characterized by axonal degeneration of peripheral nerve fibres with earlier and more frequent involvement of sensory fibres and lower limbs. Moreover, positive family history of alcoholism, but above all alcoholic disease duration and TLDE, could be more important factors than malnutrition in determining neuropathy.

Gender and peripheral neuropathy in chronic alcoholism: a clinical-electroneurographic study.

In some alcohol-related pathologies of chronic alcoholism women are more vulnerable than men. A consecutive sample of 62 chronic alcoholics was studied, 18 females and 44 males, aged between 28 and 69 years to assess the incidence and distribution of peripheral neuropathy with regard to gender. All patients underwent clinical and neurological observations, laboratory tests, and electroneurography. Total lifetime dose of ethanol (TLDE) and other risk factors for neuropathy (disease duration, age, nutritional status) were calculated and correlated to sural nerve sensory-evoked potential (SEP) amplitude. In 42 patients (67.7%), we observed the presence of clinical and/or infraclinical neuropathy, mostly axonal, in 29 males (65.9%) and 13 females (72.2%). In women, compared to men, TLDE and disease duration were significantly inversely correlated to sural nerve SEP amplitude, i.e. in women, SEP amplitude is significantly reduced in relation to TLDE and disease duration increase. These data indicate a higher sensitivity of females towards the toxic effects of ethanol, other than malnutrition, on peripheral nerve fibres.

Determination of plasma alpha-glutathione-S-transferases in chronic alcohol abusers: relationship with alcohol intake and liver involvement.

UNLABELLED: Alpha-gluthathione-S-transferases (alpha-GSTs) are enzymes involved in the cellular detoxifying processes; elevated circulating alpha-GSTs activity is considered to be an early index of liver damage. Glutathione (GSH) is the substrate for alpha-GST action. THE AIMS OF OUR STUDY WERE: (1) to evaluate plasma GSH levels and alpha-GST activity in chronic alcohol abusers with or without liver cirrhosis; (2) to define the relationship between these two biochemical parameters; (3) to establish their clinical relevance in patients with alcohol abuse and/or liver damage. We studied 69 subjects (18 healthy subjects and 51 chronic alcohol abusers: 29 without liver cirrhosis and 22 with). Plasma alpha-GST activity was determined on baseline samples and every following day for a total of 10 days in five alcoholics by HEPKIT (Alpha-Biotech, Biotrin International, Dublin, Ireland). GSH was determined on all subjects' baseline samples by fluorescent high-performance liquid chromatography. Alcohol intake was evaluated in all patients by determining blood-alcohol concentrations. Significant increases in plasma alpha-GSTs were observed in 9/29 (31%) alcoholics and 3/22 (13.6%) cirrhotics irrespective of their alcohol intake. GSH was significantly lower than normal values (P < 0.001) in all alcoholics with or without cirrhosis (controls 10.4 +/- 4.8; alcoholics without cirrhosis 3.9 +/- 1.4; alcoholics with cirrhosis 3.3 +/- 1.6). No correlation was observed between plasma alpha-GST and GSH levels. Our data indicate that: (1) alpha-GST activity does not correlate with GSH levels in the plasma; (2) alpha-GSTs do not have clinical relevance as markers of recent alcohol intake; (3) in cirrhotics, alpha-GST does not provide more information than other liver function tests. However, plasma alpha-GST determination may be useful in selecting a subgroup of alcoholics in whom routine biochemical markers of liver damage are within reference ranges.

Free radicals and not acetaldehyde influence the circulating levels of glutathione after acute or chronic alcohol abuse: in vivo and in vitro studies.

BACKGROUND: The oxidation of ethanol and acetaldehyde enhances the production of various free radicals involved in membrane lipoperoxidation, and decreases glutathione levels. AIMS: We evaluated the effects of acute and chronic ethanol use in vivo, with or without the administration of S-adenosyl-methionine (SAME, 2 g I.v.), and the effects of ethanol and acetaldehyde in vitro, on the erythrocyte levels of malonyldialdehyde and glutathione, and of its principal synthesizing enzymes, gamma-glutamyl-cysteine-synthetase and glutathione-synthetase. METHODS: Twelve healthy volunteers (age range 26-44 years, median 32 years) and 20 chronic alcohol abusers without liver disease (age range 26-57 years, median 44 years) were studied. Malonyldialdehyde was evaluated by thiobarbituric acid; glutathione and its enzymes by high performance liquid chromatography using a fluorescent detector. RESULTS: In the healthy subjects, an acute load of ethanol induced a significant decrease in plasma levels of glutathione, which was inhibited by the infusion of S-adenosyl-methionine. In the erythrocytes of alcoholic patients, glutathione and glutathione-synthetase were decreased while malonyldialdehyde was increased. In vitro, acetaldehyde did not affect either the glutathione or the glutathione-related enzyme levels. CONCLUSIONS: Our data suggest that the alterations in glutathione metabolism in the erythrocytes of alcoholics may be due principally to the production of free radicals, as supported by the high levels of malonyldialdehyde observed.

Effect of S-adenosyl-L-methionine administration on red blood cell cysteine and glutathione levels in alcoholic patients with and without liver disease.

We measured glutathione and cysteine concentrations in erythrocytes of chronic alcohol misusers with (20 subjects) and without liver cirrhosis (20 subjects). Glutathione levels were decreased, whereas those of cysteine were increased in all patients. Parenteral treatment with S-adenosylmethionine (SAME); (2 g daily in 250 ml 0.15 M NaCl for 15 days) corrected the erythrocyte thiol alterations. We conclude that parenteral treatment with SAME affects the metabolism of SH compounds in erythrocytes of alcoholic patients.

Increased GH responsiveness to dopamine receptor stimulation in alcohol addicts during the late withdrawal syndrome.

In humans the release of growth hormone (GH) elicited by dopamine (DA) and DA agonists may represent a reliable model to assess change in sensitivity of DA receptors. We now report that in chronic alcoholics, 4-7 days after the suspension of alcohol consumption, the increase of GH response to DA infusion was higher than that seen in non alcoholic volunteers. The specificity of this GH response to DA administration was demonstrated by the use of domperidone, a novel peripheral antagonist of DA receptors. These results suggest the development of hyper-responsiveness of DA receptors involved in the control of GH secretion in chronic alcoholics during the later phases of the "withdrawal syndrome".