Background-Oesophageal motor abnormalities have been reported in alcoholism. Aim-To investigate the effects of chronic alcoholism and its withdrawal on oesophageal disease. Patients-23 chronic alcoholic patients (20 men and three women; mean age 43, range 23 to 54). Methods-Endoscopy, manometry, and 24 hour pH monitoring 7-10 days and six months after ethanol withdrawal. Tests for autonomic and peripheral neuropathy were also performed. Motility and pH tracings were compared with those of age and sex matched control groups: healthy volunteers, nutcracker oesophagus, and gastro-oesophageal reflux disease. Results-14 (61%) alcoholic patients had reflux symptoms, and endoscopy with biopsy showed oesophageal inflammation in 10 patients. One patient had an asymptomatic squamous cell carcinoma. Oesophageal motility studies in the alcoholic patients showed that peristaltic amplitude in the middle third was >150 mm Hg (95th percentile (P95) of healthy controls) in 13 (57%), the ratio lower/ middle amplitude was <0 9 in 15 (65%) (>0.9 in all control groups), and the lower oesophageal sphincter was hypertensive (>23.4 mm Hg, P95 ofhealthy controls) in 13 (57%). All three abnormalities were present in five (22%). Abnormal reflux (per cent reflux time >2.9, P95 of healthy controls) was shown in 12 (52%) alcoholic patients, and was unrelated to peristaltic dysfunction. Subclinical neuropathy in 10 patients did not effect oesophageal abnormalities. Oesophageal motility abnormalities persisted at six months in six patients with ongoing alcoholism, whereas they reverted towards normal in 13 who remained abstinent; reflux, however, was unaffected.Conclusions-Oesophageal peristaltic dysfunction and reflux are frequent in alcoholism. High amplitude contractions in the middle third of the oesophagus seem to be a marker of excessive alcohol consumption, and tend to improve with abstinence. (Gut 1996; 38: 655-662)

There seems to be a dose-dependent effect of ethanol on systolic and diastolic heart function. Diastolic function impairment is present in one third of alcoholics with normal systolic function and is even more frequent when systolic dysfunction coexists.

Ethanol consumption frequently leads to a number of skeletal muscle disorders, including acute and chronic alcoholic myopathy. Ethanol has been found to interfere with signal transduction mechanisms in cardiac and smooth muscle cells. We studied the effects of ethanol on the intracellular calcium ([Ca2+]i) transients responsible for excitation-contraction coupling in human myotubes from chronic alcoholic patients and healthy controls. Cultured myotubes were loaded with the fluorescent Ca2+ indicator fura-2 and evaluated on a single-cell basis. Following electrical stimulation, ethanol caused a significant reversible dose-dependent reduction in [Ca2+]i transient amplitude, achieving a mean decrease of 36+/-5% at 300 mM ethanol (p < 0.01), without modifying the basal [Ca2+]i. This acute effect of ethanol was similar in myotubes obtained from chronic alcoholics and controls. Similarly, ethanol caused a dose-dependent reduction of [Ca2+]i transient amplitude in control samples when depolarization was elicited by 100 mM KCl (p < 0.01). Several potential mechanisms of ethanol action were studied in control muscle samples. Sarcolemmal Ca2+ entry was measured indirectly by monitoring Mn2+-quenching of intracellular fura-2 via the nitrendipine-sensitive Ca2+ channels during electrical pacing. Ethanol at doses of 100 mM and greater caused a dose-dependent reduction in the rate of quench (p < 0.01). In addition, the intracellular pool of Ca2+ releasable by caffeine was found to be reduced at 300 mM ethanol (p < 0.05). We conclude that ethanol reduces the [Ca2+]i transients underlying excitation-contraction coupling in human myotubes, and that this occurs to a similar extent in cells obtained from chronic alcoholics and controls. This acute effect of ethanol was primarily due to an inhibitory effect of ethanol on sarcolemmal Ca2+ influx via voltage-operated Ca2+ channels, although there may also be an effect on the Ca2+ sarcoplasmic reticulum loading state.

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To assess the pathogenetic importance of capillary damage and its relationship with degenerating muscle fibers in dermatomyositis (DM), an electron microscope study of eight muscle biopsy specimens (adult and juvenile forms) and seven muscle specimens from patients with other neuromuscular diseases was conducted. There was a 49% reduction of capillaries in the muscle specimens of DM patients. Capillary damage also was more frequent in the DM group than in control group (p less than 0.001). We found a striking relation between capillary and muscle damage in the DM group (p less than 0.002) but not in the control group. The diagnostic value of undulating tubules within endothelial cells is also discussed.

Antioxidant muscle enzyme activities are partially disturbed in chronic alcoholism, although not related to the presence of myopathy, amount of ethanol consumed, or the nutritional status of the patients. Further studies should assess other aspects not included in the present study such as muscle site-specific changes in antioxidant status/oxidative damage, specific fiber-type sensitivity to alcohol, and type and quantity of antioxidant content of the diet or in the alcohol beverages.

A case of a 44-year-old man in whom κ light chain multiple myeloma and rhabdomyolysis (RDM) were diagnosed simultaneously is reported. Deposition of the κ light chain in the cellular membrane of muscle fibers (observed with immunofluorescence techniques and ultrastructural examination) suggests a possible pathogenic mechanism for RDM.

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