Severe statin-induced rhabdomyolysis mimicking Guillain-Barré syndrome in four patients with diabetes mellitus treated with fusidic acid.

BACKGROUND: An interaction between fusidic acid and HMG coenzyme A reductase inhibitors (statins), resulting in rhabdomyolysis, has been described. Pain and mild weakness are common presenting symptoms. CASE REPORT: We report four patients with Type 2 diabetes prescribed long-term statin treatment who, following treatment with fusidic acid, presented atypically with painless, severe flaccid paralysis suggestive of Guillain-Barré syndrome. This, together with nerve conduction studies consistent with Guillain-Barré syndrome, resulted in the delayed recognition of rhabdomyolysis in these cases. CONCLUSIONS: The addition of fusidic acid can precipitate rhabdomyolysis in patients with diabetes already taking a statin. This can present with rapidly progressive weakness resembling Guillain-Barré syndrome. We recommend that creatine kinase is checked in patients with diabetes on statin therapy who present with profound weakness and routinely in those commenced on prolonged courses of fusidic acid.

Muscle hypertrophy in multifocal motor neuropathy is associated with continuous motor unit activity.

Multifocal motor neuropathy (MMN) is typically associated with distal upper limb weakness and wasting. However, proximal muscle bulk, particularly of biceps brachii, may be well preserved even in the presence of severe proximal weakness. Here we report 3 patients with MMN who had true muscle hypertrophy of severely weakened biceps muscles and positive motor symptoms including cramp and fasciculations in these muscles. Electromyographic studies demonstrated markedly impaired recruitment in the affected muscles and continuous motor unit activity comprising multiple fasciculation potentials at a frequency of up to 30 per minute. We propose that this continuous motor unit activity may have contributed to the hypertrophy in these muscles.

Monosaccharide composition of haptoglobin in liver diseases and alcohol abuse: large changes in glycosylation associated with alcoholic liver disease.

Liver damage through prolonged intake of high amounts of alcohol is a serious problem that affects many members of the population. The aim of this study was to investigate changes in the glycosylation of haptoglobin (Hp) resulting from alcoholic liver diseases. The monosaccharide composition was measured in Hp isolated from 48 healthy individuals, 15 alcohol abusers (AA); 25 patients with alcoholic liver disease, including those with alcoholic cirrhosis (ALD/AC), and 17 other patients with either chronic active hepatitis (AH) or primary biliary cirrhosis (BC). Fucose was elevated per mol of Hp in 70%, 44%, and 33% of the individuals in the ALD/AC, BC and AA groups, respectively. Fucose was not elevated in the AH group. N-acetylglucosamine was also elevated in the ALD/AC group. Expressing results per 3 mol of mannose suggested the presence of higher branching with increased fucose content in Hp from all the abnormal groups except the AH group. More structural information is required to develop the diagnostic potential of carbohydrate measurements of Hp in alcoholic liver diseases.

Contraction of human umbilical artery, but not vein, by oxygen.

The O2 tension of umbilical arterial blood in utero is 15 mmHg. The contractile effect of increasing the O2 tension above this value was studied quantitatively in vitro in preparations of human umbilical artery and vein. The umbilical arterial smooth muscle was contracted in a concentration-related manner by stepped increments in O2 tension. The threshold for O2-induced contraction was estimated to be 36 mmHg at pH 7.28 and the maximum contraction occurred at 297 mmHg. The sensitivity of the preparations to low O2 tensions (less than 100 mmHg) was reduced by increasing the pH of the bathing medium from 7.28 to 7.36, at which the threshold was 69 mmHg and the maximum contraction occurred at 282 mmHg. Reducing the pH to 7.18 did not significantly change the sensitivity from that found at pH 7.28. Indomethacin (0.1 microM) virtually abolished responses to O2. The results indicate that the increase in the physiological O2 tension at birth, from 15 to 100 mmHg, may be an adequate stimulus to effect the closure of the umbilical artery. In the physiological range O2 did not contract the umbilical venous smooth muscle. This may allow the transfusion of blood from the placenta to the fetus at birth when the O2 tension of umbilical cord blood increases after the onset of breathing.