Aggravation of thiamine deficiency by magnesium depletion. Acta Med Scand 1985; 218: 12!3-31.A patient with Crohn's disease and long-standing diarrhea resulting in a combined thiamine and magnesium deficiency is presented. Despite massive doses of thiamine i.v., the symptoms of thiamine deficiency could not be suppressed until the magnesium deficiency was corrected as well. This case report emphasizes the dependence of thiamine on magnesium for an adequate function in the body.

Summary A methodological study of the influence of local stasis and mechanical pressure on the continuous transcutaneous oxygen tension electrode (tcPO2 electrode) during intrapartum monitoring is presented. No effect of mechanical pressure up to 7.3 kPa (55 mm Hg) on the electrode membrane was found. Reduced blood flow in the capillaries of the tissue beneath the electrode caused by stasis or pressure effect resulted, below a certain threshold value, in tcPO2 decrease. The results emphasize that an attempt to differentiate between a methodologically caused decrease and a decrease due to impaired oxygenation must be made when evaluating the absolute fetal arterial oxygen tension from fetal tcPO2. The consistently observed decrease in relative local perfusion (‘flow’) may be a help in this respect.

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Sixteen patients with familial amyloidosis and polyneuropathy (FAP) and 14 health subjects underwent oesophageal manometry. Six of the patients had a severe oesophageal dysmotility with almost completely abolished propulsive pressure waves on swallowing in the lower 2/3 of the oesophagus. Ten patients had moderate dysfunction with reduced propulsive pressure wave amplitudes. Neostigmine increased the pressure wave amplitudes in healthy subjects but less so in the FAP patients. Scopolamine (Scopyl)-terbutaline (Bricanyl) almost abolished the propulsive pressure waves in healthy subjects and all patients in the lower 2/3 of the esophagus. Oesophageal distensibility, tested by inflating a rubber balloon in the oesophagus, was similar in FAP patients and healthy subjects. Thus, it is unlikely that amyloid deposits in the mucosal wall increased the oesophageal stiffness. An autonomic, predominantly vagal, denervation probably explains the disturbed function.

Fifty-two patients with a confirmed diagnosis of familial amyloidosis with polyneuropathy living in northern Sweden were investigated. Gastrointestinal symptoms, mainly in the form of changed bowel habits, were found in 47 patients. Symptoms of polyneuropathy of the peripheral nerves usually preceded the gastrointestinal symptoms, but in 12 patients gastrointestinal dysfunction started either before or simultaneously with the neurological symptoms. Steatorrhea was found in 30 patients (58%) and an impaired D-xylose absorption in 52%. Diarrhea, anal incontinence, and a high degree of peripheral denervation indicating a severer disease were related to the presence of steatorrhea. The results of oral lactose and glucose tolerance tests were essentially normal. The results suggest that the main reason for the gastrointestinal dysfunction is a disruption of the gut autonomic nervous system rather than a barrier to the absorption of nutrients across the intestinal wall.