Jejunoileal bypass and electrolytes. A follow-up study of intra- and extra-cellular electrolytes with special emphasis on magnesium.

It is generally believed that patients operated on for gross obesity with jejunoileal shunt develop electrolyte malabsorption. In follow-up studies electrolyte abnormalities have been reported in 6-37% of the cases. We have not been able to find any description of simple diagnostic tools to help indicate which patients should be treated with electrolyte supplements. The aim of this study was to evaluate different diagnostic tools to determine whether they would identify which patients to treat. Ten patients with end-to-side jejunoileostomies were investigated. Our attempt failed. We were not able to identify the patients who needed supplementary therapy. The reason for this may be absence of severe electrolyte abnormalities or insufficient diagnostic methods.

Amiodarone during pregnancy.

A case study is presented in which amiodarone (A) was given during the whole of pregnancy and during the breast feeding period. An intensive observation of thyroid tests, serum concentrations of A and its metabolite, desethylamiodarone (DEA) was undertaken. The child was observed in the same way from birth until 2 months of age. The milk was analyzed for A and DEA. As reported in other published cases, transplacental passage was found and there was a relatively high concentration of amiodarone in the milk. Our child like the other children was healthy at birth, being euthyroid and with no goiter or corneal deposits. No effect was observed of the medication on growth, thyroid tests or cornea. It is concluded that amiodarone can be given during pregnancy but it is advisable to use as low doses as possible and control the serum concentrations at regular intervals. Breast feeding need not be forbidden.

The familial magnesium-losing kidney.

Magnesium deficiency is often secondary to existing disease. Over a period of 20 years, 17 cases of primary magnesium-losing kidney have been reported. This report describes two additional cases, and a comparison with previous cases is made. The familial magnesium-losing kidney appears to be caused by a congenital tubular defect in the reabsorption of magnesium. Its manifestations may be various but the diagnosis is established by the presence of hypomagnesemia with an unappropriately high urinary magnesium excretion in patients with no other renal disorder.

The prognosis for patients referred with suspected acute myocardial infarction.

A follow-up investigation of the prognosis of 381 patients admitted with suspected acute myocardial infarction (AMI) has been carried out in respect of later AMI or death. During hospitalization the patients were divided into groups with particular attention to patients with no demonstrable myocardial infarction but with ischaemic heart disease (non-AMI) and patients with confirmed AMI. All patients were subjected to follow-up for 43 months (range 37-54). The mortality from cardiovascular causes after four years was 26.2% of 130 non-AMI patients and 25.8% of AMI patients. The majority of new infarctions were found in the AMI patients, but with even increase in both groups, 50% occurring within the first 12 months. The groups were studied with regard to earlier manifestations of ischaemic heart disease and heart failure during hospitalization, without any difference being observed. Due to the poor prognosis the question is raised whether non-AMI patients as a group should be offered prophylactic therapy.

Variation of serum lipoproteins in postmyocardial infarction patients treated with verapamil or placebo.

The effect of verapamil on plasma lipids and lipoproteins was studied in 64 patients taking part in a double blind controlled trial of verapamil versus placebo in post myocardial infarction. During a six month treatment period no significant difference was seen in plasma cholesterol, triglycerides, high density lipoproteins or low density lipoproteins.

Haemolytic uraemic syndrome and accumulation of haemoglobin-haptoglobin complexes in plasma in serum sickness caused by penicillin drugs.

2 patients treated with penicillin and ampicillin, respectively, suffered from haemorrhagic diathesis, haemolysis, cerebral symptoms and renal insufficiency, resembling a haemolytic-uraemic syndrome. Their plasma was red due to the presence during several days of haemoglobin-haptoglobin complexes, the P-haemoglobin being 2.8 and 1.6 g/l, respectively. Coagulation tests showed an unusual pattern with prolonged activated partial thromboplastin times, an extremely long thrombin time and very high levels of fibrinogen degradation products. Repeated transfusion had no effect. The patients were considered to have developed a drug-induced serum sickness associated with insufficient function of the reticuloendothelial system, and secondary to this an accumulation of haemoglobin-haptoglobin complexes in plasma. When the penicillin drugs were discontinued, all measured variables rapidly normalised and the patients recovered completely. Thus, the haemolyticuraemic syndrome seemed to be caused by the serum sickness, possibly via circulating or cell-associated immune complexes. The possibility of a type III allergic reaction should be considered in patients with haemolytic-uraemic-like syndromes.