Acta medica Scandinavica最新文献

We compared three representative population samples aged 70 (n = 312), 75 (n = 486) and 81 (n = 404) years. Anaemia defined either as blood haemoglobin concentration below the corresponding health-related lower reference limits or according to WHO was, in the total study groups, more common at age 81. Anaemia of unknown cause was rare, but somewhat more common at age 81. Mean blood haemoglobin concentrations in subsamples without definable disorders were significantly lower at age 81 than at ages 70 and 75, whereas the lower health-related reference limits did not differ significantly. White blood cell counts tended to be lower and iron deficiency was somewhat more common at age 81. No significant differences were found in platelet counts or in the prevalence of low plasma cobalamin concentrations. These results indicate a fall in blood haemoglobin with advancing age. The arbitrary WHO criteria for anaemia are clinically applicable at age 70-81.

In a prospective study, 57 patients with a preliminary diagnosis of myocarditis were investigated. Twenty-four patients were considered to have an acute myocarditis, 14 had a suspected myocarditis, while in 19 patients myocarditis was excluded. Episodes of frequent supraventricular and/or ventricular extrasystoles during hospital stay were seen in 8/24 cases (33%) with myocarditis and in 1/19 cases (5%) without myocarditis. On follow-up 1 month later, no supraventricular extrasystoles were observed in either group. Echocardiographic signs consistent with left ventricular insufficiency were noted in 7/24 cases (29%) with myocarditis, in 1/14 cases (7%) with suspected myocarditis and in no case without myocarditis. With a "routine" serologic test battery covering influenza viruses A and B, adenovirus, Coxsackie virus group B, ECHO viruses, Chlamydia psittaci, Mycoplasma pneumoniae and hemolytic streptococci group A, a possible etiology could be documented in 9/24 cases (38%) with myocarditis and in 4/19 cases (21%) without myocarditis. Enterovirus-specific IgM was detected with solid-phase reverse immunosorbent test (SPRIST) in 12/23 (48%) cases with myocarditis and in 3/16 cases (19%) without myocarditis. In SPRIST-IgM-positive cases, IgM antibodies were detected in 15/20 (75%) of the sera taken on admission. The overall serological results indicated a recent infection in 16/24 cases (67%) with myocarditis and in 5/19 cases (26%) without myocarditis (p less than 0.05).

One year's experience of an acute revascularization program for unstable angina pectoris is presented. In the total material of 63 patients, significant coronary artery stenosis was found in 61 and normal coronary arteries in two. Coronary artery bypass grafting was performed in 39 patients (62%) and percutaneous transluminal angioplasty in nine (14%). There were two perioperative myocardial infarctions and one hospital death. Thirteen patients were not eligible for revascularization. At follow-up (14-26 months) 60 patients were still alive (95%). In the revascularization group, one patient had died, but of the remaining 46 patients, 30 (65%) were free of angina pectoris, and in addition six had only minor symptoms.

One hundred consecutive patients admitted in 1980-82 for direct current conversion of chronic atrial fibrillation (AF) were followed. The first attempt to convert was made without the institution of class I antiarrhythmics. If AF relapsed, patients were selected for further conversions, in connection with which quinidine or disopyramide treatment was instituted. The proportion of patients maintaining sinus rhythm (SR) one and two years after the first conversion was 23% and 16%, after the second conversion 40% and 33% and after any number of conversions [1-12] 54% and 41%. Fifty-three per cent of the patients were symptomless before at least one conversion. Of the patients maintaining SR two years after conversion, 46% did not receive antiarrhythmic therapy. More than two conversions should be exceptional since symptoms of AF are often absent and the additional effect of further conversions is minor. A first attempt to convert without antiarrhythmics identifies a substantial proportion of patients maintaining SR without any prophylactic antiarrhythmic therapy.

We analyzed patients who died on chronic dialysis because they stopped the treatment, although there was no technical dialysis complication or new medical complication. These patients preferred death to the stress of dialysis. This occurred in 26/1766 (1.5%) patients, and was responsible for 26/704 (4%) of all deaths. We compared these 26 patients to 40 competent patients who discontinued treatment when a medical complication arose. The patients were similar in most respects (age, sex, diagnosis, duration of dialysis, living situation, and type of dialysis) and had the same number of medical complications when starting dialysis. However, the patients who stopped dialysis were more often on home dialysis, 8/24 vs. 3/40 of the other patients (p less than 0.05). Overall, stopping was three times more common in home than in center patients (3.0% vs. 1.1%) (p less than 0.02). Relatives responding to a written interview felt that nurses and social workers but not physicians had been helpful in the difficult time surrounding the patient's decision and death. This study indicates that particularly home dialysis patients are at a high risk of discontinuing dialysis because of the stress of the dialysis procedure. A realistic introduction to and realization of their dialysis problems, better training and better psychological support, particularly from physicians, are necessary to eradicate this avoidable cause of death in chronic dialysis patients.

Split products of complement component 3 (C3) and complement component 4 (C4) derived from activation of the alternative and classical complement pathways were measured in untreated outpatients, 20 with Crohn's disease and 19 with rheumatoid arthritis. Elevated levels of the d split product of C4 (C4d) were observed in 12 of 19 patients with rheumatoid arthritis and in 9 of 20 patients with Crohn's disease. Levels of the d split product of C3 (C3d) were increased in 14 of 19 patients with rheumatoid arthritis and in 6 of 20 Crohn's disease patients. The median values of C4d and C3d were significantly increased in both groups of patients. C3d concentrations correlated positively with C4d levels (rs = 0.51-0.56, p less than 0.005). The complement activation was not reflected in reduced plasma levels of native C3 and C4. The data indicate activation of the classical complement pathway in both rheumatoid arthritis and Crohn's disease.

One hundred and one representative post-myocardial infarction (MI) patients were investigated with radionuclide angiocardiography (RNA) and exercise test within 1 month of the MI and after 6 and 12 months. From the RNA were calculated the left ventricular ejection fraction (LVEF) and a quantified phase image, the phase standard deviation (phase-SD), representing the timing of the left ventricular contraction. The mean phase-SD was significantly higher among these patients (18 degrees, 19 degrees and 18 degrees, respectively, at the three investigations) compared to phase-SD in normals (6 degrees), indicating an impaired timing of the left ventricular (LV) contraction. At all three investigations a significant correlation was found between the phase-SD and the LVEF (r = -0.58, r = -0.74 and r = -0.75, respectively) and the corrected QT interval (r = 0.27, r = 0.44 and r = 0.39, respectively). Maximal serum ASAT in patients with their first MI correlated significantly to phase-SD. Low exercise capacity or unfavourable NYHA classification was associated with high phase-SD. Phase-SD higher than mean was also associated with significantly increased mortality during the follow-up year (p = 0.0057). In conclusion, phase-SD, reflecting the timing of the LV contraction wave, is easily accessible and clinically relevant. It merits further investigation as a prognostic factor after an MI.

In eight of 10 consecutive cases of IgM monoclonal gammopathy of undetermined significance (MGUS), the M-protein had specificity towards various tissues as estimated by direct and indirect immunofluorescence studies of skin and/or sural nerve biopsies. Five of the cases had neuropathy. In three of them, including two siblings with a demyelinating peripheral neuropathy, the IgM was bound to the myelin-associated glycoprotein (MAG) of peripheral nerves. One had axonal neuropathy with IgM activity against the peri- and endoneurium, while another case with post-infectious neuritis had IgM activity against structures in the endoneurium but no IgM autoimmunity in the direct fluorescence test. The latter improved clinically in parallel with a decrease in the M-protein indicating a pathogenetic role of the autoantibody. In three other cases, the IgM was bound to connective tissue structures, two of them also had plasma antibodies against the peri- and endoneurium in the indirect fluorescence test. Finally, two cases showed no reaction of the M-protein against any tissue structures. Since an autoimmune pathogenesis is suspected, the HLA types of seven patients are reported.

Liver function tests and prevalence of different symptoms generally said to occur in Gilbert's syndrome were analysed in male conscripts and in male and female participants in two cross-sectional population studies in Göteborg, in total 2395 subjects. The serum bilirubin levels showed a skew distribution without bimodality. We observed no tendency to higher prevalence of symptoms in subjects with high serum bilirubin levels, but normal alkaline phosphatase and aminotransferase values compared to subjects with normal bilirubin. The findings contradict the existence of a disease entity named "Gilbert's syndrome".