Transplantation of teeth to lost abutments sites--an alternative to removable dentures.
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Biomedical subjects
Publications and source records attributed to O Larsson.
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In juvenile--onset diabetes uremia is the main cause of death. Since 1972 until Oct. 1979 a total of 47 diabetics have been transplanted in Gothenburg, of these 40 were juvenile--onset diabetics without concomitant renal disease. Twenty-four were male and 16 female. The diabetic nephropathy was not an isolated phenomenon. Complications from other organs were present parallel with the kidney disease. Hypertension was present in 39 of 40 patients before transplantation. Most patients have been transplanted in terminal uremic stage, 21 were on dialysis. The overall mortality at the end of the observation period was 33% but during the later part, that is from 1976 onwards only 2 out of 26 transplanted patients have died so far (8%). Fourteen of these 26 patients were grafted with kidneys from living related donors compared to one of fourteen during the first period. This may be one of the main reasons to the improved results during the last years.
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Strokes occurring among persons between 15 and 65 years of age (population 300 000) have been registered since 1970 in Göteborg, Sweden. Control of the validity showed that less than 10% of all cases of stroke were undetected. During the period Nov. 15, 1970-May 14, 1975, 986 stroke events occurred in 941 patients, giving an annual average incidence rate of 73 (89 for men and 58 for women) per 100 000 individuals 15-65 years of age. The incidence for all ages was estimated to be about 200/100 000. The rates were higher for men than for women in all age groups. There was a female preponderance for subarachnoid haemorrhage but a male preponderance for other types of stroke. Incidence rates increased with age, most rapidly for brain infarcts and unspecified stroke. Fatality rates levelled out 3 weeks after onset of stroke; they were high for subarachnoid and intracerebral haemorrhage and low for cerebral infarction and unspecified stroke. Incidence rates were lower than those found in two similar studies from Denmark and Finland, and even greater variations were found with respect to types of stroke. Fatality rates were similar to those reported by other authors.
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Out of 27 patients with advanced diabetic nephropathy accepted for renal transplantation. 11 had cardiac symptoms and 10 others had advanced neuropathy. The former group had a poor outcome with 100% mortality within one year, seven patients dying before transplantation. Neuropathy also indicated a poor prognosis. Early transplantation, before the stage of terminal uraemia, was at no advantage in this material.
Two patients presented with initial symptoms of pericarditis. Palpable lymph nodes developed a few weeks later and a diagnosis of Hodgkin's disease was made. Although rare, this mode of presentation of Hodgkin's disease has been reported previously, and it should be considered in the differential diagnosis of any patient with pericarditis with severe general symptoms or a prolonged course.
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The effects of intravenous glycerol and intravenous dextrose were compared using a double-blind trial in twenty-seven patients with acute stroke. Administration continued for up to 6 days. A standard scoring system was used for neurological evaluation. There was no difference in mortality or in improvement in neurological score between the two groups.
The antihypertensive effect and side-effects during 12 months' treatment with bendroflumethiazide and propranolol have been compared in two randomly selected, equally large groups (n= 53) of previously untreated male hypertensives. Systolic BP above 170 or diastolic BP above 105 mmHg on two occasions were defined as hypertension. The same BP reduction was achieved in both groups. During the 12 months' treatment one subject on bendroflumethiazide developed diabetes mellitus and one on propranolol developed cardiac decompensation. None developed gout. Contrary to what had been presumed, glucose tolerance improved during 12 months' treatment with both agents, while there were no changes in fasting blood sugar, insulin or triglyceride concentrations. No changes were found in serum potassium or total body potassium during 12 months' bendroflumethiazide treatment, while serum potassium increased during treatment with propranolol. Uric acid increased slightly during treatment with both agents. Prolongation of the follow-up to 24 months did not change any of the findings regarding metabolic changes during treatment. The frequency of subjective side-effects decreased to the same extent during treatment with both drugs. It is concluded that bendroflumethiazide and propranolol are equally useful as antihypertensive agents and that the risk of impariment of glucose metabolism and potassium balance seems to be very slight during treatment with bendroflumethiazide in mild hypertension.
Body fat, body cell mass, fasting blood sugar, glucose tolerance and fasting insulin have been determined in 106 hypertensive males aged 47-54years and in 41 normotensive 50-year-old males. Both groups were derived from screening examinations in random population samples. The hypertensive subjects were more often obese and had more often an impaired glucose tolerance and a higher fasting insulin compared with the normotensive subjects. The metabolic differences were not explained simply by the higher degree of obesity in the hypertensive subjects, as the differences remained when the hypertensive subjects were matched for body fat with normotensive controls. The impaired glucose metabolism demonstrated quantitatively in an unselected group of hypertensive subjects, might be one of the factors explaining the variable prognosis in hypertensive subjects.
A 45-year-old man developed in 1965 skin lesions on cold exposure and was found to have cryoglobulinemia due to an M-component of IgG class. Glomerular damage was first noted in 1970, and progressed to renal impairment and nephrotic syndrome during the next two years. Reduced serum levels of complement components C3 and C4 were found, indicating in vivo complement activation. Renal biopsy revealed proliferative glomerulonephritis and deposition of IgG and C3 along the glomerular basement membrane. Electron microscopical examination revealed a striking deposition of a 'fibrillar' or microcrystalline material in the glomerular basement membrane. This material had an ultrastructure similar to that found in the cryoprecipitate from serum. There were no tubular changes of myeloma type, neither were there any monoclonal light chains detected in the urine. So far, there are no other signs of myeloma or lymphoma. Immunosuppressive treatment with prednisone and cyclophosphamide resulted in a decrease in the serum M-component as well as a decrease in protein leakage through the glomeruli and a return to normal of glomerular filtration rate. The finding of monoclonal cryoglobulinemia, demonstrable at room temperature, in a patient developing proliferative glomerulonephritis with complement activation is unusual. It is probably that the M-component is causally related to the glomerular lesions.
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