The purpose of this study was to investigate if insulin-dependent diabetes mellitus (IDDM) and non-insulin-dependent diabetes mellitus (NIDDM) predispose to the development of acute myocardial infarction (AMI) and modify the prognosis. The study includes 832 AMI patients consecutively hospitalized over a 3-yr period. The prevalence of diabetes mellitus among the AMI patients was 9.7% and is significantly higher than in an age-matched population, where it is 6.1% (P less than 0.001). The prevalence of diabetes was higher for women than for men (14.9% versus 7.6%). The risk of AMI was found to be twice as high among IDDM than among nondiabetic patients (P less than 0.001). Men with NIDDM were not found to have a significantly higher risk of AMI (P greater than 0.1), but the risk of AMI in women with NIDDM was approximately doubled (P less than 0.01). During the first month following AMI the mortality rate for nondiabetic patients was 20.2% compared with 42.0% for diabetic patients (P less than 0.001). Insulin treatment in NIDDM was associated with a reduced mortality rate compared with treatment with oral agents (P less than 0.05). The mortality rate was significantly higher in patients with poor metabolic control compared with patients in good control, whether before AMI or at the time of hospitalization. Diabetic patients had a higher risk of developing cardiogenic shock and conduction disorders than nondiabetic patients. We conclude that diabetes mellitus disposes to AMI and that the mortality rate of AMI is significantly increased among diabetic patients. Poor metabolic regulation of the diabetes may aggravate the prognosis for AMI.
The purpose of this study was to identify characteristics of patients with steroid-sensitive nephrotic syndrome (SSNS) that point to a high risk of frequent relapsing (FR) or steroid-dependent (SD) SSNS. A retrospective analysis of 54 consecutive patients with SSNS was performed. In this cohort, the incidence of idiopathic NS was 1.9/100,000, age at debut was 5.5 years, and the mean follow-up was 4.0 years. A total of 56% (30/54) of our patients were classified with FR/SD SSNS. FR/SD patients were significantly younger at debut than non-FR/SD patients (3.5 vs. 8.5 years, respectively; p < 0.002). Males were overrepresented in the FR/SD group (69 vs. 38%; p = 0.03). No differences were found in terms of haematuria, hypoalbuminaemia, or days to achieve remission. In total, 31 and 23 patients were on a 6 + 6-week (pred-long) and 4 + 4-week (pred-short) steroid treatment regimen, respectively. There was a reduction in the number of FR/SD patients in the pred-long group relative to the pred-short group (38 vs. 80%, respectively). In the pred-long group, the 12 FR/SD patients were younger than the 19 non-FR/SD patients (4.4 +/- 3.1 vs. 8.4 +/- 4.1 years; p<0.005). Low age at debut and male gender was associated with a high risk of SD/FR in this unselected series of SSNS patients despite the prolongation of the steroid course at debut of SSNS.
Abstract. Ultrasonic scanning has been used to estimate changes in goitre size during and after treatment with a daily dose of either 100 μg thyroxine (T4) (n = 30), 150 μg T4 (n = 33), 200 μg T4 (n = 17) or 60 μg triiodothyronine (T3) (n = 30) for one year in patients with diffuse non-toxic goitre. The thyroid volume was measured before and every 3 months during and 3 months after withdrawal of therapy. All 4 treatments resulted in a decrease in goitre size after 3 months' therapy (P < 0.05) but only in the patients given 200 μg T4 and 60 μg T3 was the decrease long lasting during additional 9 months' therapy. The mean reduction in thyroid volume after 12 months therapy was 30 ± 26 sd and 22 ± 30 (sd)%, respectively. The free-T4-index was found significantly raised throughout the treatment with all three T4 doses, whereas the free-T3-index did not change. During treatment with 60 μg T3 no persistent rise in free-T3-index was seen while free-T4-index was decreased all 12 months. No increase in goitre size was observed 3 months after withdrawal of the T3 therapy (n = 15), whereas all goitres in the T4 treated groups had returned to the pre-treatment values at that time. No rebound phenomenon was observed. The serum T3 and T4 levels were normalized 3 months after withdrawal in all four groups. Seven out of 8 patients on 200 μg T4 daily and 20 out of 25 patients on 60 μg T3 daily had no TSH response to TRH (200 μg iv) after 3 months' therapy. Forty-three out of 61 patients in the 4 groups showed no TSH response to TRH after 3 months' therapy. Only the group of patients showing no TSH response to TRH after 3 months' treatment had a significant decrease in goitre size in contrast to the group with a positive response to TRH.
Characteristics of primary breast tumours were related to the extent of dissemination, the anatomical location of metastases, and the rate of progression in 863 patients with recurrent breast cancer. The following features were examined: tumour laterality, location within the breast, size, invasion of skin or fascia, presence of residual cancer tissue (RCT) in the mastectomy specimen, and number of positive lymph nodes. Increasing tumour size, increasing number of nodes, and the presence of local invasion and RCT were all associated with a short duration of survival both from initial diagnosis and from first recurrence. None of the factors were related to either the extent of dissemination or the rate of progression. Patients who had their primary tumours located in the medial or central part of the breast had an increased incidence of mediastinal and pleural recurrences respectively. Primary tumours greater than 5 cm, invasion of skin or fascia, and presence of RCT were all associated with an increased incidence of local recurrences. In addition, both RCT and fascial invasion were associated with increased occurrence of brain metastases. Most differences were explainable on the basis of local and regional lymphodynamics. Since the status of the features examined here all vary with time from tumour inception, it is suggested that the impact on prognosis is related to variations in tumour age from inception to primary diagnosis rather than to qualitative biological differences.
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