Twenty-one patients with familial amyloidosis and polyneuropathy have been examined for the presence of skin lesions, localized to the lower legs and feet. The lesions were classified as atrophic skin lesions, hypertrophic scar-like skin lesions, rubeosis plantarum, spontaneous blisters, necrotic skin lesions, yellow nails, traumatic skin lesions, purpura and abundant pigmented small non-atrophic spots. Skeletal destructions in the feet were also demonstrated. In many respects these lesions are similar to those of long-standing diabetes mellitus. I studied the cutaneous reactions to local thermal trauma with heat and cold to the legs and forearms in 11 patients. Petechiae were observed within the area of traumatization with either heat or cold more often in patients than in controls. Four of the 11 patients developed atrophic circumscribed skin lesions at the site of traumatization.

A male patient with ketosis-prone diabetes of 55 years' duration is described. To our knowledge, this is the longest duration of diabetes reported. His daughter also has a ketosis-prone diabetes. The low degree of long-term diabetic complications in both father and daughter is remarkable.

A consecutive series of 189 diabetic patients with manifest gangrenous lesions localized to the feet were studied. These patients had 293 gangrenous lesions localized to 5 different areas: toes 58%, interdigital spaces 6%, dorsa of the feet 10%, metatarsal heads 10% and heels 16%. Cardiac decompensation with edema and edema from other causes were the dominant precipitating factors for the gangrenous lesions. Arterial insufficiency alone or together with other precipitating factors was seen considerably less often. Gangrenous lesions localized to the toes were especially common in patients with long duration of diabetes and in men. In women gangrenous lesions localized to the interdigital spaces and to the heels were more common. Multiple gangrenous lesions were more common in patients with cardiac decompensation, while the occurrence of only one lesion was especially common in patients with signs of arterial insufficiency and in men.

PURPOSE:To examine the prevalence of diabetic retinopathy and its relation to certain risk factors (glycosylated hemoglobin, blood pressure, serum creatinine, proteinuria, smoking) in a population-based study on a specific age-group of patients with diabetes mellitus in the county of Umeå, Sweden.METHODS:All diabetic patients aged 15-50 years living in the county of Umeå were invited to the study. A standard clinical and eye examination was performed, and seven-field stereoscopic photographs were taken of each eye. Blood and urine samples were collected. Univariate and multivariate statistical analyses were performed.RESULTS:Of the eligible 395 patients 285 (91%) participated in the study. 285 patients (79%) had diabetes mellitus type 1, 71 (20%) subjects had diabetes mellitus type 2, and 3 patients (1%) had secondary diabetes. In the statistical analysis performed on patients with type 1 diabetes mellitus, duration, presence of hypertension, systolic blood pressure, plasma glucose, glycosylated hemoglobin, serum creatinine, proteinuria and smoking all were significantly related to increasing degree of retinopathy when a univariate model was applied. However, when a multivariate analysis was performed only duration, proteinuria, glycosylated hemoglobin and male gender were statistically significantly associated with severeness of retinopathy.CONCLUSION:Increased duration of diabetes, inadequate metabolic control as measured by glycosylated hemoglobin, proteinuria and male gender are factors that are associated with a higher incidence of diabetic retinopathy in diabetes mellitus type 1.

HLA-associated relative risks of type 1 (insulin-dependent) diabetes mellitus were analysed in population-based Swedish patients and controls aged 0-34 years. The age dependence of HLA-associated relative risks was assessed by likelihood ratio tests of regression parameters in separate logistic regression models for each HLA category. The analyses demonstrated an attenuation with increasing age at onset in the relative risk for the positively associated DQB1*0201-A1*0502/B1*0302-A1*0301 (DQ2/8) genotype (P = 0.02) and the negatively associated DQB1*0602-A1*0102 (DQ6.2) haplotype (P = 0.004). At birth, DQ6.2-positive individuals had an estimated relative risk of 0.03, but this increased to 1.1 at age 35 years. Relative risks for individuals with DQ genotype 8/8 or 8/X or DQ genotype 2/2 or 2/X, where X is any DQ haplotype other than 2, 8 or 6.2, were not significantly age-dependent. An exploratory analysis of DQ haplotypes other than 2, 8 and 6.2 suggested that the risk of type 1 diabetes increases with age for DQB1*0604-A1*0102 (DQ6.4) and that the peak risk for the negatively associated DQB1*0301-A1*0501 haplotype is at age 18 years. There was also weak evidence that the risk for DQB1*0303-A1*0301 (DQ9), which has a positive association in the Japanese population, may decrease with age. We speculate that HLA-DQ alleles have a significant effect on the rate of beta cell destruction, which is accelerated in DQ2/8-positive individuals and inhibited, but not completely blocked, in DQ6.2-positive individuals.

Lipid abnormalities and their associations with degree of retinopathy in diabetes mellitus type 1.

Diabetic MedicineVolume 12, Issue 2 p. 180-180 Diabetes and Dementia F.G. Lithner, F.G. Lithner Department of Medicine, University Hospital S-90185 Umeå, SwedenSearch for more papers by this author F.G. Lithner, F.G. Lithner Department of Medicine, University Hospital S-90185 Umeå, SwedenSearch for more papers by this author First published: February 1995 https://doi.org/10.1111/j.1464-5491.1995.tb00452.xCitations: 1AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onEmailFacebookTwitterLinkedInRedditWechat No abstract is available for this article. References 1 Amiel, S.A. Diabetes and dementia: A causal association? Diabetic Med; 11: 430–431. 2 Bucht, G., Adolfsson, R., Lithner, F., Winblad, B.. Changes in blood glucose and insulin secretion in patients with senile dementia of Alzheimer type. Acta Med Scand 1983; 213: 387–392. Citing Literature Volume12, Issue2February 1995Pages 180-180 ReferencesRelatedInformation

This study was performed to evaluate hypothalamic-pituitary hormone regulation in patients with familial amyloidotic polyneuropathy. Twenty-two patients without clinically overt endocrinological dysfunction were studied. A thyrotropin-releasing hormone test revealed abnormal growth hormone regulation in 9 of 17 (53%) patients, and abnormal prolactin regulation in 9 of 18 (50%) patients. Abnormalities in either growth hormone or prolactin regulation were found in 12 of 17 (71%) patients. Serum somatomedin C levels were normal in all 22 patients. In 3 of 18 (17%) patients the plasma arginine vasopressin levels were low relative to the serum osmolality levels. Thus abnormalities in hypothalamic-pituitary hormone regulation may be common in familial amyloidotic polyneuropathy.

To evaluate a possible relationship between Mg deficiency and the development of microvascular disease in diabetes mellitus, quadriceps muscle biopsies for estimating Mg content and capillary basement membrane thickness, were studied in 16 patients with type I diabetes. The diabetic individuals had a slightly but significantly reduced muscle Mg content as compared with 13 healthy controls. There was a significant, positive correlation between capillary basement membrane width and age in the diabetic group, but no relationship between membrane thickness and muscle or serum concentration of Mg. However, diabetic patients with retinopathy (n = 6) showed a nonsignificant inverse correlation between basement membrane thickness and Mg parameters. The opposite tendency was found in patients without retinal lesions.

The impact of diabetes was prospectively studied during a 5-year period in 428 unselected and consecutive patients with acute cerebrovascular disease of whom 18% were diabetic. Cerebral infarction was more frequent in diabetics (81 vs 70%, p less than 0.02) whereas transient cerebral ischaemia was less frequent (4 vs 14%, p less than 0.01). Case fatality rate during hospitalization was higher in the diabetic than in the non-diabetic patients (28 vs 15%, p less than 0.02). Patients who died during hospitalization, diabetic as well as non-diabetic, had significantly higher blood glucose concentrations on admission compared with patients who survived. Hematocrit values were higher in the diabetic than in the non-diabetic patients (p less than 0.02). Diabetics had higher systolic blood pressure levels than the non-diabetics in the acute phase (p less than 0.005). The diabetic stroke patients more often had a history of hypertension, atrial fibrillation, heart failure and angina pectoris than non-diabetics stroke patients and diabetic control patients without stroke. Stroke patients, not known to be diabetic, had larger mean oral glucose tolerance test curve areas when compared with healthy controls but not when compared with hospitalized controls. We propose that diabetes increases the risk for stroke through other concurrent risk factors, cardiac disorders in particular.

SUMMARYA basal plasma Cortisol value taken in a physically unstressed state in 68 patients with or without hypothalamic‐pituitary‐adrenocortical disease was compared with the maximal plasma Cortisol concentration during an insulin tolerance test. There was a strong positive correlation between the values. Basal Cortisol levels above 300 nmol/1 (RIA method) almost excluded ACTH‐cortisol insufficiency and those below 100 nmol/1 strongly suggested dysfunction. A repeated basal Cortisol estimation within a month was especially valuable in categorizing patients with levels between 100 and 200 nmol/1. We suggest that a basal Cortisol measurement may be used as a first laboratory test in patients evaluated for possible hypothalamic‐pituitary‐adrenocortical insufficiency; in many patients, this approach obviates more sophisticated and expensive testing.

Clinical features of different types of stroke were investigated in a sample of 409 patients representative of all cases admitted for acute stroke, except subarachnoidal hemorrhages, within a well defined population. A specific cerebrovascular diagnosis was obtained by detailed clinical investigation, including CT scan. In people > 50 years old, men/women risk for stroke was estimated to be 1.40:1. The risk was higher in men up to the age of 80; above this age similar risk for the two genders was observed. Eleven per cent had intracerebral hemorrhage, 13% TIA, 51% non-embolic and 25% embolic brain infarction. In all diagnostic categories there were similar proportions of patients who had a history of hypertension and previous stroke, neither did hemoglobin and hematocrit levels differ between the different stroke disorders. TIA preceded intracerebral hemorrhage in 11% and brain infarction in 15–20%. As opposed to patients with ischemic lesions, subjects with intracerebral hemorrhage had higher systolic blood pressure levels and more severe symptoms on admission to hospital. Ischemic stroke was associated with male predominance, different ischemic manifestations of heart diseases and diabetes.

We have studied the extrinsic fibrinolytic system in survivors, below 70 years, from myocardial infarction (AMI) treated in Umeci during 1983; in 43 type-1 diabetics; and in controls. Elderly controls underwent chest x-ray, ECG, EEG, brain CT scan to verify their health. Tissue plasminogen activator (tPA) activity was measured with a fibrin-stimulated rate assay, before and after a 10 min venous occlusion test (VO), tPA antigen (Ag) with an ELISA, and plasminogen activator inhibitor (PAI) by incubating samples with purified tPA and measuring remaining tPA with a polylysine-stimulated rate assay. In the diabetics, PAI and tPA:Ag were similar to the controls. tPA:Ag correlated with age (r=0.6). Diabetics had much higher specific activity of tPA (61,300 vs 21,900), and had also much higher tPA activity after VO (2.2 vs 1.2 U/ml). The tPA activities after VO correlated well with HbA1c (r=0.39). A significant effect of smoking was disclosed. Smoking diabetics had higher PAI and tPA antigen but also lower specific activity of tPA (60,600 vs 115,700 U/mg). Ex-smokers were very similar to smokers, not to the non-smokers. Retinopathy, nephropathy, or hypertension didn’t appear to affect fibrinolysis independently. In the AMI survivors (sampled 3 months after discharge from hospital), PAI was 6-fold higher than in elderly controls (p less than 0.0001). tPA activity after VO was much higher (3.2 vs 1.2 U/ml), as was tPA:Ag. tPA specific activity was lower. Among AMI patients with PAI over 10 U/ml, PAI correlated with triglycerides (r=0.4) and negatively with age (r=™0.4): these relations were not seen in the patients with PAI less than 10. The effects of smoking seen in diabetics were not observed among the AMI patients, von Willebrand factor was not increased among AMI nor diabetic patients, except for those with retinopathy. The results suggest that the tPA/PAI system is a more sensitive indicator than vWF of endothelial cell dysfunction. It relates to effects of age, atherosclerotic vascular disease, and among diabetics also to degree of metabolic control and to tobacco smoking habits.

A thyrotropin-releasing hormone (TRH) test with serum thyroid-stimulating hormone (TSH) assays was performed in 22 euthyroid stroke patients without thyroid disease and the results were compared with those in 17 age-matched euthyroid controls. Basal and maximum TSH levels after TRH injection were significantly lower in the stroke group without elevation of basal serum thyroid hormone levels. There was a tendency towards an inverse relationship between TSH levels and the degree of pareses of the extremities. The test was repeated in 7 stroke patients 3-4 months after the onset of stroke with essentially the same results. The abnormal TSH parameters in stroke patients seem to be the result of the brain lesion per se.

The clinical outcome in 110 patients admitted to a non-intensive stroke unit was compared to that in 183 patients treated for acute stroke in general medical wards. At entry, the two groups of patients were closely similar in all prognostic indicators. Subsets of patients were analyzed in an attempt to identify groups that benefit more than others from stroke unit care. The stroke unit regime had little effect on short-term and long-term mortality rates in the entire stroke population as well as in subgroups. But after the care in the stroke unit, the need for long-term hospitalization in survivors was reduced (p = 0.0001). This difference in favour of the stroke unit was independent of the patients' age, the extent of neurological deficit on admission and previous history. In subgroups where the general prognosis is fair or good (minor neurological deficits and less than 75 yrs), SU care accelerated the process of rehabilitation, but the need for institutional care very late after the stroke was influenced only little. In groups with a poor general prognosis (major deficits and greater than or equal to 75 yrs), the ultimate proportion of patients able to return home was enhanced by SU care. It is concluded that care in a stroke unit benefits the great majority of stroke patients and that such a unit should be designed to admit all acute stroke patients without selection.