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Immune thrombocytopenia due to passive transfer of anti-PI(A1) alloantibody has been noted as a rare but potentially dangerous complication of plasma transfusions. We report a patient with a preoperative platelet count of 241 x 10(9)/l who developed severe thrombocytopenia within 2 hr following transfusion of 2 U of fresh frozen plasma. The plasma donor was found to be a PI(A1)-negative woman. The platelet count of the PI(A1)-positive patient recovered within 7 days to normal values. In the frozen plasma, excessive antibody binding to GPIIb-IIIa on the recipient's platelets was detected. The antibody was shown to have anti-PI(A1)-specificity. Only 40 min after transfusion of the frozen plasma, no antibody was detected in the plasma of the recipient. This case suggests that passively administered anti-PI(A1) alloantibody is immediately adsorbed onto the recipient's platelets and thus removed from circulation.

This prospective study defines the clinical and biochemical features of acromegaly in a large cohort of patients. There was no difference in sex distribution, and for men and women the mean ages at diagnosis (40 +/- 12 and 40 +/- 14 yr, respectively) were similar. Nearly three-quarters of patients were overweight and some 12% severely overweight; the frequency and severity of obesity also was not different between the sexes. Half of patients were hypertensive or were taking anti-hypertensive drugs. Neither GH nor insulin levels were significantly different between normotensive and hypertensive patients. Acral growth and facial coarsening, soft tissue swelling, and excessive perspiration were present in the majority (98%) of patients. Mean serum GH, Sm-C, and PRL levels did not differ between the sexes. Sm-C levels correlated with mean GH concentration (r = 0.31, p0.001), both variables inversely related to age. With each decade of life, mean GH and Sm-C levels declined by 7.6 +/- 0.2 ng/mL and 0.5 +/- 0.2 U/mL, respectively. Impaired glucose tolerance was diagnosed in 36% and frank diabetes mellitus in 30% of patients. Hyperprolactinemia was noted in 18% of patients. Galactorrhea was noted in 43 (9%) patients, most of whom were female; the mean GH levels of patients with galactorrhea (60.1 +/- 13 ng/mL) were higher than those of patients without (35.4 +/- 2.6 ng/mL, p = 0.02). Acromegaly appears to afflict men and women equally with a preponderance of presentation in the fourth decade of life.(ABSTRACT TRUNCATED AT 250 WORDS)

Circulating levels of insulin, proinsulin-like component, glucagon, growth hormone, and pancreatic polypeptide were measured in 12 patients with functioning insulinomas, and the suppressibility of serum insulin by somatostatin and diazoxide was assessed before surgical removal of the tumors. The hormone content of the tumors was evaluated by radioimmunoassay and by immunofluorescence and the structure of the tumor cells by electron microscopy. Based on these findings, we propose a new classification of insulinomas in two groups: group A is characterized morphologically by abundant well-granulated typical B-cells, trabecular arrangement of tumor cells, and uniform insulin immumofluorescence; functionally, these tumors are associated with a moderate elevation of proinsulin-like component and with an almost complete suppressibility of serum insulin by somatostatin and diazoxide. In contrast, tumors of group B are characterized by scarce well-granulated typical B-cells, a medullary-type histologie structure, and irregular insulin immunofluorescence; functionally these tumors show elevated circulating levels of proinsulin-like component and a marked resistance of insulin secretion to somatostatin and diazoxide inhibition. This way of separating human insulinomas in groups A and B represents a simplification of existing classifications and emphasizes the quantitative ultrastructure in relationship to suppressibility of insulin secretion. The proposed classification of human insulinomas in groups A and B, however, does not allow the assessment of the clinical or histopathologic malignancy of the tumors.

The effect of treadmill training on intravenous glucose tolerance and insulin sensitivity was investigated in Zucker rats (fafa). In 25-week-old fafa animals with the typical metabolic syndrome of massive obesity, glucose intolerance, hypertriglyceridaemia and insulin resistance, treadmill exercise of only very mild intensity was carried out for 6 weeks. The training programme induced a marked reduction in basal and post-glucose challenge plasma insulin levels and a slight but significant improvement of intravenous glucose tolerance. No alteration in insulin sensitivity of the isolated perfused hindquarter was demonstrable. In another study a 9-week training programme was started in 7-week-old fafa rats before the development of their metabolic syndrome. In the sedentary control animals glucose intolerance and insulin resistance developed during the study period; in the training group, both the deterioration of glucose tolerance and the decrease of insulin sensitivity were prevented. This study demonstrates in fafa rats that (a) in young animals physical training may prevent a genetically predisposed deterioration of glucose tolerance and insulin sensitivity and (b) in adult animals mild physical training may improve intravenous glucose tolerance and insulin sensitivity.

Acarbose, an alpha-glucosidase inhibitor, lowers the glycemie excursion following the ingestion of carbohydrates, in particular, sucrose. This was confirmed with increasing doses of acarbose (0, 50, and 100 mg) and the causes investigated. The absorption of the glucose moiety of sucrose was determined from plasma tracer concentrations when overnight-fasted normal subjects received a 100-g oral sucrose load labeled with sucrose ([1-14C]glucose) and a simultaneous intravenous infusion of [3-3H] glucose. As the dose of acarbose given with the sucrose load was increased from 0 to 100 mg, the percentage of the load appearing in the peripheral circulation decreased from 90% to 62%. Malabsorption was confirmed by the appearance of breath hydrogen. Simultaneously, absorption time increased from 243 to 411 min. Maximal glycemie excursions were therefore lowered from 64 to 31 mg/dl. The plasma concentrations of gastric inhibitory polypeptide and insulin decreased with the acarbose dose so that the fractional disappearance rate of glucose also decreased. However, the concentrations of glucagon-like immunoreactivity (GLI) rose, confirming the ileal appearance of malabsorbed sucrose.

The effect of physical training on glucose tolerance in vivo and skeletal muscle glucose metabolism in vitro was investigated in normal rats. Treadmill running for 10 days up to 240 min/day led to a decrease of basal and glucose-stimulated plasma insulin levels without major alterations of the IV glucose tolerance (1 g/kg body weight). Swim training of two weeks' duration, i. e. exercise up to 2×75 min/ day, which did not induce significant changes in body composition, skeletal muscle glycogen levels or citrate synthase activity, resulted in a significant improvement of IV glucose tolerance and substantial reductions of basal and glucose-stimulated plasma insulin levels. Associated with this apparent improvement of insulin sensitivity in vivo, significant increases of the insulin-stimulated glucose uptake (+ 55%) and lactate oxidation (+ 78%) in vitro were found on perfusion of the isolated hindquarter of swim-trained animals. It is suggested that mild physical training can improve glucose tolerance and insulin sensitivity in normal rats, at least in part, due to an increase of insulin sensitivity of skeletal muscle glucose metabolism.

The effects of a new sulfonylurea (Ro 6-4563) have been studied on glucose tolerance, plasma insulin, lipids, and lipoprotein pattern in 29 patients with maturity onset diabetes. After 4 weeks of treatment 3 different reactions have been distinguished and are discussed: I. No response, viz. same glucose tolerance and insulin levels before and after treatment. II. Improved glucose tolerance without increased insulin levels. III. Improved glucose tolerance with higher insulin levels. Sulfonylurea treatment had no effect on plasma lipids or lipoprotein pattern. Clinically “good blood sugar control” could not be correlated with good lipid control. Response II supports the view that sulfonylurea compounds do not necessarily act by increasing plasma insulin levels.

Radioactivity in adipose tissue triglycerides was followed after giving an intravenous injection of 25 g of glucose with 50 μCi of U-14C-glucose to 12 obese and 7 control patients. Seventy-five minutes after injection the radioactivity could be measured with sufficient precision. Recirculation of label was probably small during this period. Total adipose tissue glucose uptake could therefore be estimated knowing the variation of adipose tissue triglyceride radioactivity in different selected regions, and total body fat, and was found to be only a few per cent of all assimilated glucose in the body. Triglyceride radio-activity per gram of adipose tissue was similar in obese subjects and controls. Consequently total adipose tissue label was higher in the obese. Triglyceride radioactivity per fat cell correlated positively with fat cell size which in turn correlated positively with plasma insulin concentration. During the two first weeks after injection adipose tissue triglyceride radioactivity increased after which it began to fall in some patients.

The neutralizing capacity of two antacids (Alucol = A, Syntrogel = S), differing both in their composition and theoretical neutralizing capacity, was evaluated in vitro and in vivo. In vitro at pH 3.5, 1 ml of A or S neutralizes 3.9 and 1.6 meq of acid, respectively, in an aqueous solution. When tested in vivo in the absence of food during near maximal acid secretion, induced by impromidine, 60 ml of either A or S reduced the 4-hr mean H+ activity by 83% and 65%, respectively. In contrast, the reduction of the 12-hr H+ activity observed after repeated administration of 30-60 ml of A or S at the end of the postprandial hour failed to reach significance with both preparations. This suggests that interaction with food produces a considerable loss of in vivo antacid neutralizing capacity, not quantitatively predictable from in vitro tests.

The classification of obesity into a hypertrophic and a hyperplastic type is apparently becoming less accepted since preadipocytes are not covered by investigation of adipose tissue cellularity. Obesity-associated insulin resistance is probably due to a decrease in number of insulin receptors, induced by hyperinsulinemia. Metabolic factors may contribute to insulin resistance. Long-standing hypersecretion of insulin may exhaust the B-cell, resulting in glucose intolerance and diabetes. There is increasing interest in the (possibly) disturbed energy metabolism in obesity, though clearcut conclusions are not yet possible. For the management of obesity an integrated treatment schedule is recommended including a 1000 calorie mixed diet, intensive nutritional education, motivation, group and individual psychotherapy, physical exercise and physiotherapy. Drastic methods for the treatment of obesity are critically reviewed.

There is a close epidemiological association between obesity and elevated blood pressure for all age groups, although not every obese individual becomes hypertensive. In populations without age-related increases in body weight, an elevation of blood pressure with age is not seen. Mechanisms included in the development of hypertension in obesity are hyperinsulinemia, insulin induced sodium retention and increased sympathetic tone. Overnutrition with over intake of sodium and lack of physical exercise contribute to the metabolic syndrome of obesity. Thus, weight reduction by decreased energy uptake and increased physical exercise is recommended in the treatment of hypertension in obese patients. The resulting fall in insulin levels may lead to decreased sodium absorption in the kidney. Although treatment of obesity by weight loss decreases blood pressure substantially, a minority of patients do not respond to the weight loss. Blood pressure generally decreases before normal weight is achieved. Salt intake reduction does not appear to explain why weight reduction lowers blood pressure. Reduced levels of plasma renin activity, serum aldosterone levels, catecholamine levels and serum insulin levels may be involved in the blood pressure lowering associated with weight loss. Since the risk of cardiovascular disease in the hypertensive patient is not only determined by the blood pressure, an overall treatment which aims at reduction of other risk factors such as glucose intolerance and hyperlipoproteinemia is advocated. Thus, in any obese hypertensive patient normalization of excess body weight and increased physical activity appears to be the first and most important step of any rational therapeutic strategy.

In 1332 patients with different degrees of obesity (344 men, mean age 36 +/- 13 years, Broca Index 1.46 +/- 0.23; 988 women, mean age 37 +/- 13 years, Broca Index 1.67 +/- 0.30), cardiovascular risk factors (RF), serum HDL-cholesterol, and insulin levels were investigated. The most frequent RF was diastolic hypertension (68 per cent), followed by systolic hypertension (56 per cent), glucose intolerance (55 per cent), hypertriglyceridemia (31 per cent), hyperuricemia (19 per cent) and hypercholesterolemia (18 per cent). Only 9.4 per cent of the patients were without RF, and these patients were younger and less obese than patients with RF. Compared with controls, HDL-cholesterol levels were decreased in obese patients, however, the negative linear correlation between relative body weight and HDL-cholesterol levels was only significant in women, not in men. HDL-cholesterol levels were higher in women than in men. Serum insulin levels were correlated positively with relative body weight and negatively with age. Partial correlation analysis revealed a stronger influence of age than body weight on blood pressure, serum levels of total cholesterol, LDL-cholesterol, triglycerides and blood glucose levels. Uric acid levels correlated positively, and HDL-cholesterol levels negatively with relative body weight alone and not with age. On the basis of prevalence of RF, low serum HDL-cholesterol and high insulin levels, obese patients must be considered at high risk with respect to the development of cardiovascular disease.

Epidemiological studies on the relationship of obesity, morbidity and mortality revealed the following results: In life insurance studies, excess mortality of obese people was found with more than 30 percent overweight. Mortality was caused by cardiovascular disease and diabetes mellitus. Obesity at issue of the policy in younger age was a greater risk than in the older age group. In prospective studies with long follow-up periods (greater than 16 years) it could be shown that obesity alone was a risk factor for coronary heart disease, the risk being greatest for men and middle aged women. However, the prevalence of accepted risk factors in an obese population is so high that the question whether obesity alone is a risk factor for coronary heart disease is of little interest. The correlations between obesity and risk factors were of minor magnitude; therefore other factors, such as age or HDL-cholesterol, should be considered in the elucidation of the relationship between obesity and coronary heart disease. HDL-cholesterol appears to be a powerful independent protective factor which is diminished in obesity. Despite the fact that studies proving a prolongation of life by treating obesity are not available, the treatment of obesity may be beneficial for the patient by diminishing risk factors.

In a controlled study on 121 patients with peripheral vascular disease (PVD) (75 patients with primary hyperlipoproteinemia, 15 diabetics, 31 patients without metabolic disease) the relationship between risk factors (hyperlipoproteinemia, obesity, hypertension, abnormal glucose tolerance, smoking) and the degree and localisation of sclerotic lesions was investigated by angiography. The degree was directly related in all patients to the number of risk factors, in Type IIa to cholesterol levels, in diabetics and Type IV with abnormal glucose tolerance to age. The latter patients were 5-10 years older than patients with Type IIa and showed 2 or more additional risk factors. The sclerotic lesions affected in Type IIa, less in Type IIb, predominately the pelvic vessels. Diabetics and Type IV patients showed a distal arterial involvement. The difference was significant. The degree of sclerotic lesions in arteries of the pelvis and the distal lower limb was positively correlated with the cholesterol-triglyceride ratio. Smoking aggravated the pelvic lesions in Type IV. Hypertension lead to more pronounced lesions of the distal lower limb in Type II. S-shaped tortuosities of the big vessels were shown to be typical, independent of localisation or degree.

In a retrospective study over the years 1978-1982, 729 cases of acute pulmonary embolism were analyzed in relation to history, clinical signs and laboratory findings and the results compared with the findings of the urokinase pulmonary embolism trial. As far as history and clinical symptoms were concerned, breathlessness, chest pain, tachypnea, tachycardia and cyanosis were the dominating features. Among laboratory tests, the radiological and electrocardiographic findings of pulmonary hypertension were of little value. In contrast, arterial hypoxemia and isotope scanning provided the most reliable diagnostic information. The most frequent problem in differential diagnosis was acute myocardial infarction.

In 500 obese patients (146 men, mean age 37 +/- 13 years, Broca index 147 +/- 24; 354 women, mean age 36 +/- 14 years, Broca index 151 +/- 28) cardiovascular risk factors (RF) were investigated. The most frequent RF was hypertension (71 per cent), followed by glucose intolerance (49 per cent), hypertriglyceridemia (31 per cent), hypercholesterolemia (22 per cent) and hyperuricemia (22 per cent). Only 12 per cent of the patients were without RF. These patients were younger and less obese than the patients with RF. The prevalence of RF increased with increasing age and overweight. Analysis revealed significant correlations between overweight and blood pressure, blood glucose, insulin and age. Significant correlations between age and hypertension, blood glucose cholesterol, triglycerides and overweight were detected. The correlation between overweight and the sum of all RF was higher (r = 0.35) than the one between age and the sum of all (r = 0.23). Obese patients had a high prevalence of RF. Increasing overweight and (to a lesser extent) age are both associated with increased prevalence of RF. On the basis of the prevalence of RF, patients with gross obesity (Broca index greater than around 150) were considered to be at a high risk in respect of coronary heart disease.

Home blood glucose monitoring by diabetic patients has recently been advocated as an effective means to improve metabolic control. The Glucocheck apparatus, a pocket-size battery-driven reflectance-meter (in Germany commercially available under the name Glucose-meter), has been evaluated for accuracy and practicability. In 450 blood glucose measurements, the variance between the values obtained using the Glucocheck apparatus and routine clinical laboratory procedures was +/- 11.7%. Especially in the low range of blood glucose concentrations, the Glucocheck method was very reliable. The quantitative precision of the Glucocheck method depends, however, quite considerably on the ability of the patient to use the apparatus correctly. In order to profit from Glucocheck in clinical practice, particular efforts to educate the patients in its use are necessary.

The effect of 4-[p-chloro-N-(p-methoxyphenyl)-benzamido] butyric acid (clanobutin, Bykahepar) on bile formation was studied in anesthetized male Sprague-Dawley rats and in non-anesthetized female boxer dogs. Following i.v. injection of 40 mg/kg body weight of clanobutin, a marked choleresis paralleling the biliary excretion of the drug was observed in both species. The biliary elimination of 1 mumol clanobutin (and metabolites) caused on the average an increment of bile flow of 90 microliter and 11.5 microliter in the rat and dog, respectively. Bile flow was linearly related to clanobutin excretion in rat and dog. Within the period of observation 55% of the dose of clanobutin in the rat, and 80% of the dose in the dog were eliminated via the bile; urinary excretion amounted to 3% of the dose. In rat bile, 32% of the clanobutin was present as the parent compound; the remaining 68% consisted of 3 metabolites. Measurement of the erythritol clearance in the dog suggests that clanobutin stimulates the bile salt-independent, canalicular bile formation. In addition, however, the observed changes in the bile/plasma concentration ratio of erythritol, as well as a predominant excretion of bicarbonate and chloride point to a possible ductular effect of clanobutin. In these acute studies, the drug did not influence the bile salt, phospholipid or cholesterol excretion. Cholesterol saturation of bile was unaffected.

The interrenal (adrenocortical) cells of the common dogfish show the ultrastructural features characteristic of steroid hormone producing cells. Their endoplasmic reticulum consists predominantly of smooth surfaced tubules. They are rich in mitochondria with tubular and vesicular cristae and in liposomes. This last characteristic differentiates them from the interrenal cells of Teleosts, which are devoid of liposomes. In addition, the interrenal cells of the common dogfish are strikingly rich in microfilament-like inclusions.

The long-term results of total fasting during hospitalisation were evaluated an average of 21 months after the end of the hospital stay in 42 patients treated for obesity between 1971 and 1975. Further weight reduction occurred in 14, while the remainder had regained some weight. Nine of the latter had, in fact, surpassed their prehospitalisation weight. Neither age not sex, social status, time interval since fasting had any influence on the long-term results of total fasting. It is concluded that, in view of the poor correlation between cost and long-term result of such total-fasting regimen, it should be undertaken in this form only exceptionally.

Chronic ITP is a common hematologic illness. Approximately three fourths of the patients respond to corticosteroids or splenectomy and need no further treatment. Patients refractory to these two therapeutic approaches are relatively resistant to present forms of treatment and are at much greater risk for morbidity and mortality. Future clinical studies evaluating therapy in this refractory group would be best performed in a cooperative group setting in which large numbers of patients could be treated in a prospective randomized manner.

To investigate whether leg exercise accelerates the absorption of exogenous insulin from Its subcutaneous depot in insulin-treated diabetics, and whether the glycemie response to exercise in these patients is related to alterations in the insulin absorption process, we studied nine insulin-dependent diabetics and four normal subjects during rest and exercise. The diabetics received the regular dose of intermediate-acting insulin, reduced by 20 U, and their morning breakfast. One hour after the meal, 20 U regular insulin (Actrapid, labeled with 125I or unlabeled) was injected into the arm or the leg. Exercise (90 ± 10 W) was initiated 35 min later for three consecutive 10-min periods. In controls, no insulin was injected. Plasma glucagon and C-peptide levels were not changed during exercise, but blood ketone bodies and lactate levels increased significantly. Whether the insulin was injected into the moving or resting limb, external counting over the injection site demonstrated no exercise-induced alteration of the disappearance of 125I-radiation during the exercise period, but revealed a small postexercise enhancement of 125I disappearance only after leg injection. Determination of plasma insulin levels in four diabetics with newly insulin-treated diabetes revealed that circulating insulin had increased by 70% 30 min after the subcutaneous administration of regular insulin and had then plateaued for 45 min. Leg exercise had no additional effect on plasma insulin levels during the physical activity. In normals, exercise lowered circulating plasma insulin to a level approximately one-fifth that in diabetics. Regardless of the insulin injection site, there was an identical glycemie response to exercise, i.e., a pronounced fall of glycemia by 15% immediately and by 50% 30 min after the onset of exercise. In normals glucose homeostasis was not disturbed by exercise. This study demonstrates that moderate leg exercise does not necessarily accelerate the absorption of exogenous insulin; however, it can induce an acute and profound fall in glycemia, which presumably is due to the presence of a fixed hyperinsulinemic state in these patients rather than an alteration of the mobilization of insulin from its subcutaneous depot. Although this study investigated only a specific situation, the results indicate the possibility that exercise-induced hypoglycemia in insulin-treated diabetics is not necessarily prevented by changing the insulin injection site to nonmoving parts Of the body.

Glucagon secretion before and during arginine infusions was tested in 11 patients with diabetes associated with haemochromatosis. The results were compared with those obtained in six normal subjects and five patients with haemochromatosis but normal glucose tolerance. The patients with haemochromatosis, regardless of glucose tolerance, exhibited higer level of plasma immunoreactivity for glucagon (antiserum 30-K) suggesting hyperglucagonaemia. However, additional analysis revealed that a considerable amount of this glucagon immunoreactivity was due to cross-reacting material of high molecular weight, the levels of which were significantly higher in patients with idiopathic haemochromatosis. When this was deducted from the total immunoreactivity measured, the resulting values for true glucagon concentrations were similar to those of normal subjects. The data suggest that (1) patients with idiopathic haemochromatosis, whether or not associated with diabetes, exhibit plasma glucagon levels comparable with those of normal subjects; (2) the plasma of the same patients contains significantly more high-molecular-weight substances reacting with glucagon antiserum 30-K than is present in plasma of normal subjects; and (3) 'hyperglucagonaemia' may be erroneously suggested when glucagon is measured with certain antisera reputed to be specific for glucagon.

A lethal paradoxical air embolism (PLE) occurred in a 21-year-old secundigravida during general anaesthesia for cervical cerclage on account of cervical insufficiency. The diagnosis of PLE was verified postmortem; we initially diagnosed venous air embolism intraoperatively because of typical symptoms (cyanosis, pulmonary dysfunction, and vascular obstruction) and aspiration of air from the subclavian catheter. We also suspected an arterial embolism due to prominent neurologic deficits. In spite of corrective positioning, controlled ventilation (CPPV and PEEP), volume therapy, and sympathomimetics, resuscitation remained unsuccessful. This very rare complication depends upon several conditions: (1) opened, non-collapsible veins; (2) a pressure gradient from outside to inside the veins; (3) a patent foramen ovale; and (4) a right atrial pressure greater than that on the left, which can cause an air embolism to either the coronary or cerebral circulations. The pathophysiology and causative factors are discussed extensively as the immediately started resuscitation could not alter the lethal course.

The effects of physical activity on blood glucose homeostasis in diabetes mellitus and the potential benefits of exercise in the treatment of diabetic patients, are reviewed. Mild physical exercise results in a fall of blood glucose levels in controlled diabetic patients; this acute effect of exercise might be used in particular to inhibit the rise of blood glucose seen in insulin-treated diabetics after food intake. In contrast, physical activity will further deteriorate the metabolic situation in decompensated diabetic patients by an increase in blood glucose and a rapid aggravation of ketosis. On the other hand exercise potentiates the blood glucose lowering effect of subcutaneously injected insulin; therefore precautions have to be taken in order to avoid hypoglycemia in insulin-dependent diabetics especially during and after more strenous exercise. In juvenile-type diabetes, physical activity can be used as an efficient therapeutic adjunct only in cooperative, well-instructed patients who are used to check their metabolic situation on a regular basis. Physical training increases the tissues' sensitivity towards (endogenous) insulin. Hence, in addition to the diet, training might represent the most appropriate treatment in maturity onset-type diabetic patients. However, direct evidence for an improvement of glucose tolerance in diabetic patients by physical training is still lacking. In order to formulate detailed, generally applicable recommendations on how to carry out a useful therapeutic program of physical exercise and/or training in diabetic patients, further clinical studies assessing the quantitative effects of physical activity on carbohydrate metabolism are needed.

Type-I and type-II diabetics receiving antidiabetic therapy, comprising of diet, or diet plus sulphonylureas or insulin, were additionally treated with acarbose for a period of 12 months in an open, multi-centre study carried out under general practice conditions. This was followed by an observation period without acarbose. After 3 months on acarbose, the mean fasting and post-prandial blood glucose concentrations were 30 and 40 mg/dl, respectively, lower, thereafter remaining virtually unchanged up to the end of treatment. After withdrawal of acarbose the mean blood glucose values rose to their pretreatment levels, except in patients with proven poor acarbose compliance. All three treatment subgroups mentioned above showed the same pattern of glucose reduction. The mean blood glucose values of patients previously treated by dietary measures alone fell under acarbose therapy below the upper limit of normal. The percentage of glycosuric patients in the above subgroups was halved under acarbose and rose after discontinuation of acarbose approximately to the initial numbers. The number of patients with blood-glucose control classified as "good" rose fourfold during the acarbose treatment. In the course of the trial acarbose had to be discontinued due to intestinal side effects in only 5% of the patients. Frequency and intensity of the intestinal symptoms related to increased bacterial carbohydrate cleavage (flatulence, meteorism, occasionally diarrhoea), decreased during treatment. Other subjective complaints or side effects were neither reported nor could be detected objectively.

The effects in vivo of a biguanide (Metformin) on intestinal enzyme activities and vitamin B12 and folic acid absorption can be summarized as follows. 1. The enzyme activities of the brush border of the mucosal cell of the upper intestine were influenced. 2. The disaccharidase activities were reduced, although not to such an extent as to be expected to impair disaccharide absorption. 3. Vitamin B12 absorption was significantly reduced, as measured by Schilling test. 4. Serum folic acid levels were significantly reduced, possibly due to a decreased intestinal absorption of dietary folic acid.

Autoantibodies against platelet glycoproteins (anti-GP) are found in the majority of patients with autoimmune thrombocytopenia (AITP) as well as in thrombocytopenia associated with systemic lupus erythematosus (SLE). Some of these patients may have anti-phospholipid antibodies (anti-PL). To evaluate the pathogenetic significance of anti-PL and anti-GP antibodies in AITP and SLE patients, we investigated anti-cardiolipin (anti-CL), anti-phosphatidylserine (anti-PS) and anti-GP antibodies (anti-GPIIb-IIIa and anti-GPIb-IX) in 71 patients with AITP and 3 thrombocytopenic patients with SLE. Anti-GP antibodies were detected in 52 (70%) patients. Fifty-six (73%) patients showed anti-PL antibodies. Seven patients (6 AITP, 1 SLE) with both anti-GPIIb-IIIa and IgG anti-PL antibodies were followed during treatment with corticosteroids. Antibodies were measured before treatment and at the time of platelet-peak. Anti-GPIIb-IIIa antibodies decreased in all or became undetectable in five. In contrast, IgG anti-PS and IgG anti-CL antibodies decreased only moderately or remained positive. Adsorption experiments, using gelfiltered platelets, erythrocyte (Ec)-inside-out-vesicles and purified GPIIb-IIIa, showed that anti-GP and anti-PL antibodies have distinct specificities and do not crossreact. We conclude that anti-PL and anti-GP antibodies may be present simultaneously in some patients with immune mediated thrombocytopenia. Although anti-PS as well as anti-CL antibodies may be responsible for thrombocytopenia, we speculate that anti-GPIIb-IIIa antibodies are more related to the severity of thrombocytopenia.