Assessing genetic and environmental influences on epicardial and abdominal adipose tissue quantities: a classical twin study.

BACKGROUND/OBJECTIVES: Various adipose tissue compartments play an important role in the development of cardiometabolic diseases. The quantity of different fat compartments is influenced by genetic and environmental factors. The aim of our study was to evaluate the magnitude of genetic and environmental effects on epicardial, subcutaneous and visceral adipose tissue (EAT, SAT and VAT) quantities in a cohort of adult twin pairs. SUBJECTS/METHODS: In this cross-sectional study we investigated adult twins (57 monozygotic (MZ) and 33 dizygotic (DZ) same-gender twin pairs; 180 twin subjects). We measured EAT volume using electrocardiogram-gated native computed tomography (CT) scan of the heart, and abdominal SAT and VAT areas were quantified between the third and fourth lumbar vertebra on native CT images. We calculated genetic and environmental impact on the size of various adipose tissue compartments by analyzing co-twin correlations in MZ and DZ pairs separately, and furthermore by using genetic structural equation models. RESULTS: In co-twin analysis, MZ twins had stronger correlations than DZ twins for EAT (rMZ=0.81, rDZ=0.32), similar to SAT and VAT quantities (rMZ=0.80, rDZ=0.68 and rMZ=0.79, rDZ=0.48, respectively). In multi-trait model fitting analysis, the overall contribution of genetic factors to EAT, SAT and VAT volumes were 80%, 78% and 70%, whereas environmental factors were 20%, 22% and 30%, respectively. Common pathway model analyses indicated that none of the EAT, SAT and VAT phenotypes was independent of the other two. CONCLUSIONS: Genetic factors have substantial influence, while environmental factors have only a modest impact on EAT volume, abdominal SAT and VAT quantities. There is a considerable amount of common genetic background influencing the quantities of all three adipose tissue compartments.

Is there a connection between postprandial hyperglycemia and IGT related sensory nerve dysfunction?

BACKGROUND AND AIMS: To assess the risk factors for sensory nerve dysfunction in subjects with isolated impaired glucose tolerance (IGT). METHODS AND RESULTS: Seventy-two people with isolated IGT (WHO 1999 criteria) and 39 gender and age-matched healthy volunteers underwent detailed clinical and neurological assessment including quantitative sensory testing using the Neurometer device (current perception threshold measurement on four limbs at three different frequencies). Sensory nerve dysfunction was defined as at least two abnormalities on any frequencies on the upper or lower limbs. Sensory nerve dysfunction was more prevalent among subjects with IGT compared to controls (58.3 vs. 10.3%, OR: 11.23, 95%CI: 3.57-35.35). This association was not influenced by BMI, systolic and diastolic blood pressure, heart rate and autonomic neuropathy (multiple adjusted OR: 13.87, 95%CI: 3.18-60.58), but further adjustment for glycaemic measures abolished the association (OR: 1.58, 95%CI: 0.07-35.68). Assessing the components of glycaemic measures separately, the association between sensory nerve dysfunction and IGT was not affected by HbA1c (OR: 13.94, 95%CI: 1.84-105.5). It was, however, substantially attenuated by fasting plasma glucose (OR: 6.75, 95%CI: 1.33-34.27) while the significance was lost after adjustment for 120 min postload glucose level (OR: 3.76, 95%CI: 0.26-54.10). In the pooled population assessed, independent determinants of sensory nerve dysfunction were older age, 120 min glucose, higher height and cardiovascular autonomic neuropathy at near significance. CONCLUSIONS: Sensory nerve dysfunction amongst subjects with IGT was not explained by cardiovascular covariates, only by glycaemic measures. In addition to 120 min glucose, cardiovascular autonomic neuropathy at borderline significance, age, and height were the independent determinants of sensory nerve dysfunction.

Impact of treatment with saxagliptin on glycaemic stability and ß-cell function in the SAVOR-TIMI 53 study.

AIMS: To study the effects of saxagliptin, a dipeptidyl peptidase-4 inhibitor, on glycaemic stability and ß-cell function in the SAVOR-TIMI 53 trial. METHODS: We randomized 16,492 patients with type 2 diabetes (T2D) to saxagliptin or placebo, added to current antidiabetic medications, and followed them for a median of 2.1 years. Glycaemic instability was defined by: (i) a glycated haemoglobin (HbA1c) increase of ≥ 0.5% post-randomization; (ii) the initiation of new antidiabetic medications for ≥ 3 months; or (iii) an increase in dose of oral antidiabetic medication or ≥ 25% increase in insulin dose for ≥ 3 months. ß-cell function was assessed according to fasting homeostatic model 2 assessment of ß-cell function (HOMA-2ß) values at baseline and at year 2 in patients not treated with insulin. RESULTS: Compared with placebo, participants treated with saxagliptin had a reduction in the development of glycaemic instability (hazard ratio 0.71; 95% confidence interval 0.68-0.74; p < 0.0001). In participants treated with saxagliptin compared with placebo, the occurrence of an HbA1c increase of ≥ 0.5% was reduced by 35.2%; initiation of insulin was decreased by 31.7% and the increases in doses of an oral antidiabetic drug or insulin were reduced by 19.5 and 23.5%, respectively (all p < 0.0001). At 2 years, HOMA-2ß values decreased by 4.9% in participants treated with placebo, compared with an increase of 1.1% in those treated with saxagliptin (p < 0.0001). CONCLUSIONS: Saxagliptin improved glycaemia and prevented the reduction in HOMA-2ß values. Saxagliptin may reduce the usual decline in ß-cell function in T2D, thereby slowing diabetes progression.

Autonomic dysfunction and circadian blood pressure variations in people with impaired glucose tolerance.

AIMS: To assess circadian blood pressure variability in people with impaired glucose tolerance and a healthy control population. METHODS: Seventy-five people with impaired glucose tolerance and 40 healthy volunteers (frequency matched on 10-year age bands and sex) underwent a detailed neurological assessment. Autonomic neuropathy was detected by the five standard cardiovascular autonomic tests and heart rate variability was characterized by the triangle index. Diurnal indices were assessed by 24-h ambulatory blood pressure monitoring. Systolic and diastolic diurnal indices were defined as: (mean daytime blood pressure - mean night-time blood pressure) × 100/mean daytime blood pressure. RESULTS: Mean 24-h systolic and diastolic blood pressure was significantly higher in the group with impaired glucose tolerance compared with the control group [126 ± 12 (mean ± SD) vs. 117 ± 10, 75 ± 7 vs. 71 ± 6 mmHg, both P < 0.05). Systolic and diastolic diurnal indices and heart rate variability triangular index were significantly lower in people with impaired glucose tolerance compared with control subjects (9.1 ± 7.8 vs. 13.2 ± 5.4, 14.5 ± 9.7 vs. 18.4 ± 7.1 mmHg, 28.0 ± 8.4 vs. 39.5 ± 9.3, all P < 0.05). Differences in mean diastolic blood pressure, heart rate variability triangular index and the frequency of non-dippers between those with impaired glucose tolerance and control subjects seemed to be independent of BMI and the presence of cardiovascular autonomic neuropathy, as simultaneous adjustment for BMI and cardiovascular autonomic neuropathy had no major effect on the results. CONCLUSION: Our data suggest that people with impaired glucose tolerance have increased diastolic blood pressure and abnormal circadian blood pressure regulation, independent of obesity and the presence of cardiovascular autonomic neuropathy.

Screening for metabolic syndrome within a minority ethnic group (adult Gypsy people) in Hungary.

BACKGROUND: Metabolic syndrome occurs more often among people living in poorer social conditions. The health status of the largest minority ethnic group in Hungary lags in many aspects behind that of the general population. METHODS: To estimate the prevalence of metabolic syndrome a screening was initiated in the city of Gyor among subjects aged 20-70 years who declared themselves as Gypsy. Subjects with known diabetes and cardiovascular disease were excluded. The diagnosis of metabolic syndrome was based on the ATP-III criteria. RESULTS: Among the 77 individuals screened (35 men, 42 women, age 46.9 ± 10.6 years, x ± SD) diabetes mellitus was found in 14 cases (18.2 %), and pre-diabetes (impaired fasting blood glucose (IFG) or impaired glucose tolerance (IGT) could be diagnosed in further 14 cases (18.2 %). Individual components of the metabolic syndrome occurred as follows: hypertension in 47 subjects (61.0 %), abnormal waist circumference in 40 individuals (51.9 %), abnormal HDL-cholesterol in 39 cases (50.6 %), abnormal triglycerides in 35 individuals (45.5 %) and abnormal fasting blood glucose in 15 subjects (19.5 %). Within the cohort metabolic syndrome could be diagnosed in 39 individuals (50.6 %) without a significant gender difference (males 20/35 = 57.1 %; women: 19/42 = 45.2 %, p>0.05). CONCLUSION: The occurrence of metabolic syndrome and that of glucose intolerance is high among adult Gypsy people in Hungary. In order to recognise cardio-metabolic risks and to prevent their cardiovascular consequences, continuous health promotion and adequate medical care should be provided for the Gypsy population in Hungary (Tab. 5, Ref. 32).

Effects of genetic vs. environmental factors on cardiovascular autonomic function: a twin study.

AIMS: Cardiovascular autonomic function is often assessed in patients with diabetes by measuring heart rate variability and baroreflex sensitivity, the heritability of which is not fully understood. The present study was aimed to determine the effects of genetic and environmental factors on heart rate variability and baroreflex sensitivity in monozygotic and dizygotic adult healthy twin pairs. METHODS: A total of 101 (63 monozygotic, 38 dizygotic) adult twin pairs (n = 202; mean age 44.3 years) were investigated. Anthropometric variables and serum metabolic markers were measured, while environmental characteristics were evaluated by questionnaires. Linear and spectral indices of heart rate variability and baroreflex sensitivity were determined by non-invasive methods. All measurements were adjusted for age and gender (model 1) and for all significantly relevant covariates (model 2). Heritability A-C-E structural equation models were used for characterizing the proportion of additive genetic, shared and unshared environmental influences. RESULTS: Genetic influence of different cardiovascular autonomic indices was estimated between 10.3 and 39.4%, common environmental influence was found between 0.0 and 33.2%, while unshared environmental influence was observed between 60.6 and 81.4% in model 1 analysis. In multivariable-adjusted heritability estimates (model 2), the magnitude of the genetic effects decreased to 0.0%, common environmental influence was nearly unchanged (values between 4.4 and 14.5%), while unshared environmental influence slightly increased (values between 85.5 and 96.5%). CONCLUSIONS: Unshared environmental but not genetic factors have substantial influence on cardiovascular autonomic function, suggesting that appropriate treatment of all modifiable environmental factors is of importance in order to prevent or ameliorate cardiovascular autonomic neuropathy.

Day-night blood pressure variation in normotensive and hypertensive NIDDM patients with asymptomatic autonomic neuropathy.

In order to assess the characteristics of day-night blood pressure (BP) variation in normotensive and hypertensive non-insulin-dependent diabetic (NIDDM) patients with asymptomatic autonomic neuropathy, 54 NIDDM patients and 13 healthy control subjects were studied by casual BP measurements and 24-h ambulatory blood pressure monitoring. Signs but not symptoms of autonomic neuropathy were documented by results of standard cardiovascular function tests in each patient. Daytime (06:00-22:00) and nighttime (22:00-06:00) BP values were separately analyzed and delta day-night BP values and diurnal index were determined. Patients were classified as being normotensive or having hypertension according to the casual BP values and medical history. In normotensive NIDDM patients (n = 30), nighttime systolic BP was significantly higher, whereas delta day-night systolic and delta day night diastolic BP values as well as diurnal index were considerably lower than those in control subjects (n = 13). In hypertensive NIDDM patients (n = 24), similar alterations were found at higher BP levels. No significant difference was found in BP values if normoalbuminuric and microalbuminuric NIDDM patients were compared. 'Non-dipper' phenomenon could be found in normotensive and hypertensive NIDDM patients with asymptomatic autonomic neuropathy, suggesting that relative sympathetic overdrive due to incipient and predominantly parasympathetic impairment of cardiovascular innervation might play a role in early alterations of circadian BP variation.

Impairment of the NO/cGMP pathway in the fasting and postprandial state in type 1 diabetes mellitus.

The assessment of the postprandial state in diabetes mellitus has gained importance due to postprandial hyperglycemia being considered as an independent risk factor for cardiovascular disease. Hyperglycemia may contribute to vascular dysfunction through the alteration of the nitric oxide/cyclic guanosine monophosphate (NO/cGMP) pathway. The authors assessed the NO/cGMP pathway in the fasting and postprandial state in 20 type 1 diabetic patients (age: 34.1 +/- 2.6 years, body mass index (BMI): 24.1 +/- 1.3 kg/m (2), duration of diabetes: 16 +/- 2.2 years, HbA (1C): 8.3 +/- 0.4 %, [x +/- SEM], 10 without, 10 with late complications) and 20 matched control subjects (age: 39.7 +/- 1.9 years, BMI: 25.3 +/- 1.1 kg/m (2)). In the fasting state NO end product (nitrite/nitrate) levels did not differ between the diabetic and control group, cGMP levels were found to be significantly lower in the diabetic group (2.5 +/- 0.2 vs. 4.6 +/- 0.6 nmol/l, p = 0.01). A higher level of lipid peroxidation end products (TBARS) was found in diabetic subjects (6.7 +/- 0.4 vs. 5.0 +/- 0.3 micro mol/l, p = 0.004). The diabetic subgroup without late complications had significantly higher nitrite/nitrate levels compared to the patients with complications (57.8 +/- 6.6 vs. 30.4 +/- 4.3 micro mol/l, p = 0.006), their TBARS and cGMP levels were similar. The control subjects responded to the test meal with an increase in the cGMP levels (4.6 +/- 0.6 to 5.5 +/- 0.6 nmol/l, p = 0.02), while in the diabetic group no change was detected. Postprandial nitrite/nitrate levels decreased in both groups, they were significantly lower in the diabetic group. There was no difference between postprandial nitrite/nitrate, cGMP, or glucose levels in the diabetic subgroups. Postprandial glucose levels showed a significant negative correlation with cGMP levels in the diabetic group (r = - 0.50, p = 0.02). The results suggest that in subjects with type 1 diabetes mellitus NO might have an impaired ability to induce cGMP production in the fasting state prior to the development of late specific complications or microalbuminuria under hyperglycemic conditions. Postprandial hyperglycemia is suggested to interfere with endothelial NO action, as shown by the decreased nitrite/nitrate and unchanged cGMP plasma levels in the diabetic group. The impairment of the NO/cGMP pathway both in the fasting and postprandial state that was shown in patients without diabetic complications may be an early sign of hyperglycemia induced vascular damage in type 1 diabetes mellitus.

Hypoglycemia factitia: Munchhausen syndrome in diabetes mellitus.

The medical history of a 43-year-old non-insulin-dependent diabetic patient with severe and repetitive hypoglycemic episodes is reported. The exact diagnosis proved to be difficult. Finally, surreptitious insulin administration was documented by high serum insulin and low C-peptide values with an elevated molar ratio of insulin to C-peptide in peripheral venous blood during hypoglycemia. Confronting the patient with evidences of surreptitious insulin administration, hypoglycemic episodes abruptly stopped. Hypoglycemia factitia was assessed as a manifestation of Munchhausen syndrome in diabetes mellitus.

Clinical consequences of cardiovascular autonomic neuropathy in diabetic patients.

A wide range of clinical consequences of cardiovascular autonomic neuropathy (CAN) can be observed in diabetic patients and contributes to the clinical picture of the diabetic heart. Resting heart rate and cardiovascular reflexes as well as circadian heart rate variability may be altered by CAN in diabetes. Moreover, blood pressure is also influenced by sympathovagal imbalance. Postural hypotension is a clinical characteristic in diabetic subjects with CAN. Painless myocardial infarction, ischaemia and left ventricular dysfunction are also observed in some cases. Impairment of cardiac parasympathetic and sympathetic innervation as well as QT-interval prolongation may play a partial role in the pathogenic mechanism of sudden unexpected death in diabetic patients. The risk of surgical intervention and that of anaesthesia are increased due to abnormal cardiovascular reactions. Clinical symptoms and signs of CAN should be assessed as severe diabetic complication and the therapy is difficult in some cases. Taken together, symptoms and signs of CAN carry a poor prognosis in diabetic patients.

Cardiac autonomic neuropathy and QT interval length. A follow-up study in diabetic patients.

For evaluating the clinical significance of QT interval prolongation in diabetics with cardiac autonomic neuropathy (CAN), 53 diabetic patients were followed-up for 5 years or to death and the results of cardiovascular function tests as well as the values of QT intervals were repeatedly determined. At baseline investigation, the QTc intervals were significantly longer in diabetics with definitive (456 +/- 5 ms, mean +/- SEM, n = 17) than those with early (435 +/- 5 ms, n = 13, p less than 0.01) and without (413 +/- 4 ms, n = 23, p less than 0.001) signs of CAN or in controls (414 +/- 5 ms, n = 15, p less than 0.001). Thirteen patients died during the follow-up period (1 without, 2 with early and 10 with definitive signs of CAN) but QTc intervals did not differ significantly between patients with cardiac (456 +/- 9 ms, n = 8) and non-cardiac (459 +/- 15 ms, n = 5) causes of death. At reinvestigation of 40 patients, the severity of CAN worsened in 22 patients, remained unchanged in 15 patients and improved in 3 patients. Accordingly, the mean values of autonomic function tests decreased (beat-to-beat variation from 15 +/- 2 to 9 +/- 1 beats/min, p less than 0.01; 30:15 ratio from 1.19 +/- 0.03 to 1.09 +/- 0.02, p less than 0.01) while QTc interval increased (from 424 +/- 3 to 431 +/- 4 ms, p less than 0.01). It was concluded that CAN carries a poor prognosis in diabetic patients. Nevertheless, QTc interval prolongation could be evaluated as rather an additional sign of CAN than the only explanation for mechanism in the pathogenesis of sudden cardiac death in diabetic patients.

Myocardial systolic alterations of insulin-dependent diabetics in rest.

Left ventricular systolic function was tested in 27 insulin-dependent diabetic patients by measuring the systolic time intervals. In diabetics longer pre-ejection period, and higher PEP/LVET quotient were found showing a good correlation with the values of glycosylated haemoglobin. These findings emphasize the importance of metabolic control in the development of cardiac dysfunction.

[Factitious hypoglycemia--Munchausen syndrome in diabetes mellitus]. / Hypoglykaemia factitia--Münchhausen-syndroma diabetes mellitusban.

The medical history of a 43-year-old non-insulin-dependent diabetic patient is presented. The exact diagnosis of the cause of repetitive and severe hypoglycaemic episodes proved to be difficult. Finally, high serum insulin and low C-peptide values were found in peripheral venous blood during hypoglycaemia resulting in an elevated (> 1.0) molar ratio of insulin to C-peptide. The laboratory findings were assessed as consequences of surreptitious insulin administration. Factitious hypoglycaemia could be considered as a clinical manifestation of Munchhausen syndrome. Confronting the patient with evidences of surreptitious insulin injections, hypoglycaemic episodes abruptly discontinued to occur.

[Metabolic syndrome-x at the turn of the millennium (Theoretical aspects with practical consequences)]. / Metabolikus x-szindróma az ezredfordulón. (Elméleti vonatkozások és gyakorlati teendók).

The authors give an overview on the hypothesis of the metabolic syndrome-x in accordance with insulin resistance and hyperinsulinism in triggering the development of type 2 diabetes mellitus with its clinical complexity. Dealing with the criticism of the original hypothesis, they touch the problem of protein-insufficient feeding in utero and consequences later in life. They discuss the recently emerging importance of postprandial hyperglycaemic condition, which might be even more responsible in leading to atherosclerotic lesions than the hyperinsulinism itself. Finally, they deal with the non-pharmacological intervention and drug therapy as well. A short overview of the results of the UKPDS (United Kingdom Prospective Diabetes Study) are also given, pointing out the clinical importance of correct antihyperglycaemic and antihypertensive treatment. The authors emphasise the utmost importance of early prevention in behalf of avoiding type 2 diabetes and cardiovascular complications as well.

[Granulomatous dermatitis caused by surfen in diabetics treated with Insulin-depot-S-Richter]. / Surfen okozta granulomás börgyulladás Insulin-depot-S-Richter terápia kapcsán.

Two cases of local cutaneous reaction in diabetics treated with Insulin-depot-S-Richter are reported. Intracutaneous test and histological examination revealed that the granulomatous inflammation of the skin was due to surfen. Insulin-depot-S-Richter was changed to insulin preparation free from surfen (Monotard MC, Novo) and no further local reactions could be observed in the same patients.

[Thiazolidinediones--a new class of oral antidiabetic drugs]. / Tiazolidindionok--az oralis antidiabeticumok új hatástani csoportja.

The discovery of a new class of oral antidiabetic drugs was stimulated by difficulties with the treatment currently available for patients with type 2 diabetes mellitus. Thiazolidinediones can lower blood glucose values due to their special insulin-sensitiser effect. In this way, these drugs seem to be very effective in the treatment of type 2 diabetic patients with characteristics of metabolic syndrome. The intracellular action caused by thiazolidinediones differs markedly from that of other oral antidiabetic drugs available. Apart from antihyperglycaemic effect, thiazolidinediones have further beneficial effects in experimental diabetes which require corroboration by clinical studies. Troglitazone was the first drug which reached the market. Unfortunately, this drug was withdrawn soon due to its hepatotoxicity. Rosiglitazone proved to be much safer in clinical studies. Pioglitazone is being tested nowadays in clinical studies. Thiazolidinediones have been already listed among oral antidiabetic drugs in international therapeutical guidelines. Nevertheless, further clinical studies and experiences are needed to determine the final exact indication of thiazolidinediones for the treatment of type 2 diabetic patients.

[Human insulin-induced lipoatrophy]. / Humán inzulin okozta lipoatrophia.

The medical history of a 14-year-old diabetic adolescent female patient is presented. The patient has been exclusively treated by human insulin since the manifestation of diabetes at age of 11. As a clinical curiosity lipoatrophy developed at different sites of insulin injections (upper arm, thigh, abdominal wall, buttock). The insulin administration technique by pen-devices was correct. The patient proved to be non-atopic without signs of insulin allergy on intracutan tests. On histological examination, "lipoblastoma-like" alterations without signs of local immune mechanisms and no inflammatory cell infiltrates were found at the site of lipoatrophy. The histological findings suggested dedifferentiation of adipose tissue mediated probably by elevated local tumor necrosis factor-alpha. Immunological consequences of previous human insulin treatment were documented by high insulin-specific IgG and IgE antibody titer, however, no clinical signs of immunogenic insulin resistance were found. Switching to insulin analogue (insulin lispro) before main meals no further lipoatrophic areas were observed despite of using human NPH-insulin for basal insulin supplementation. Insulin analogue (insulin lispro) may be useful for treating diabetic patients with lipoatrophy secondary to previous human insulin treatment.

[Variability of the circadian heart rate in diabetes mellitus-related autonomic neuropathy]. / A szívfrekvencia napszaki ingadozásainak vizsgálata autonom neuropathiával szövödött diabetes mellitusban.

For assessing the alterations of circadian heart rate variability 66 diabetic patients (age: 52.9 +/- 1.0 years; x +/- SEM) and 23 control subjects (age: 52.7 +/- 1.7 years) were investigated using 24 hours Holter monitoring. Autonomic neuropathy (AN) was evaluated by tests for cardiovascular reflexes and patients were classified as being without AN (n = 26), having mild (n = 25) or definitive (n = 15) signs of AN. Minimal heart rates were significantly higher while maximal heart rates were considerably lower in patients with than without AN (60 +/- 2 min-1 versus 54 +/- 1, min-1, p < 0.05 and 125 +/- 4 min-1 versus 146 +/- 4 min-1, p < 0.01). Diabetic groups were comparable regarding values of averaged heart rates. The difference between the mean waking and sleeping averaged heart rates was the smallest in diabetic patients with definitive signs of AN (9 +/- 2 min-1) differing from those of control subjects (17 +/- 1 min-1, p < 0.01) and diabetic patients without (17 +/- 1 min-1, p < 0.001) or with mild (15 +/- 1 min-1, p < 0.05) signs of AN. Characteristic alteration, i.e. a reduction in circadian heart rate variability could be found in diabetic patients with signs of AN. This phenomenon has primarily been a consequence of more frequent sleeping heart rates due to dominant impairment in cardiac parasympathetic innervation.

[Connection between painless abnormal ST-deflection and autonomic neuropathy in diabetes mellitus]. / Fájdalommal nem kísért kóros ST-szakasz depresszió és autonom neuropathia összefüggésének vizsgálata cukorbetegségben.

In order to assess the relationship between abnormal but silent ST-segment depression and autonomic neuropathy 63 diabetic patients (age: 40-71 years, duration of diabetes: 2-32 years) without a history of angina pectoris were investigated. Transient ST-segment depression was assessed by 24 hours Holter monitoring and, in addition, dynamic exercise on bicycle ergometer was also performed in all but 7 patients. Autonomic neuropathy was evaluated by cardiovascular function tests (deep breathing, Valsalva manoeuvre and lying-to-standing). Abnormal ( > or = 2 mm) ST segment depression was observed in 11 patients (18%) while signs of autonomic neuropathy were found in 37 diabetics (59%). Signs of autonomic neuropathy were significantly (p < 0.01) more often documented in patients with (11/11) than without (26/52) abnormal ST-segment depression. It was concluded that autonomic neuropathy could be a possible explanation for lacking symptoms from abnormal ST-segment depression in diabetic patients.

[Screening for microalbuminuria in diabetic patients in the primary health care system]. / Alapellátásban nyilvántartott cukorbetegek microalbuminuria szúrése.

In order to detect the prevalence of microalbuminuria, a screening procedure was carried out in 1016 adult (age > 14 years) diabetic patients registered in primary health care system at the 17st district of the capital. The clinical characteristics of patients were investigated and microalbuminuria was measured by immunoturbidimetric method using first void morning urinary samples. In this way, the urinary albumin/creatinine ratio was calculated (abnormal value in men > or = 2.5 mg/mmol, in women > or = 3.5 mg/mmol). Moreover, serum creatinine, blood glucose, serum cholesterol and triglycerides were measured in fasting blood samples. After applying exclusion criteria data of 933 diabetic patients [129 insulin-dependent (IDDM) and 804 non-insulin-dependent (NIDDM) patients; 424 men, 509 women] were analysed. Abnormal urinary albumin/creatinine ratio was found in 315 (33.8%) patients. Microalbuminuria was detected in 32 (24.8%) IDDM and in 201 (25.0%) NIDDM patients. Macroalbuminuria was found in 13 (10.1%) IDDM and in 69 (8.6%) NIDDM patients. Abnormal urinary albumin/creatinine ratio was more often found in men than in women (IDDM men 41.3%, IDDM women 28.8%; NIDDM men 38.0%, NIDDM women 30.0%). Significant difference was found between diabetic patients with (n = 315) and without (n = 618) abnormal urinary albumin/creatinine ratio regarding age (64.3 +/- 0.7 years vs. 61.4 +/- 0.5 years; p < 0.001), duration of diabetes (10.3 +/- 0.5 years vs 7.9 +/- 0.3 years; p < 0.001) systolic blood pressure (151 +/- 1 mmHg vs 146 +/- 1 mmHg; p < 0.01), serum creatinine (99 +/- 2 mumol/l vs 88 +/- 1 mumol/l; p < 0.001) and blood glucose (10.4 +/- 0.2 mmol/l vs 9.4 +/- 0.1 mmol/l; p < 0.001). One third (33.8%) of diabetic patients in primary health care setting exhibited signs or were at risk of renal involvement of diabetes. Diabetic patients with micro- or macroalbuminuria should be carefully controlled in order to prevent or to decrease deterioration of renal function due to diabetic nephropathy.