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Biomedical subjects

K Wiefels

Publications and source records attributed to K Wiefels.

12 recordsLinked to original sources
PubMed2000

[Diabetic muscle infarct].

HISTORY AND CLINICAL FINDINGS: A 64-year-old diabetic man with secondary failure of treatment with oral hypoglycemic agents was admitted to our clinical department to initiate insulin therapy. The patient was otherwise in good health. Before his dismissal he acutely developed symptoms of pain in his left calf. In addition, the patient was unable to move his left leg and presented palpable pea-sized nodules of his left calf. INVESTIGATIONS: Laboratory investigations revealed elevated serum creatine kinase levels on day two after the onset of clinical symptoms (peak value: 2238 U/I). There was evidence for antinuclear antibodies, c-reactive protein was normal. An ultrasound investigation showed a focal edema or bleeding located to the musculus gastrocnemius. Duplex-sonography excluded thrombosis or embolisation. Magnetic resonance imaging showed a diffuse enhancement of signal intensity within the musculus soleus and in areals of the musculus gastrocnemius, as signs of increased blood supply. All clinical findings were consistent with the diagnosis of diabetic muscle infarction. TREATMENT AND COURSE: Under symptomatic treatment with tramadol, diclofenac ointment, and fragmented heparin serum creatine kinase returned to normal levels (105 U/I) within 14 days. In accordance, symptoms of local pain disappeared completely. After two weeks of treatment the patient was able to move his leg without pain. CONCLUSION: This is the first presentation of a patient with diabetic muscle infarction from the onset of symptoms until full recovery. In addition, this case confirms previous descriptions that this condition can be diagnosed by clinical and sonographic findings in combination with magnetic resonance imaging without invasive histologic techniques.

Diabetes Mellitus, Type 2↗
PubMed1995

Insulinkinetic and -dynamic in diabetic patients under insulin pump therapy after injections of human insulin or the insulin analogue (B28Asp).

In this double blind randomized study we compared the insulinkinetic, insulindynamic and the frequency of hypoglycemic events after s.c. injection of human insulin and the insulin analogue (B28Asp). Fourteen c-peptide negative patients treated with continuous subcutaneous insulin infusion (CSII) were included in the study. Their mean age was 42.9 (range 26-60 yrs), duration of diabetes 18.5 (5-29) and mean duration of CSII 6.3 yrs (3-10). Serum free insulin (FIRI) was determined from 8:00 to 11:00 h, and blood glucose from 7:00 to midnight. Maximum FIRI values were obtained after 45 min for (B28Asp) and after 90 min for Actrapid HM. Maximum blood glucose increase (Tmax) was obtained 60 min after injection of (B28Asp) and 90 min after Actrapid HM. The AUCBC was greater after administration of Actrapid HM compared to (B28Asp) (p < or = 0.05). A total number of 16 hypoglycemias (BG < or = 3.3 mmol.l-1) were registered. 8 episodes were induced equally by (B28Asp) and by Actrapid HM. We conclude that in insulin dependent diabetic patients the insulin analogue (B28Asp) showed a faster absorption and less hyperinsulinemia than Actrapid HM after s.c. administration. The corresponding BG-values were higher after s.c. administration of Actrapid HM compared to (B28Asp). These findings in patients support the concept of a more physiological effect of rapid acting insulin analogues than of regular insulin.

Adult↗
PubMed1991

Glucose counterregulation in type 1 diabetic patients with decreased symptoms of hypoglycemia after insulin pump treatment.

We were interested in studying whether impaired hypoglycemic awareness after intensified insulin treatment with insulin pumps is associated with impaired glucose counterregulation. Glucose counterregulatory hormones were measured in 7 type I diabetic patients with altered symptoms after 6 months of continuous subcutaneous insulin infusion (CSII) (group 1) and in 9 patients with unchanged symptoms of hypoglycemia under CSII (group 2). The groups did not differ in diabetic control, duration of diabetes, or prevalence of neuropathy. Counterregulatory hormone response to an insulin-induced episode of hypoglycemia was measured before (first test) and after 6 months (second test) of CSII. Glucose nadirs and glucose recovery were similar in both groups and both tests. The mean plasma glucagon values demonstrate a lack of glucagon response in both groups and both tests. Growth hormone and cortisol increased in both groups and both tests without any difference between the groups or first and second tests. Epinephrine response was similar in both tests of group 2 (first test: 50 +/- 5 to 416 +/- 73; second test; 45 +/- 5 to 456 pg/ml), while in group 1 the response was not increased significantly in the second test [first test: 32 +/- 6 to 346 +/- 63; second test: 44 +/- 7 to 575 +/- 91 pg/ml; areas under curve (AUC) 11,977 and 16,345 pg x ml-1 x 90 min-1 (p = 0.36)].(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1990

Elevated platelet activation in type I diabetics with chronic complications under long-term near-normoglycemic control.

A prethrombotic state with altered, hyperactive platelets may contribute to the development of diabetic late complications. Whether increased platelet 'in vivo' activation can be reduced by tight metabolic control is controversial. We studied plasma markers of platelet activation in 64 long-term, microangiopathic type I diabetics after at least 18 months of intensive treatment for near-normoglycemia. Both platelet factor 4 and beta-thromboglobulin proved to be significantly (p less than or equal to 0.05) elevated in comparison with healthy controls: 15.8 (sdf 2)/77.6 (sdf 1.9) vs. 8.9 (sdf 1.6)/45.1 (sdf 2) ng/ml (sdf = standard deviation factor). We found no significant correlations with any metabolic parameter (actual blood glucose, mean blood glucose, HbA1, triglycerides, cholesterol) or with the duration of intensive treatment. It is therefore concluded, that platelet 'in vivo' activation takes place in type I diabetics even after long-term near-normoglycemic control. This deviation could be regarded as indicator of an additional risk for the development of vascular complications.

Adolescent↗
PubMed1988

The natural course of peripheral and autonomic neural function during the first two years after diagnosis of type 1 diabetes.

Motor and sensory nerve conduction velocities (MNCV, SNCV), beat-to-beat variation (BBV) at rest, speed of pupillary dilation (SPD), and pupillary latency time (PLT) were measured in 32 patients aged 12-36 years after 19 +/- 2 (mean +/- SEM) days and again after 3, 12, and 24 months of insulin treatment. Moreover, BBV under deep respiration was determined after 12 and 24 months, and thermal discrimination thresholds (TDT) as well as pain and vibration perception thresholds (PPT; VPT) were evaluated after 24 months. Mean HbA1 levels during months 3-24 within the normal range (7.2 +/- 0.2%; mean +/- SEM) were observed in 20 patients (group 1), while in 12 patients (group 2) mean HbA1 of months 3-24 was elevated (10.1 +/- 0.4%). There were no significant differences between both groups with regard to the nerve function tests at baseline and after 3 months. After 12 months mean median MNCV and median, ulnar, and sural SNCV were significantly lower in group 2 than in group 1 (p less than 0.05). After 24 months mean median MNCV, peroneal MNCV, median SNCV, and sural SNCV as well as both BBV tests and PLT were significantly impaired in group 2 as compared to group 1 (p less than 0.05). In addition, mean malleolar VPT and PPT to heat and cold stimuli on the thenar and the foot were significantly elevated in group 2 as compared to group 1 (p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1988

Effects of one year of near-normoglycemia on peripheral nerve function in type 1 (insulin-dependent) diabetic patients.

Ninety poorly controlled C-peptide negative type 1 (insulin-dependent) diabetic patients with chronic complications were allocated to intensified insulin treatment with either continuous subcutaneous insulin infusion or multiple insulin injections; 83 were studied over 1 year (seven patients dropped out of the study). Peripheral nerve function was assessed by clinical examination, malleolar vibration perception threshold, and motor and sensory nerve conduction velocities (MNCV; SNCV) in the median, ulnar, peroneal, and sural nerves. In order to assess the effect of metabolic control on peripheral nerve function, the results in patients with normal mean HbA1 levels during months 3-12 of the study less than 8.6% (tight control (tc); n = 50) were compared with those with abnormal mean HbA1 greater than or equal to 8.6% (poor control (pc); n = 33). Mean blood glucose was significantly higher in pc than in tc at months 2-9 and 11 (P less than 0.05). In pc median and ulnar SNCV were significantly lower at 6 and 12 months, and ulnar and peroneal MNCV at 12 months than in tc (P less than 0.05). No significant differences between the groups were observed for median MNCV, sural SNCV, and vibration sensation. Further analysis revealed that in well-controlled patients who showed abnormal peripheral nerve tests at baseline, median, and ulnar MNCV and SNCV but not peroneal MNCV, sural SNCV, and vibration sensation were significantly improved after 12 months as compared with poorly controlled patients with initially abnormal tests (P less than 0.05). There were no differences in nerve function between well- and poorly-controlled patients who had normal nerve tests at baseline.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1988

Somatic and autonomic nerve function during the first year after diagnosis of type 1 (insulin-dependent) diabetes.

Somatic and autonomic nerve function was assessed by motor and sensory nerve conduction velocities (MNCV; SNCV), beat-to-beat variation at rest, speed of pupillary dilation, and pupillary latency time in 35 newly diagnosed type 1 diabetic patients aged 12-36 years. The nerve function tests were performed 18 +/- 2 (mean +/- SEM) days after the correction of initial ketosis and hyperglycaemia and again after 3 and 12 months of insulin therapy. Mean HbA1 levels of months 3 and 12 within the normal range less than 8.6% (mean: 7.2 +/- 0.2%) were observed in 24 patients (group 1) and greater than or equal to 8.6% (mean: 10.1 +/- 0.6%) in 11 patients (group 2). Group 1 showed no significant changes from baseline in the mean nerve conduction and autonomic functions after 3 and 12 months. In group 2 there was no change until three months, however, at 12 months there was a significant decrease in mean MNCV in the median, ulnar and peroneal nerves (p less than 0.05) and in mean SNCV in the median (p less than 0.05) and sural nerves (p less than 0.01), when compared to the baseline values. The autonomic function tests remained unchanged. No patient had symptoms of neuropathy during the period studied. These findings suggest that the deterioration of motor and sensory nerve conduction precedes that of cardiac and pupillary autonomic function in poorly controlled asymptomatic type 1 diabetic patients during the first year of the disease. Effective glycaemic control prevented progression of subclinical neuropathy, but did not reverse abnormalities which were present at diagnosis.

Adolescent↗
PubMed1987

Peripheral and autonomic nerve function in long-term insulin-dependent diabetes.

In a cross sectional study, motor nerve conduction velocity (MNCV) and sensory nerve conduction velocity (SNCV), beat-to-beat variation (BBV) at rest and speed of pupillary dilatation (SPD) have been investigated in 127 nonketonuric long-term insulin-dependent diabetics aged 19-72 yr and in age-matched control subjects. 84% of the patients had electrophysiologic abnormalities, 58% had symptomatic peripheral neuropathy, 35% had abnormal cardiac parasympathetic tests and 26% had abnormal pupillary tests. The most frequent pathologic feature was a decreased sural SNCV (66%). Among the patients without symptomatic peripheral neuropathy, 71% showed electrophysiologic abnormalities. MNCV and SNCV in median, peroneal and sural nerves correlated with BBV (p less than 0.005), but only peroneal MNCV was related to SPD (p less than 0.005). There was also a relationship between BBV and SPD (p less than 0.05). Glycosylated hemoglobin (HbA1) levels correlated inversely with median MNCV (p less than 0.001), and SNCV (p less than 0.03), peroneal MNCV (p less than 0.05) and sural SNCV (p less than 0.05). Patients with abnormal peripheral or autonomic nerve function tests or symptomatic peripheral neuropathy had significantly higher HbA1 levels than those with normal tests (p less than 0.04) or asymptomatic patients (p less than 0.01). Median MNCV and SNCV, sural SNCV and BBV deteriorated with age (p less than 0.05) and median SNCV and peroneal MNCV deteriorated with the duration of diabetes (p less than 0.001). Our findings show an association between peripheral and autonomic nerve dysfunction in long-term insulin-dependent diabetics.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMedDate not supplied

Differential effects of near-normoglycaemia for 4 years on somatic nerve dysfunction and heart rate variation in type 1 diabetic patients.

To evaluate the long-term effects of near-normoglycaemia on somatosensory and autonomic nerve dysfunction, 55 poorly controlled Type 1 diabetic patients were allocated to intensified insulin treatment using continuous subcutaneous insulin infusion or multiple insulin injections and were studied prospectively for 48 months. They were divided into three groups according to their mean HbA1 levels during the study. Group 1 (n = 19) had mean HbA1 during months 3-48 in the normal range of less than 7.8% (near-normoglycaemic control), Group 2 (n = 18) showed moderately elevated mean HbA1 between 7.8 and 8.5% (satisfactory control), and Group 3 (n = 18) had clearly elevated mean HbA1 of greater than or equal to 8.6% (poor control). In the three groups studied, the changes in nerve conduction over baseline in the median and peroneal motor nerves as well as median and ulnar sensory nerves after 4 years were inversely related to the mean HbA1 levels of months 3-48 (all p less than 0.05). No significant associations with mean HbA1 were noted for the ulnar motor and sural sensory nerve conduction, vibration perception threshold, and heart rate variation. The percentages of patients with neuropathic symptoms decreased from 32 to 14% in Group 1, remained fairly constant in Group 2, and increased from 41 to 73% in Group 3 after 48 months when compared to baseline (p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗