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F A Gries

Publications and source records attributed to F A Gries.

At least 73 records · Page 4Linked to original sources
PubMed1992

[Diabetes type II].

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Diabetes Mellitus, Type 2↗
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↗
PubMed1991

Increase in the cytosolic concentration of calcium in platelets of diabetics type II.

The intracellular concentration of calcium (Cai) was measured in platelets of healthy control subjects and diabetics type II. Cai was elevated in platelets of diabetics type II under basal conditions, after stimulation by collagen, in the presence and absence of calcium in the incubation medium. The increase in Cai after stimulation by collagen was inhibited by nitrendipine in both kinds of platelets, however Cai remained elevated in platelets of diabetics. Our data and findings of others may be understood as indications of disturbances in the handling of Cai in diabetes.

Aged↗
PubMed1991

[Successful insulin therapy in lipoatrophic diabetes].

Two and a half years after manifestation of treatment-refractory lipoatrophic diabetes a 16-year-old girl had blood-sugar levels of about 500 mg/dl and hypertriglyceridaemia with fasting levels of about 3000 mg/dl, while there was no increase in ketone bodies. All the clinical, histological and radiological findings were those of generalized fatty tissue atrophy. In addition, she had marked axillary and periorbital acanthosis nigricans. Main symptoms were fatigue, weakness and excessive appetite. Intravenous insulin of at first 1200 IU daily reduced blood-sugar levels to normal. A good metabolic state was maintained by intensive insulin treatment with four intramuscular injections daily. On a dosage of 600-700 IU daily the HbA1 value dropped from 16.7% to 7.8%, triglyceride concentration to 300-400 mg/dl. The symptoms also regressed with normalization of the metabolic state.

Adolescent↗
PubMed1991

Follow-up of cyclosporin A treatment in type 1 (insulin-dependent) diabetes mellitus: lack of long-term effects.

In the Canadian/European randomized controlled study on cyclosporin A (CsA) in recent onset Type 1 (insulin-dependent) diabetes, treatment with the immunosuppressive drug had increased and maintained Beta-cell function and clinical remission during the first 12 months. Following discontinuation of the study drug and double-blinding after a mean of 13.8 months former CsA patients doubled the daily insulin dose within 6 months reaching the level of former placebo patients. The difference in Beta-cell function between the two groups was also lost. Metabolic control (HbA1c) was transiently worse in the former CsA group. Adverse effects of cyclosporin A on systolic blood pressure, haemoglobin levels, serum potassium and creatinine levels also remitted during that time. We conclude that treatment with cyclosporin A for a mean of 13.8 months had no long-lasting effect on the course of Type 1 diabetes persisting beyond drug discontinuation.

Adolescent↗
PubMed1991

The natural history of somatosensory and autonomic nerve dysfunction in relation to glycaemic control during the first 5 years after diagnosis of type 1 (insulin-dependent) diabetes mellitus.

The natural evolution of neural dysfunction was studied prospectively over 5 years following diagnosis of Type 1 (insulin-dependent) diabetes in 32 patients aged 12-36 years. Motor and sensory nerve conduction velocities, heart rate variation at rest and during deep breathing, and pupillary function were measured at diagnosis and after 3, 12, 24, 48, and 60 months. Thermal and vibration sensation thresholds were determined after 24, 48, and 60 months of diabetes. Mean HbA1 levels of months 3-60 within the normal range of less than 8.3% (7.3 +/- 0.2%) were observed in 13 patients (Group 1), while a mean HbA1 of months 3-60 greater than or equal to 8.3% (10.0 +/- 0.3%) was found in 19 patients (Group 2). Mean nerve conduction was significantly diminished in Group 2 as compared with Group 1 in at least 4 out of 6 nerves tested during months 12-60 (p less than 0.05). Both tests of heart rate variation were significantly impaired in Group 2 as compared with Group 1 after 24 and 60 months (p less than 0.05), but no differences in pupillary function were observed between the groups. Thermal discrimination but not vibration perception thresholds on the foot were significantly higher in Group 2 than in Group 1 at 40 and 60 months (p less than 0.05). Abnormalities in nerve conduction, thermal discrimination, and heart rate variation, but not vibration perception threshold and the pupillary function tests were significantly more frequent in Group 2 than in Group 1 at 60 months (p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1991

Proinsulin autoantibodies are more closely associated with type 1 (insulin-dependent) diabetes mellitus than insulin autoantibodies.

The disease association of autoantibodies to proinsulin and insulin was compared in patients with Type 1 (insulin-dependent) diabetes mellitus and first-degree relatives. Following the recommendation of the Fourth International Workshop on the Standardization of insulin autoantibodies, autoantibodies were determined by fluid-phase radioimmunoassay using equimolar concentrations of mono-125I-A14-insulin or -proinsulin to detect insulin or proinsulin autoantibodies, respectively. A higher prevalence of proinsulin autoantibodies vs insulin autoantibodies was found in 97 patients with Type 1 diabetes prior to insulin treatment (34.0% vs 22.7%, p less than 0.05) and in 16 islet cell antibody-positive relatives (43.8% vs 31.3%, NS). There was only one serum positive for insulin and proinsulin autoantibodies in 110 islet cell antibody-negative first degree relatives (0.9%). None of 88 normal sera contained proinsulin autoantibodies or insulin autoantibodies. There was a close correlation of proinsulin autoantibody and insulin autoantibody titres in individual sera (r = 0.95, p less than 0.01) due to crossreaction of all insulin autoantibodies with proinsulin. However, some proinsulin autoantibodies did not crossreact with insulin. Background binding in normal sera was lower for proinsulin autoantibodies. We conclude that proinsulin autoantibodies have a higher association to acute Type 1 diabetes than insulin autoantibodies.

Adult↗
PubMed1991

One-year treatment with the aldose reductase inhibitor, ponalrestat, in diabetic neuropathy.

A double blind placebo controlled trial was performed to evaluate the effects of the aldose reductase inhibitor, ponalrestat, on symptomatic diabetic neuropathy. After a 4-week placebo run-in phase, 60 patients were 2:1 randomized to receive either 600 mg ponalrestat or placebo once daily over 12 months. Forty-six patients, 30 of whom were treated with ponalrestat and 16 with placebo, completed the study. Motor and sensory nerve conduction, thermal and vibration sensation thresholds, heart rate variation at rest, E/I ratio, pupillary dilation velocity and pupillary reflex latency were determined at baseline and after 6 and 12 months. Neuropathic symptom scores were assessed every 3 months. Among the fifteen nerve function parameters studied, only trends in favour of ponalrestat were noted for heart rate variation and E/I ratio after 6 months (P = 0.06), but no significant differences between the groups could be demonstrated during the study. No adverse reactions were observed. It is concluded that one-year treatment with ponalrestat has no beneficial effects on symptoms or electrophysiological parameters in diabetic neuropathy.

Aldehyde Reductase↗
PubMed1991

Large platelets circulate in an activated state in diabetes mellitus.

Diabetes mellitus is associated with aggravated development of vascular complications. Yet, it has not been established whether platelet hyperreactivity contributes as a pathogenetic factor. In order to study the role of activated platelets in diabetes mellitus, we investigated the expression of the membrane activation markers CD63 (GP53) and CD62 (GMP-140) as direct indicators of in vivo activation. The CD63-positive fraction was significantly higher in patients (6.1% X 3.7 +/- 1) than in controls (2.7% X 3 +/- 1). In parallel, the CD62-positive fraction was significantly elevated in patients to 5% X 2.5 +/- 1 in comparison to controls (3% X 2 +/- 1). Patients with angiopathy had a mean increase of 304% in CD63-positive and of 223% in CD62-positive platelets. Patients without clinically detectable angiopathy showed a trend to an increased fraction in CD63-/CD62-positive platelets. There was no correlation of the activation markers with fasting blood glucose, HbA1 or platelet count. CD63 platelet bound fluorescence significantly increased with platelet size in the patient group. We conclude that in diabetes mellitus an increased number of large platelets circulate in an activated state predominantly in patients with angiopathy. This could imply that platelets become activated by vascular lesions. The trend in patients without vascular disease, however, suggests that activated platelets may also basically contribute to the prethrombotic state in diabetes mellitus.

Adult↗
PubMed1991

Sodium lithium countertransport is acutely influenced by heparin-induced extracorporal LDL precipitation.

Sodium lithium countertransport may be a genetic marker for arterial hypertension and for the risk of diabetic nephropathy in type 1 diabetic patients. Since various factors seem to influence the transport velocity including serum lipid alterations, erythrocytes of seven patients with severe hyperlipoproteinaemia who were chronically and intermittently treated with LDL apheresis were examined before and immediately after therapy. The LDL apheresis reduced sodium lithium countertransport significantly (0.383 vs 0.269, P less than 0.02). Therefore, we conclude that serum lipid composition must be considered when interpreting sodium lithium countertransport velocity.

Adult↗
PubMed1991

Changes in brainstem auditory evoked potentials during insulin-induced hypoglycaemia in type 1 diabetic patients.

To determine whether the central and peripheral auditory pathways are disturbed during hypoglycaemia, brainstem auditory evoked potentials were measured in 16 Type 1 diabetic patients aged 17-55 years during intravenous insulin infusion. Within 60 min mean blood glucose declined from 5.0 mmol l-1 to a nadir at 1.7 mmol l-1 followed by an increase to 2.8 mmol l-1 30 min after the insulin infusion had been discontinued. The latency of wave I of brainstem auditory evoked potentials remained unchanged during hypoglycaemia. However, latencies of waves III and V and interpeak latencies I-III, III-V, and I-V were significantly prolonged at average blood glucose levels of 1.7 or 2.1 mmol l-1 when compared with baseline: III 3.96 +/- 0.03 (+/- SE) vs 4.01 +/- 0.04 ms; V 5.69 +/- 0.07 vs 5.81 +/- 0.07 ms; I-III 2.30 +/- 0.05 vs 2.37 +/- 0.05 ms; III-V 1.73 +/- 0.06 vs 1.83 +/- 0.07 ms; and I-V 4.01 +/- 0.05 vs 4.14 +/- 0.06 ms (all p less than 0.05). When blood glucose was allowed to increase to 2.8 mmol l-1, these conduction delays were no longer demonstrable. The depression of the brainstem was approximately paralleled by the activation of counter-regulatory hormones and development of hypoglycaemic symptoms. We conclude that hypoglycaemia results in a rapidly reversible delay of the transmission time in the brainstem but not in the auditory nerve. The dysfunction in the brainstem suggests that not only cortical centres are involved in response to hypoglycaemia in Type 1 diabetic patients.

Adult↗
PubMed1991

Diabetes and arterial disease.

Macroangiopathy (or atherosclerosis) is a common and chronic complication in diabetic patients. Unlike other diabetic complications, atherosclerosis is not unique to diabetes, confounding analysis of its relationship with the diabetic condition. Evidence of an independent role for diabetes in the development of atherosclerosis remains equivocal. The main determinant of macrovascular disease may be an interaction between diabetes and the aging process. Similarly the question of a relationship between macrovascular disease and good metabolic control remains unanswered. Macroangiopathy in diabetic populations seems to be related to similar predictors and pathological mechanisms operating in the general population. However, after analysis of these common risk factors for macroangiopathy, a diabetes-specific risk remains. Low-density lipoprotein metabolism is markedly disturbed in poorly controlled diabetic patients. This is manifest as a concert of actions which increase formation of foam cells and fatty streaks. The next step in the atherosclerotic process, the formation of fibrous plaques, may be associated with the platelet hyperactivity seen in diabetes. This may promote overshooting of repair mechanisms at the vessel wall. Release of a specific diabetic serum growth factor from the platelets may be responsible for the later stages of fibrous plaque development and the increased atherosclerotic risk in diabetes.

Adult↗
PubMed1991

Regression of carotid plaques during low density lipoprotein cholesterol elimination.

We performed serial prospective ultrasound examinations of four flat and 17 soft carotid plaques during an average of 17 months in seven patients with heterozygous hypercholesterolemia during heparin-induced extracorporeal low density lipoprotein elimination on precipitation from plasma. By means of a specially designed quantitative three-dimensional ultrasound analysis, significant plaque volume reduction could be evaluated in all subjects, along with a marked reduction of total and low density lipoprotein cholesterol and fibrinogen serum levels.

Adult↗