[How I take charge and treat type II diabetes resistant to usual treatment].
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Blood Glucose↗
Biomedical subjects
O Ziegler
Publications and source records attributed to O Ziegler.
[Medical treatment of diabetic arteriopathy].
Medical care of arteriopathy of leg in a diabetic patient involves control of diabetes combined with a series of non specific measures applicable to all atheromatous arteriopathies. Allowance must be made for the often silent nature of the arterial lesion, explicable by the associated peripheral neuropathy and the site of the lesions, generally more distal or staged than in non diabetics. A stable blood sugar level must be obtained to provoke improvement in hemorrheologic parameters and to slow the atheromatous process. A dietary regimen is associated with oral hypoglycemic agents or insulin therapy, the latter systematically for trophic disorders, administered as multiple injections or by insulin pump until complete healing is obtained. Insulin therapy normalizes abnormal blood lipid levels secondary to an uncontrolled diabetes. Other vascular risk factors (primary hyperlipoproteinemia, hypertension, smoking) must be allowed for. Of major importance in these patients at risk are foot hygiene, prevention of local trauma and correction of plantar anomalies. Aggravating factors in patients with arteritis are diabetic neuropathy and foot deformities. Regular walking is encouraged. Drug therapy (oral or injectable vasoactive agents, platelet antiaggregants, prostacyclin, normal blood volume restoration) depends on the severity of the arteriopathy and any complications. Analgesics are often required in advanced stages. Local therapy and sometimes antibiotics are necessary for trophic disorders. The frequent asymptomatic character up to the stage of gangrene should not, because of the diabetic diathesis, induce a wait and see attitude, and revascularization by angioplasty or shunt operation should be envisaged. A frequent complication of sugar diabetes, arteriopathy of the leg should be diagnosed early before it is revealed by a gangrenous lesion.(ABSTRACT TRUNCATED AT 250 WORDS)
Arterial Occlusive Diseases↗
[Insulin in type 2 diabetes. Why, when, how?].
Non insulin-dependent diabetes is often associated with obesity and always with some degree of insulin resistance. First choice treatment consists of appropriate and sometimes hypocaloric diet and oral hypoglycemic agents. Using insulin becomes mandatory in patients with associated pathology or at risk of metabolic imbalance. Insulin administration must be discussed in each individual case when it aims at a long-term improvement of blood glucose control, taking into account the lack of consensus on this point and the potential drawbacks of insulin therapy, notably weight increase and risk of hypoglycaemia.
Diabetes Mellitus, Type 2↗
A multicenter comparison of the effects of simvastatin and fenofibrate therapy in severe primary hypercholesterolemia, with particular emphasis on lipoproteins defined by their apolipoprotein composition.
This multicenter, double-blind, randomized study was designed to compare the effects of simvastatin (20 mg/d and 40 mg/d) and fenofibrate (400 mg/d) on plasma lipids, lipoproteins, apolipoproteins (apo), and lipoprotein particles defined by their apo composition (Lp A-I, Lp A-II:A-I, Lp E:B, Lp C-III:B) in primary hypercholesterolemia. After 6 and 10 weeks of therapy, both drugs lowered plasma cholesterol, low-density lipoprotein (LDL) cholesterol, and apo B. The effect on LDL and apo B was significantly more pronounced for simvastatin (P = .01). Simvastatin increased Lp A-I, but did not change Lp A-II:A-I, while fenofibrate decreased Lp A-I and increased Lp A-II:A-I. Lp E:B and Lp C-III:B were decreased with both drugs, but fenofibrate was significantly more effective in reducing these particles than simvastatin. This study demonstrates that both drugs have beneficial effects on the parameters positively or negatively correlated with the atherosclerotic risk, with simvastatin being more effective in reducing some of them. These results suggest that the drugs led to different structural modifications of the lipoproteins, which would not be revealed by examination of lipoprotein density classes. These differences are probably related to the different mechanisms of action of the agents.
Adolescent↗
Lipoprotein particle analysis comparing simvastatin and fenofibrate.
This study compares the effects of fenofibrate and simvastatin in primary hypercholesterolemia, with particular regard to lipoprotein particles, as defined by their apolipoprotein composition: LpAI, LpAII: AI, LpE:B, LpCIII:B. This was a double-blind study in which patients were randomized to 2 groups, one receiving simvastatin 20 mg once daily and the other receiving fenofibrate 200 mg b.i.d., if their total cholesterol and their LDL cholesterol remained above 7.60 mmol/l (300 mg/dl) and 4.95 mmol/l (195 mg/dl) after a 4-week placebo period. Simvastatin dosage was doubled at the end of 6 weeks of therapy if the LDL-cholesterol level remained above 3.55 mmol/l (140 mg/dl). Analyses were done after 6 and 10 weeks of therapy. Apolipoprotein AI was increased significantly only at week 10 with fenofibrate (+7.4%). Simvastatin had a more pronounced effect than fenofibrate on apolipoprotein B. There was a significant difference between drugs at weeks 6 and 10. No change was observed in the LpAII:AI level with simvastatin, whereas fenofibrate increased these particles quite significantly (+13.9 and +22.3%). The drugs had opposite effects on LpAI (+2.5 and +5.6% with simvastatin; -12.8 and -15.1% with fenofibrate). LP E:B (-33.0 and -40.8% with simvastatin; -53.8 and -52.2% with fenofibrate) and LpCIII:B (-23.8 and -31.8% with simvastatin; -35.1 and -43.5% with fenofibrate) were decreased by both drugs, but fenofibrate was significantly more effective in reducing these particles than simvastatin at week 6. This study suggests that both drugs led to different structural modifications of the lipoproteins, which would not be revealed by total apolipoprotein analysis. These differences are probably related to the mechanisms of action of these drugs.
Adolescent↗
Hemobiological activity of gliclazide in diabetes mellitus.
The hemovascular abnormalities encountered in diabetes include platelet alterations, shifts in prostaglandin metabolism and disorders of fibrinolysis. Diabetes is thus associated with increased platelet adhesiveness, increased platelet aggregation with hypersensitivity to proaggregants, increased plasma levels of beta-thromboglobulin and platelet factor 4 as an expression of platelet hyperactivity, increased levels of thromboxane A2 (TXA2) and prostacyclin (PGI2), and reduced levels of tissue plasminogen activator (t-PA). It is not clear which, if any, of these abnormalities are generated by chronic hyperglycemia and can be corrected by adequate glycemic control. Studies with gliclazide have demonstrated that it exerts hemovascular effects which can be valuable to patients. Thus, treatment with gliclazide leads to a decrease in platelet adhesiveness and aggregability. This treatment also reduces thromboxane levels and increases TPA levels. The mechanisms of action of gliclazide are not fully known but it has been demonstrated that its antiplatelet action is independent of its hypoglycemic activity and is not accompanied by clinical abnormalities of blood clotting. The mechanism of direct action on platelet activity may be mediated by inhibition of activated glycogen synthetase, activation of adenylate cyclase, modulation of arachidonic acid release from platelet membranes, stimulation of PGI2 production, and inhibition of the proaggregant action of TXA2. Thus, gliclazide not only has a hypoglycemic action but also improves hemovascular parameters in type 2 diabetes when used at normal therapeutic doses.
Blood Platelets↗
Rheological properties and membrane fluidity of red blood cells and platelets in primary hyperlipoproteinemia.
Lipid fluidity of the erythrocyte membrane and intact platelets was examined in 32 male patients affected by types IIA, IIB and IV primary hyperlipoproteinemia and 15 control subjects. Lipid fluidity was determined by fluorescence polarization using two probes: DPH and TMA-DPH which are localized in different lipid areas of the cell membrane. Classical haemorheological tests were also performed including plasma viscosity, whole blood viscosity and erythrocyte aggregation. As compared to a control group, plasma viscosity and whole blood viscosity at low shear rate was significantly increased in types IIB and IV, but not in type IIA patients. In contrast, the increase in erythrocyte aggregation was significant in all HLP types. Concerning lipid fluidity, the results recorded with red cells and platelets were not significantly different for type IIA HLP compared to the control group. In contrast, erythrocyte membranes from patients with types IIB and IV HLP had a significantly higher level of fluidity in lipid regions characterized by TMA-DPH. Using DPH as a fluorescent probe, identical results were only noted in type IIB patients. Regarding intact platelets of IIB and IV patients, an increase in lipid fluidity was noted for two fluorescent probes. These findings suggest that HLP associated erythrocyte and platelet fluidity alterations are not related to hypercholesterolemia but to the triglyceride level.
Adult↗
Safety, tolerability, and efficacy of simvastatin and fenofibrate--a multicenter study. Simvastatin-Fenofibrate Study Group.
Five centers participated in a double-blind, randomized, active-drug controlled study. The selected patients had a diagnosis of primary hypercholesterolemia (phenotype IIa or IIb, total cholesterol [TC] greater than 300 mg/dl, low-density lipoprotein [LDL] cholesterol greater than 195 mg/dl, triglycerides [TG] less than 350 mg/dl). Throughout the study the patients observed a lipid-lowering diet (American Heart Association). After a baseline placebo period (4 weeks), the patients were randomly assigned to simvastatin 20 mg q.p.m. or fenofibrate 200 mg b.i.d. If after 6 weeks of treatment the LDL cholesterol level remained over 140 mg/dl the dose of simvastatin was doubled. The total duration of treatment was 10 weeks. One hundred eighty-four patients completed the study; age ranged from 17 to 72 years (mean 46; 129 men, 55 women). Seventy-nine patients had ischemic heart diseases. Simvastatin significantly reduces TC, LDL, and apolipoprotein (apo) B (30%, 35%, and 27%, respectively). These effects are larger than those of fenofibrate (19%, 22%, and 14%, respectively). Fenofibrate decreased very-low-density lipoprotein and TG, and increased high-density lipoprotein and apo A1, to a larger extent than simvastatin. However, the difference reached statistical significance only for TG (29% versus 17%). Both drugs were well tolerated. Clinical adverse experiences occurred with a low frequency, and few of these were considered drug related (6 and 8% in the simvastatin and fenofibrate groups, respectively). Only two patients had serious laboratory adverse experiences considered drug related or possibly drug related (one in each treatment group with increased SGPT, gamma-GT, and/or creatine phosphokinase).
Adolescent↗
[Efficacy of 2 cholesterol apheresis systems].
A new generation of techniques can be applied to the selective removal of some well-defined molecules from plasma. This is the field of plasma treatment. We investigated the selective removal of LDL cholesterol, by double filtration and dextran sulfate cellulose column plasmapheresis, from 3 to 4 liters of plasma from 4 hypercholesterolemic patients. The extraction rate of Apo A1 lipoprotein in dextran sulfate was less than 25% and Apo B was between 50 and 90%. Cascade filtration gave an extraction rate for Apo A1 between 25 and 50%; the extraction rate for Apo B was about the same as that found using the dextran sulfate procedure. Both techniques decreased the concentrations of coagulation factors (V, VIII and fibrinogen). In conclusion, we obtained good removal of LDL cholesterol with both systems. Dextran sulfate (from Kaneka) was more selective but very expansive. However, we observed side effects with this product that probably result from the release of dextran sulfate from the column.
Cholesterol, LDL↗
[HMG CoA reductase inhibitors: a new class of hypocholesterolemic agents].
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Anticholesteremic Agents↗
Effect of simvastatin on plasma lipids, apolipoproteins and lipoprotein particles in patients with primary hypercholesterolaemia.
The effect of treatment with simvastatin, a new HMG-CoA reductase inhibitor, has been investigated in 27 patients with primary hypercholesterolaemia. It produced a significant decrease of cholesterol and phospholipids in plasma, LDL and apolipoprotein B-containing lipoproteins. Plasma apolipoproteins B, C-III and E were also significantly lowered. The concentration of lipoprotein particles recognized by monoclonal antibodies (BL3, BL5 and BL7), associated with atherosclerotic disease, was also lowered by the treatment. Lipoproteins LpA-II:A-I were not changed, while LpA-I, which has been suggested to be the protective fraction of the apo A-I-containing lipoproteins, was slightly and inconsistently increased.
Adolescent↗
Reliability of self-monitoring of blood glucose by CSII-treated patients with type I diabetes.
The reliability of patient-generated data from self-monitoring of blood glucose (SMBG) was studied in 14 patients with type I (insulin-dependent) diabetes mellitus treated by continuous subcutaneous insulin infusion (CSII) (7 women, 7 men). The reflectance meters (Glucometer I, Ames, Elkhart, IN) used by the patients were replaced for a period of 21 days by memory-reflectance meters; patients were unaware of the memory capacity of the new meters and were instructed to continue their practice of recording the meter readings in their logbook. This study compares the data recorded in the memory-reflectance meters with those reported in the logbook. The number of SMBG measurements was different in 11 patients (differences ranging from 2 to 66). Mean glycemia was similar (8.23 +/- 0.36 mM in logbook vs. 8.49 +/- 0.48 mM in memory-reflectance meters), but both the M value and mean amplitude of glycemic excursions (MAGE) index were lower when calculated from logbook data (38 +/- 5 vs. 48 +/- 7 mM, P less than .05 and 6.91 +/- 0.43 vs. 7.72 +/- 0.52 mM, respectively; P less than .05). Overreporting (addition of phantom values in logbook) and underreporting (omission of SMBG measurements from logbook) indexes were 19 +/- 7 and 12 +/- 3%, respectively. Precision (percent of identical values in logbook and in memory-reflectance meters at the corresponding time) was 77 +/- 6.8%. The number of SMBG measurements recorded in the memory-reflectance meter was negatively correlated with glycosylated hemoglobin [HbA1c; (r = -.85, P less than .001)], whereas overreporting was positively correlated with HbA1c (r = .76, P less than .01).
Adult↗
Visual evoked potentials in diabetic patients.
Visual evoked potentials (VEPs) were assessed in 50 adult type I (insulin-dependent) and 19 type II (noninsulin-dependent) diabetes mellitus patients and in 54 controls. P100 wave latency was significantly longer in diabetic patients (P less than .001). Twenty-eight percent of diabetic patients had P100 wave latencies above the normal range. There was no correlation between P100 latency and type or duration of diabetes mellitus, quality of metabolic control, or presence of degenerative complications. The significance of VEP abnormalities in diabetes mellitus remains speculative.
Adult↗
[Diet therapy of hypercholesterolemia. From theory to practice].
Hypercholesterolemia, quite frequent in industrialized countries is a major risk factor of atherosclerosis, especially in the coronary arteries. Consensus conferences, in the United States as well as Europe, have established a practical approach to this field. The dietetic treatment, from a population standpoint, remains the corner-stone of the treatment of primary dyslipoproteinemias. The quality and quantity of lipids in the food, play a definite role. In order to lower cholesterolemia, the intake of total lipids and cholesterol must be lowered and the consumption of polyunsaturated or mono-unsaturated fatty acids must be increased. The advantage of fish (omega 3 fatty acid), soy-bean and food fibers, are discussed.
Dietary Carbohydrates↗
[Classification of primary dyslipoproteinemias].
The prevention of atherosclerosis implies a better knowledge of dyslipoproteinemias. The metabolic disease must first be defined before considering its treatment and evaluate the atherogenic risk. The clinician must take advantage of two different classifications. The WHO classification (WHO: World Health Organization) permits to consider six phenotypes (I, IIa, IIb, III, IV, V), according to the serum levels of cholesterol and triglycerides. The genetic classification permits to relate one or several genetic anomaly to these phenotypes. The main clinical and biological characteristics of primary dyslipoproteinemias are summarily reported.
Humans↗
[Holter erectometry. A new approach to erectile disorders].
A Holter-type portable computerised electronic system for measurement of the apparent volume of the penis, eye movements and heart rate over 12 hours, enables investigation of erectile disorders by the patient himself, under more physiological conditions at home. Data processing and ease of use will permit scientific use on a large scale.
Adult↗
[Impotence in the diabetic].
Two-hundred-and-two impotent diabetic patients gave their consent to be investigated. Impotence is linked to diabetes mellitus in 58.9% of patients so all the other etiologies have to be systematically eliminated. Neuropathy or arteriopathy, when isolated, are found with the same frequency, but these 2 etiologies are often associated (47 patients). No statistical difference between IDDM and NIDDM was found. Mercury strain gauge plethysmography and venous occlusion coupled to ECG allows detection of arterial lesions in diabetic impotence. Patients agreed to submit to all of the various therapeutic possibilities. Combination of alpha-blockade and good glycemic control induced the best results.
Adult↗
Thymulin (facteur thymique serique) and zinc contents of the thymus glands of malnourished children.
Protein-energy malnutrition (PEM) leads to an immune deficiency, which is now well documented. Some investigators have suggested that the associated zinc deficiency is important in thymic involution and changes in cellular immunity. To evaluate the respective roles of nutritional deficiency, infection, and zinc in the alteration of thymic function, we measured the amounts of thymulin (facteur thymic serique, or FTS) and of Zn in the thymus glands of 58 Senegalese children who died in various stages of malnutrition. In the severe forms (marasmus, kwashiorkor, and marasmic kwashiorkor) the thymus was tiny and contained very little thymulin. The Zn content of the thymus was high whatever the nutritional state of the subject and was related significantly only to the presence of infections. In Senegalese children thymic atrophy and depleted thymulin content are associated with severe PEM but not systemic infection or depleted thymic Zn content.
Animals↗