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S Wettre

Publications and source records attributed to S Wettre.

15 recordsLinked to original sources
PubMed1986

Batch to batch imprecision in the affinity chromatography assay of glycated hemoglobin.

An affinity chromatographic method (AC) was compared with ion exchange chromatography (IEC) for determination of glycated hemoglobin (gHb). In vitro, increasing glucose concentration produced no change on AC-determined gHb. gHb measurement by AC was highly correlated with mean blood glucose (r = 0.96). Mean values of gHb were apparently higher, and variation greater, by AC than by IEC. Intra-assay variation was 2.0% and 3.0%, respectively. Inter-assay variation was 4.8% by IEC and 6.4% by AC. When different batches of AC-columns were compared, mean values as well as precision differed considerably. The affinity chromatographic method tested here shows several expected advantages, but precision and inter-batch variation of the columns remain to be improved.

Blood Glucose↗
PubMed1986

Kinetics of glycosylated haemoglobin in uraemia determined on ion-exchange and affinity chromatography: no increase in the rate of glycosylation.

The haemoglobin glycosylation in uraemia was studied by determination of labile and stable HbA1 in patients and by kinetical experiments in vitro. The influence of uraemia on stable and labile HbA1 was investigated in a clinical study of 32 non-diabetic and 20 diabetic patients with uraemia compared with controls. Glycosylated haemoglobin (GHb) was determined with ion-exchange chromatography (IEC). A highly significant elevation of stable as well as labile HbA1 was found in uraemic non-diabetics and of stable HbA1 in uraemic diabetics. This elevation was not related to blood glucose level. Labile HbA1 does not significantly affect the increased total level of GHb. An in vitro study using IEC and affinity gel chromatography on erythrocytes sequentially incubated in glucose and saline showed identical kinetics of GHb formation and elimination in uraemic and in non-uraemic patients. No indication of changed glycosylation by the uraemia was found.

Adult↗
PubMed1984

A comparison of 100 mg atenolol and 100 mg metoprolol once a day at rest and during exercise in hypertensives.

The effects of once daily dosage of the two cardioselective beta-adrenoceptor blocking agents, atenolol and metoprolol, were studied in 26 patients with primary hypertension. The study was a randomized double-blind cross-over trial with placebo run-in and wash-out. Assessment of effect was performed about 1 and 25 hours after dosing. At rest, both atenolol and metoprolol lowered the blood pressure (BP) and heart rate (HR) compared to placebo. Atenolol induced a more effective BP reduction than metoprolol, especially 25 hours after drug intake. During exercise 1 hour after dosing both drugs reduced BP and HR to a similar extent, whereas 25 hours after dosing atenolol gave a more efficient BP and HR reduction than metoprolol. Our data show that both 100 mg atenolol and 100 mg metoprolol are effective antihypertensive beta-blockers at rest and during exercise, 1 hour after intake. Metoprolol was less effective than atenolol 25 hours after dosing probably due to its shorter plasma half-life, thus implying a twice daily regimen for metoprolol in standard preparation.

Adult↗
PubMed1984

Abnormal concentration of stable HbA1 in non-diabetic patients.

To study its specificity for hyperglycemia, stable HbA1 was determined with ion-exchange chromatography in 240 patients consecutively hospitalized in the department of internal medicine and in a non-diabetic reference population. Reference values were found to increase significantly with age in the age groups less than 30, 30-60, and greater than 60 years. 41 patients had stable HbA1 more than 2 SD above the mean of the reference group and random blood glucose less than 7 mmol/l, and 21 of these were classified as non-diabetics according to data in medical records. Four non-diabetic patients had stable HbA1 higher than + 4 SD. One of them had haemoglobinopathia, one severe anaemia under cortisone treatment, one cortisone treated myelomatosis with renal insufficiency and severe anaemia, and one patient had lymphoma and renal insufficiency. Nine patients had stable HbA1 between + 3 and 4 SD and diagnoses of coronary heart disease (4), rheumatoid arthritis (2), asthma (1), chronic renal failure (1) and malignant melanoma (1). Five of them were treated with cortisone or diuretics. Four patients had stable HbA1 slightly below the reference range. In summary marked elevation of stable HbA1 due to factors other than diabetes occurred in a few patients with haematological disorders.

Adult↗
PubMed1983

Increase in stable glycosylated haemoglobin after induction of poor glycaemic control.

Eight insulin-treated diabetic patients in good glycaemic control were studied as out-patients with frequent determinations of stable glycosylated haemoglobin (HbA1c) before, during and after 1 week of induced poor glycaemic control. Stable HbA1c was determined by cation exchange chromatography after elimination of the labile fraction by incubation in saline (0.15 mol/l). The increase in mean blood glucose was significant on the first day of reduced insulin therapy and greatest after 1 week (6.9 +/- 3.9 mmol/l above basal values). Stable HbA1c increased significantly on day 7 of the reduced insulin treatment. The increase represented, on average, 0.009% of total haemoglobin per mmol/l increase in mean blood glucose per 24 h during the period of induced hyperglycaemia. After restoring insulin therapy, a significant decrease in blood glucose was achieved on day 1 and after 2 days, the blood glucose level was similar to before the study. There was no significant decrease in stable HbA1c within the first 2 weeks of improved glycaemia.

Adult↗
PubMed1983

Characteristics of labile HbA1 in erythrocytes from normals and diabetics.

Incubation of erythrocytes from diabetic patients and non-diabetic persons in 0.15 mol/l saline at 37 degrees C was followed by a decrease in ion-exchange microcolumn determined HbA1 only during the first 4 h. The fraction removed was denoted as labile HbA1 and the remaining fraction as stable HbA1. Incubation in saline overnight at 20 degrees C did not completely remove the labile fraction. Incubation in saline overnight at 4 degrees C yielded only a slight decrease in labile HbA1. Incubation in saline containing various glucose concentrations (up to 100 mmol/l) produced increasing amounts of HbA1 during the first 3-4 h after which an equilibrium was reached. In both normal and diabetic erythrocytes incubated for 3-4 h we found a linear relationship between changes in labile HbA1 and glucose concentration. The degree of increase in labile HbA1 was the same in normals and diabetics and not dependent on pre-existing normal or moderately increased stable HbA1. In the blood from non-diabetics (n = 30) labile HbA1 was 0.5 +/- 0.3% (mean +/- SD) and in diabetics (n = 80) 1.6 +/- 0.8%. The correlation between labile HbA1 and simultaneously determined blood glucose was r = 0.72.

Blood Glucose↗
PubMed1983

Captopril, aldosterone and urinary kallikrein in primary hypertension.

The effects on blood pressure, the renin-angiotensin-aldosterone and the kallikrein-kinin systems were investigated in 32 patients with primary hypertension WHO stage I-II treated with captopril. Hydrochlorothiazide was added if needed to achieve a supine diastolic blood pressure of less than or equal to 90 mmHg. A placebo control group (n=8) was treated similarly. Supine mean arterial pressure fell from 133 +/- 10 on placebo to 114 +/- 12 mmHg after 4 weeks on captopril. At the same time plasma aldosterone decreased from 263 +/- 188 to 164 +/- 101 pmol . 1(-1), 24 h urinary excretion of aldosterone from 18 +/- 12 to 12 +/- 10 nmol and kallikrein from 9.0 +/- 6.7 to 6.2 +/- 4.1 nkat. Plasma angiotensin II was significantly reduced after two weeks treatment from 23.2 +/- 8.6 to 17.0 +/- 6.7 pmol . 1(-1). Before, but not during captopril, 24 h urinary kallikrein excretion correlated with plasma aldosterone levels and 24 h urinary aldosterone excretion (r=0.44 p, less than 0.05 and r=0.53, p less than 0.01, respectively). Mean arterial pressure reduction on captopril correlated with pretreatment PRA (r=0.44, p less than 0.05) but not with other measured hormone levels or changes therein. The addition of hydrochlorothiazide caused a further fall in blood pressure, but increased plasma aldosterone and 24 h urinary kallikrein excretion. Hydrochlorothiazide alone increased only 24 h urinary aldosterone excretion significantly. These findings indicate that, besides aldosterone secretion and renal arterial pressure, further mechanisms regulating the release of and activity of the renal kallikrein-kinin system exist.

Aldosterone↗
PubMed1982

Rapid and slow rate of decrease in HbA1a + b and HbA1c during improved glycaemic control.

The change in glycosylated haemoglobins was studied with a column chromatographic method when glycaemic control was rapidly improved in nine diabetic patients. The patients were followed for 3 weeks or more. There was a decrease in HbA1a+b and HbA1c within the first few days of improved control and this decrease was faster than later on. The initial decrease of HbA1a+b was faster than that of HbA1c. In individual patients the initial decrease in glycosylated haemoglobins correlated with the initial rate of decrease in blood glucose. It is concluded that HbA1a+b and HbA1c decrease biphasically during improved glycaemic control. The rapid initial decrease may be due to labile HbA1 and it is large enough to influence the value of HbA1 as an indicator of long-term glycaemic control in some patients.

Adolescent↗
PubMed1982

Long-term experience of captopril in the treatment of primary (essential) hypertension.

1 Forty-one patients with primary (essential) hypertension were treated with captopril alone or in combination with hydrochlorothiazide for 12-36 months. 2 During an initial dose-titration period mean blood pressure fell from 174/111 mm Hg to 134/88 mm Hg supine and from 170/116 mm Hg to 126/93 mm Hg standing after 3 months' treatment. 3 During long-term treatment with unchanged or reduced doses of captopril or hydrochlorothiazide, or both, blood pressure remained substantially reduced. Mean supine blood pressure at 24 months was 136/90 mm Hg and at 36 months 138/90 mm Hg. 4 In 12 patients with clearly defined low renin (essential) hypertension initial blood pressure reduction was less than in patients with normal renin hypertension after 1 month's treatment (162/102 mm Hg v 143/92 mm Hg). After 24 months of treatment, however, the treatment results were similar in the two groups. 5 Except for one case of reversible proteinuria no serious side effects were seen during treatment periods of up to three years. 6 Captopril alone or in combination with hydrochlorothiazide seems to be an effective and safe drug in the long-term treatment of primary hypertension.

Adult↗
PubMed1981

Captopril, an orally active converting enzyme inhibitor, in the treatment of primary hypertension. A controlled long-term study with reference to initial plasma renin activity.

Captopril (SQ 14 225), an orally active inhibitor of angiotensin converting enzyme, was evaluated in the treatment of primary (essential) hypertension in a placebo-controlled long-term study. In 24 patients allocated to captopril treatment, mean supine BP fell from 174 +/- 18/110 +/- 7 to 151 +/- 22/96 +/- 12 mmHg. Ten patients achieved a supine diastolic BP of less than or equally 90 mmHg with a mean BP fall of 28/22 mmHg after 4 weeks' captopril dose titration (75-450 mg daily). In 14 patients, BP fell 19/9 mmHg. When hydrochlorothiazide (50-100 mg daily) was subsequently added, a total supine BP reduction of 51/20 mmHg was noted. In the placebo control group (n = 16), BP changed +1/-2 mmHg from 171/110 mmHg while addition of hydrochlorothiazide caused a mean supine BP fall of 19/10 mmHg. During long-term follow-up (mean 11.8 months), no resistance to therapy developed. A weak correlation, (p less than 0.05) was seen between pretreatment plasma renin activity and initial captopril-induced BP reduction. However, in patients with clearly defined low renin hypertension, the hypotensive effect of captopril was much less than in patients with higher renin values. Captopril induced a significant decrease in urinary aldosterone excretion, which was partially reversed by addition of hydrochlorothiazide. Observed side-effects were proteinuria (1 case), rash (2 cases) and taste disturbances (3 cases). During long-term follow-up, seven patients have dropped out, four due to side-effects and three because of non-compliance.

Adult↗
PubMed1981

Captopril in primary hypertension. Effects related to the renin-angiotensin-aldosterone and kallikrein-kinin systems.

The effects of captopril (SQ 14.225), an orally active inhibitor of angiotensin converting enzyme, were investigated in a dose titration study of primary hypertension. In 32 patients 4 weeks titration with captopril gave a mean blood pressure (BP) reduction of 26/16 mmHg supine and 30/16 mmHg standing. No serious side effects were observed. The BP lowering effect was related to pretreatment plasma renin activity and was less in low renin hypertension (p less than 0.05). Captopril reduced angiotensin II (p less than 0.05), plasma (p less than 0.005) and urinary aldosterone (p less than 0.001) as well as urinary kallikrein excretion (p less than 0.005). Captopril (SQ 14.225) is a competitive inhibitor of peptidyl dipeptide hydrolase, also known as angiotensin converting enzyme (ACE) or kininase II, which converts angiotensin I (A I) into angiotensin II (A II), hydrolyzes des-Asp-angiotensin I to angiotensin III (A III) and inactivates bradykinin (BK) (19). Captopril has potent antihypertensive effects when used in human hypertension (review, 3) especially when the renin-angiotensin-aldosterone system (RAAS) is activated. To further investigate the mode of action and the hypotensive effect of captopril, we measured plasma renin activity (PRA), A II, plasma (PA) and urinary aldosterone excretion (UA) and urinary kallikrein excretion (UK) in 32 patients with established primary (essential) hypertension.

Adult↗