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Biomedical subjects

O R Nilsson

Publications and source records attributed to O R Nilsson.

At least 19 recordsLinked to original sources
PubMed1987

Value of thyroid follow-up registers.

In this study from a county in southern Sweden 269 of 271 patients (99.3%) treated with radioiodine for hyperthyroidism over a two-year period were followed up five years later. The routine procedures at hospital clinics and primary health care centres were studied. A high number of toxic multinodular goitre (n = 113; 42.0%) and toxic adenoma (n = 76; 28.3%) emerged, 80 patients (29.7%) had toxic diffuse goitre (Graves's disease). During the five-year follow-up the cumulative incidence of hypothyroidism in the various goitre groups was 10.7%, 23.9%, and 57.5% respectively. Altogether 76 patients (28.3%) were diagnosed hypothyroid. Nine patients were lost to regular follow-up; elevated TSH and low or normal T4-concentrations were found in two of them. We propose a register system to enable detection of thyroid dysfunction after radioiodine treatment and other thyroid patients in primary health care.

Adult↗
PubMed1985

Long-term effects of captopril and atenolol in essential hypertension.

Fifty patients with mild or moderate essential hypertension were randomized (double-blindly) to treatment with either captopril (n = 26) or atenolol (n = 24). Their mean supine diastolic blood pressure after placebo was 100-125 mmHg. The study included an initial dose finding phase (12 weeks) during which the dosages of captopril and atenolol were increased stepwise every second week in order to obtain normotension (supine diastolic blood pressure less than 95 mmHg). Hydrochlorothiazide was added when necessary. During the second phase of the study the patients were followed on active treatment for 2 years. After the initial 12 weeks of active treatment, recumbent and standing blood pressures had fallen significantly both in the captopril group (by 31/20 and 33/19 mmHg, p less than 0.001) and in the atenolol group (by 24/18 and 30/20 mmHg, p less than 0.01 (systolic), p less than 0.001 (diastolic)). The antihypertensive effect was maintained in both groups during long-term treatment. The antihypertensive effect of both agents was potentiated to the same extent by addition of hydrochlorothiazide. Side-effects were few and mild. It can be concluded that both captopril and atenolol are safe and effective antihypertensive drugs.

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↗
PubMed1983

Thyroid hormones and the adrenergic nervous system.

This paper reviews the various possible relationships between thyroid hormones and the adrenergic nervous system. These concern the sympathetic influence on thyroid hormone secretion, thyroid hormone - induced changes of sympathetic activity or adrenoceptor changes - the effects of catecholamines on thyroid hormone metabolism and, finally, the clinical benefits of beta-adrenoceptor blocking drugs on symptoms and signs of hyperthyroidism.

Adrenergic beta-Antagonists↗
PubMed1983

beta-Adrenoceptor-adenosine 3',5-monophosphate system in human leucocytes before and after treatment for hyperthyroidism.

Modifications in characteristics of the beta-adrenoceptor-cAMP system were observed in leucocytes from 10 patients in the hyperthyroid state after antithyroid treatment. These include 1) an increased number of beta-adrenoceptors without a change in their affinity, 2) an increased magnitude of stimulation of adenylate cyclase by isoprenaline, without a change in the NaF-stimulated enzyme activity, 3) an increased cAMP-dependent protein kinase activity ratio, and 4) an increased activity of cAMP-phosphodiesterase. Moreover, the plasma cAMP levels were markedly elevated during the hyperthyroid state. It is suggested that the above changes may in part constitute the molecular basis for the reputed catecholamine supersensitivity in the hyperthyroid state.

3',5'-Cyclic-AMP Phosphodiesterases↗
PubMed1983

Early post-operative growth hormone levels predict the result of transsphenoidal tumour removal in acromegaly.

Serum human growth hormone (hGH) measurements were performed during transsphenoidal microsurgery for acromegaly and in the early period afterwards. There were 14 patients of which 2 were operated on twice. In 11 patients (2 patients at reoperation) the serum hGH concentration was normalized to less than 5 micrograms/l within 3 h after completion of surgery. On five occasions only partial restoration of the hGH values was obtained and additional treatment was given in 2 patients by successful re-operation. The early post-operative hGH concentrations were consistent with the clinical evaluation of the patients and the hGH concentrations during follow-up for an average of 27 months. We conclude that early post-operative serum hGH measurement is of value for evaluation of the efficiency of the tumour removal and the need for further treatment.

Acromegaly↗
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

Influence of hyperthyroidism on the kinetics of methimazole, propranolol, metoprolol and atenolol.

The kinetic profiles of oral methimazole 40 mg, propranolol 80 mg, metoprolol 100 mg and atenolol 100 mg were compared in hyperthyroid patients both during the hyper- and euthyroid states. for methimazole, neither the peak concentration (Cmax), the time to reach peak concentration (tmax), the elimination half-life (t 1/2) nor the area under the curve (AUC) value was affected by the hyperthyroid state. For propranolol and metoprolol, which undergo extensive presystemic clearance, the AUC values were lower (p less than 0.02) when the patients were hyperthyroid than when they had become euthyroid, but the t 1/2's were not significantly altered. For atenolol, there were no significant kinetic differences between the hyperthyroid and euthyroid states. The findings are compatible with the assumption that hyperthyroidism does not affect the kinetics of methimazole or atenolol, but that it may enhance presystemic clearance of propranolol and metoprolol.

Administration, Oral↗
PubMed1982

Antihypertensive and metabolic effects of increasing doses of atenolol and labetalol. A comparative study in primary hypertension.

Thirty-two patients with primary hypertension were studied in a double-blind cross-over comparison between the cardioselective beta 1-blocking agent atenolol and the combined alpha- and beta-blocking agent labetalol. The doses used were atenolol 50--150 mg twice daily and labetalol 200--600 mg twice daily. Both drugs effectively reduced blood pressure and heart rate. Dose increments every second week resulted in a higher proportion of patients with normal blood pressure (les than or equal to 150/90 mm Hg) with both drugs. Labetalol was somewhat more effective in lowering upright blood pressure while atenolol caused a more pronounced heart-rate reduction. Both agents decreased plasma renin activity and urinary aldosterone excretion. Scalp tingling on labetalol (2 patients) and cold fingers with atenolol (1 patient) caused withdrawal of the drugs. Cold fingers were reported in another four patients during treatment with atenolol and in one when on labetalol. Tiredness and postural symptoms were more common during intake of labetalol.

Adult↗
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

Radioimmunoassay of extracted glucagon compared with three non-extraction assays.

Radioimmunoassay of glucagon was performed with three different antisera, i.e. E7, 30K and 4305, all directed against the carboxyl-terminal region of glucagon and thus avoiding co-determination of glucagon-like polypeptides from the gut. Plasma samples from five healthy people subjected to various A-cell stimulation and suppression tests were used and immunoreactive glucagon assessed with the three antisera. Aliquots from all plasma samples were also extracted with acetone and glucagon re-assessed with antiserum E7. Even though all four baseline glucagon concentrations obtained were different, the glucagon profiles were comparable after superimposing the baselines. The differences in baseline concentrations of immunoreactive glucagon seem due to the interference of "big plasma glucagon", a still unidentified factor in the E7 and 30K assays that can be precipitated by acetone. Since acetone extraction yielded the lowest baselines without altering the glucagon profiles, it is suggested that the baseline glucagon concentrations of acetone-extracted plasma reflect the physiological level of the biologically active hormone. Using antiserum E7, our own antiserum, the normal range of glucagon values in acetone-extracted plasma samples from 22 healthy, fasting people of both sexes was 42 +/- 16 ng/l (mean +/- 2 S.D.). These values agree well with those obtained by other assay techniques.

Acetone↗
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↗
PubMed1980

Effects and plasma levels of propranolol and metoprolol in hyperthyroid patients.

The effects and plasma concentrations of different doses of propranolol and metoprolol were studied in 34 hyperthyroid patients. The initial daily doses were propranolol 160 mg or metoprolol 200 mg. If the resting heart rate remained above 75 beats per min after treatment for 4-7 days, the dose was increased and the patient re-examined after a further 4-7 days. Propranolol (n = 17) caused a reduced heart rate, a decrease in serum 3,3',5-triiodothyronine (T3) and an increase in serum 3,3',5'-triiodothyronine (reverse T3, rT3). In 10 patients, there was no change in T3 or rT3 until the daily dose of propranolol had been increased to 240 or 320 mg. The plasma level of propranolol was significantly correlated with the decrease in T3 and the increase in rT3. Metoprolol (n = 17) caused a reduction in heart rate similar to that following propranolol. However, serum T3 was only slightly reduced even after an increase in dose to 300 or 400 mg, and serum rT3 was not altered. Metoprolol concentrations were not significantly correlated with the fall in T3. It appears that the influence of beta-blockers on T4 conversion is of little importance for the clinical improvement in hyperthyroid patients, and rather it is a consequence of beta 1-adrenergic blockade interfering with the effect of T3. In addition, the findings support the assumption that therapeutic failure with beta-blockers in hyperthyroidism may be due to suboptimal treatment, and that individualized dosage is necessary.

Adult↗
PubMed1980

Timolol and hydrochlorothiazide-amiloride in primary hypertension.

Fifty-five patients with primary hypertension, World Health Organization (WHO) stages I and II, were randomly allocated to a 9-mo multicenter, controlled, double-blind, crossover study with timolol, a nonselective beta adrenoceptor blocker, and hydrochlorothiazide combined with the potassium-sparing drug amiloride (AHCT). In 54% of the patients the blood pressure responded to timolol, in 87% to AHCT, and in 91% to a combination of the two. The diurectic was more effective than the beta blocker in patients with low-renin hypertension, who all responded to AHCT. Overall, there was no correlation between pretreatment plasma renin activity (PRA) and hypothensive effect of either drug. Timolol reduced PRA by 58% and plasma aldosterone (PA) by 23% while AHCT increased these levels threefold. Combination therapy increased PA while PRA returned towards baseline, suggesting greater aldosterone stimulation by the diuretic component. Serum triglycerides rose during timolol treatment alone and in combination. Both timolol and AHCT are effective antihypertensives. In combination they normalize blood pressure in most patients with primary hypertension (WHO stages I and II). Determination of PRA is useful as a guide to the choice of the first treatment in searching out low-renin hypertensive patients, who are best treated with diuretics.

Adult↗
PubMed1980

Cortisol, growth hormone and prolactin responses to insulin-induced hypoglycaemia in hyperthyroid patients before and during beta-adrenoceptor blockade.

Two beta-adrenoceptor blocking agents, metoprolol (beta-1-selective) and propranolol (non-selective), were used in the treatment of hyperthyroid patients. The response of pituitary stress hormones to insulin-induced hypoglycaemia was investigated before and during beta-adrenoceptor blockage. Treatment with metoprolol (n=10) or propranolol (n=10) produced no changes in the cortisol or prolactin responses to hypoglycaemia. Moreover the growth hormone response remained unaltered during treatment with metoprolol. A small, but statistically significant, augmentation of growth hormone response was obtained during treatment with propranolol. When twelve subjects, euthyroid after final conventional treatment (surger), radioiodine or thyrostatic drugs), were re-examined, the cortisol and prolactin responses were unchanged, although growth hormone concentrations reached a slightly higher maximum value (P less than 0.01). It was concluded that treatment with beta-blocking agents in hyperthyroid subjects has no clinically important influence on the release of pituitary stress hormones during hypoglycaemia.

Adrenergic beta-Antagonists↗