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Biomedical subjects

P Manhem

Publications and source records attributed to P Manhem.

At least 37 records · Page 2Linked to original sources
PubMed1989

Normal visual fields as assessed by computerized static threshold perimetry in patients with untreated primary hypothyroidism.

In this prospective study, 25 consecutive patients with untreated primary hypothyroidism were tested with a highly sensitive perimetric technique, since a high prevalence of visual field defects has been described in this condition. All patients had clinical hypothyroidism, a serum TSH value greater than 20 mU/l (reference range 0.4-4.0) and decreased/low normal serum total T4 concentration. Visual fields were tested with fully automated threshold-measuring computerized perimetry of the central 30 degrees field. Interpretation of fields included computer-assisted analysis provided by a perimetric statistical programme package. In 23 patients, conventional inspection and computer-assisted analysis showed no visual field defects. Two patients were excluded from the latter analysis: one patient who did not respond adequately at computerized perimetry and in whom manual field tests were entirely normal: one patient who had low sensitivity values in the uppermost parts of both visual fields owing to markedly swollen upper eye lids. In conclusion, although pituitary hyperplasia has been well documented in primary hypothyroidism, the present prospective study clearly indicates that visual field defects are not a common finding in patients with this disease.

Adult↗
PubMed1987

Pharmacokinetics and effects on the renin-angiotensin system of ramipril in elderly patients.

Converting enzyme inhibitors are likely to be prescribed with increasing frequency in elderly patients. The pharmacokinetics of ramipril, a new potent long-acting non-sulphydryl converting enzyme inhibitor, and its effects on blood pressure, plasma renin activity and angiotensin II concentrations were studied in a group of 8 elderly volunteers (mean age 77, range 61 to 84). Circulating concentrations of the active diacid formed from its parent drug were consistently higher in this group despite apparently normal renal function, assessed by serum creatinine and urea concentrations, compared with younger volunteers (age range 21 to 30). The initial dose of ramipril should be lower in older subjects. The study emphasizes the importance of careful extrapolation of data obtained from young volunteers to older subjects.

Aged↗
PubMed1986

Twenty-four hour changes in active and inactive renin after various oral doses of the converting enzyme inhibitor ramipril (HOE498) in normal man.

Different oral doses (5, 20, 50 mg) of the new orally active nonsulfhydryl-converting enzyme inhibitor, ramipril (HOE498), were given to 12 normotensive healthy males, and the pattern of changes in plasma active and inactive renin concentration was evaluated. Active and inactive renin increased after ramipril, and the magnitude of the response was clearly dose related. Active renin rose markedly by 4 hours and tended to decrease thereafter, although remaining higher than basal at 24 hours. In contrast, inactive renin rose more slowly, and the increase was sustained throughout the 24-hour period. The pattern of these changes is consistent with the hypothesis that circulating inactive renin is a biosynthetic precursor of the active form.

Administration, Oral↗
PubMed1984

Responses of plasma catecholamines to tilt in patients with diabetes mellitus.

The immediate heart rate acceleration, blood pressure reaction, plasma adrenaline (PA), and plasma noradrenaline (PNA) responses to a 90 degrees and 2 sec tilt were evaluated in 13 male patients with type I diabetes. A disturbed immediate acceleration, as measured by a previously described acceleration index (AI), was found in 5 patients. All patients with normal AI but only one of those with abnormal AI showed an increase in PA during the first minute after tilt (p less than 0.02). A late diastolic blood pressure fall occurred in 6 patients and the fall was minor (5 mmHg) in 5 of these. Patients with a late diastolic blood pressure fall showed a significantly lower increase in PNA 1-8 min after tilt than those without (55 +/- 13% versus 163 +/- 24% (mean +/- SE), p less than 0.005). An abnormal immediate acceleration to tilt is associated with an impaired sympatho-adrenal reaction, and even a minor diastolic blood pressure fall indicates peripheral sympathetic denervation.

Adult↗
PubMed1984

Plasma noradrenaline and blood pressure in hypothyroid patients: effect of gradual thyroxine treatment.

High plasma noradrenaline (PNA) levels have been reported in hypothyroid patients and hypothyroidism has been associated with hypertension. To explore the relationship between PNA and blood pressure (BP) in hypothyroid patients, and the effects of gradual thyroxine replacement, a prospective study was performed comparing BP, heart rate (HR) and PNA in a normotensive and a hypertensive group of hypothyroid patients before and during gradual thyroxine substitution. Thyroxine treatment reduced the BP; the reduction in supine BP was greater in the hypertensive than in the normotensive group. HR increased similarly in both groups during treatment. PNA was elevated in the normotensive group before treatment and decreased gradually during thyroxine treatment. The hypertensive group had normal PNA levels. The present study indicates that normotensive, in contrast to hypertensive, hypothyroid patients have increased sympathetic nervous activity. Although the mechanism is unclear, thyroid replacement therapy can reverse hypertension in hypothyroid patients.

Adult↗
PubMed1983

Effects of penbutolol and metoprolol on blood pressure, plasma catecholamines and renin activity in hypertensive patients.

The effects of penbutolol 20-30 mg twice daily and of metoprolol 50-150 mg three times daily were studied in five and nine patients, respectively, with moderate hypertension. Both drugs significantly reduced blood pressure and pulse rate under basal conditions and in connection with exercise. Plasma catecholamine levels were not altered in supine or upright position, neither during penbutolol nor during metoprolol treatment. Following work there was an enhanced response in both plasma noradrenaline and adrenaline during penbutolol but only in plasma noradrenaline during metoprolol treatment. Both drugs effectively reduced basal plasma renin activity but only penbutolol abolished the renin response to work. Penbutolol significantly reduced urinary aldosterone excretion whereas metoprolol caused no significant changes. Neither penbutolol nor metoprolol affected maximal working capacity.

Aldosterone↗
PubMed1983

Unsuccessful DTIC treatment of a patient with glucagonoma syndrome.

Various chemotherapeutic modalities have been tried in the treatment of patients with malignant glucagonomas. Promising results have been reported after drug treatment with dimethyltriazenoimidazole carboxamide (DTIC). We present a patient with a metastasizing pancreatic glucagonoma, in whom treatment with neither DTIC nor with the combination of streptozotocin and 5-fluorouracil resulted in any noticeable improvement.

Adenoma, Islet Cell↗
PubMed1983

Increased vascular plasminogen activity in patients with pheochromocytoma.

Fibrinolytic and coagulation components were assayed in six patients with pheochromocytoma. Blood samples and a specimen from a superficial hand vein were obtained before, and six months after removal of the tumour. Vascular plasminogen activator (PA) activity in the vein wall was significantly increased in all patients who all had increased concentrations of urinary adrenaline, or noradrenaline, or of both. After adrenalectomy catecholamines were normalized and the PA activity was within normal range in all patients. There were no significant differences in factor VIII, antithrombin III, fibrinolytic activity, plasminogen or inhibitors of the plasminogen activation in plasma.

Adrenal Gland Neoplasms↗
PubMed1982

Plasma clonidine in relation to blood pressure, catecholamines, and renin activity during long-term treatment of hypertension.

Eight patients with essential hypertension were treated with 50 microgram oral clonidine four times daily for 4 wk followed by 75 to 150 microgram four times daily for another 4 to 16 wk. Before treatment and at the end of each treatment period the patients were hospitalized and their plasma clonidine concentrations (P-CLON) were determined repeatedly during one dosage interval. The relationship of P-CLON to blood pressure, heart rate, plasma norepinephrine (PNE), and plasma renin activity (PRA), as well as to conventional kinetic parameters, was calculated. With the two dosages used the half-life (t 1/2 s) of clonidine absorption were 1.05 and 0.83 hr, the biological t 1/2 s 8.7 and 7.9 hrs, and the total oral clearances 4.7 and 5.0 ml X min-1 X kg-1. The log of P-CLON correlated with the maximum percentage decrease of mean arterial blood pressure (MAP) (r = 0.91, P less than 0.001) in five patients, whereas in three patients there was no further decrease of MAP after increase of plasma clonidine level. The logarithm of P-CLON correlated with percentage reduction of PNE (r = 0.67, P less than 0.01). In six patients in whom clonidine induced a reduction of PRA, there was a relationship between log P-CLON and percentage PRA reduction (r = 0.91, P less than 0.001) and also between the percentage PRA and PNE reduction (r = 0.74, P less than 0.01).

Blood Pressure↗
PubMed1981

Prolonged clonidine treatment: catecholamines, renin activity and aldosterone following exercise in hypertensives.

Eight patients with essential hypertension, WHO grade I-III, were studied under standardized conditions in a metabolic ward, before and after 8-20 weeks of treatment with clonidine in a maintenance dose of 300-600 micrograms/24 h. Before clonidine, plasma noradrenaline concentration (PNA), plasma adrenaline concentration (PA), plasma renin activity (PRA) and plasma aldosterone concentration (PAC) increased in response to standing and submaximal exercise for 20 min. PNA was positively correlated to pulse rate in the supine position (R = 0.74, p 0.05) and the increase in PNA to the increase in pulse rate during exercise (min 10, R=0.73, p less than 0.05; min 15, R = 0.79, p less than 0.05; min 20, R = 0.74, p less than 0.05). No other significant correlations were found between PNA, PA, PRA and PAC on the one hand and blood pressure (BP) and pulse rate on the other. Clonidine reduced BP, pulse rate, PNA and PRA under all conditions studied. PA was reduced in the upright position and in connection with exercise. PAC was reduced during clonidine after exercise but otherwise unaltered. The clonidine-induced decrease in PNA was positively correlated to the decrease in diastolic BP both in the supine (R = 0.76, p less than 0.05) and in the upright (R = 0.80, p less than 0.05) position. thus, long-term clonidine treatment lowered the BP and pulse rate, at least partly by reducing sympathetic activity via a central mechanism. However, clonidine did not block the sympathetic reflex mechanisms engaged in the maintenance of BP in the upright position. During clonidine, the adrenaline values were lower than before treatment in the supine and in the upright position and also following exercise, indicating that clonidine exerts an inhibitory effect on the sympatho-adreno-medullary system.

Adult↗
PubMed1981

The effect of captopril on catecholamines, renin activity, angiotensin II and aldosterone in plasma during physical exercise in hypertensive patients.

The studies were designed to explore the effect of the converting enzyme inhibitor captopril on the activity of the sympathetic nervous system during basal conditions and following graded physical exercise in patients with essential hypertension. Seven males and two females, aged 36-59 years, were hospitalized under metabolic ward conditions and treated for 7 days with captopril given orally in increasing dosages, the final dose being 600 mg daily. The patients were subjected to an individual, graded submaximal work test (bicycling) for 20 min before medication and then again in an identical manner during medication with 600 mg captopril. Blood samples were drawn before exercise and then after 10 and 20 min of work for the determination of plasma angiotensin II (PA II), plasma aldosterone (PAC), plasma renin activity (PRA), plasma noradrenaline (PNA) and plasma adrenaline (PA). Before medication blood pressure (mmHg) was 195/133 immediately before exercise, 230/129 after 10 min of moderate exercise and 263/105 following 20 mon of nearly maximal work. During treatment with captopril the respective blood pressure values were 154/110, 200/100 and 245/98. Captopril had no significant effect on the changes in heart rate following physical exercise. PA II and PAC were substantially reduced and PRA considerably increased by captopril. PA II, PAC and PRA increased in response to exercise both before and following captopril. The exercise stimulated increase in PNA and PA was almost identical before and during captopril. Thus, captopril had no major effect on the activity of the sympathetic nervous system in patients with essential hypertension, neither during basic conditions nor during heavy physical exercise in spite of a profound decrease in PA II.

Adult↗