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1.  Profound hypotension after the first dose of ketanserin. 
Postgraduate Medical Journal  1987;63(738):305-307.
Two patients developed profound hypotension approximately one hour after taking an initial oral dose of ketanserin 40 mg. The reaction appeared similar to that reported with prazosin, and may have been due to the alpha 1-adrenoceptor antagonist action of ketanserin. Both patients were taking regular beta-blocker therapy, which may exacerbate such a reaction.
PMCID: PMC2428148  PMID: 3684842
2.  Comparison of nifedipine, prazosin and hydralazine added to treatment of hypertensive patients uncontrolled by thiazide diuretic plus beta-blocker. 
Postgraduate Medical Journal  1987;63(736):99-103.
In 93 patients with hypertension uncontrolled by bendrofluazide 5 mg plus atenolol 100 mg daily, the effects of adding nifedipine (up to 60 mg/day, n = 31), prazosin (up to 20 mg/day, n = 31), or hydralazine (up to 200 mg/day, n = 31) were compared in a 6 month open random parallel group study. The three drugs did not differ significantly as regards antihypertensive effect, withdrawal rate, total number of side effects, or effect on serum biochemical variables. The pattern of side-effects differed. Headache, flushing and oedema were common with nifedipine, tiredness and drowsiness with prazosin, and headache with hydralazine. Nifedipine is an acceptable third-line antihypertensive drug which may have some advantage over hydralazine and prazosin.
PMCID: PMC2428247  PMID: 3671250
3.  Ketanserin in essential hypertension: a double-blind, placebo-controlled study. 
Postgraduate Medical Journal  1985;61(717):583-586.
The antihypertensive effect of the selective serotonin antagonist ketanserin was examined in a double-blind, placebo-controlled, parallel group study in 20 patients with essential hypertension. After 7 weeks treatment with ketanserin (mean dose 71 mg/d) there was a significant fall of both systolic and diastolic blood pressure, as compared to placebo, with a peak effect of 19.1/9.1 mmHg lying (P less than 0.01/P less than 0.01), and 16.5/11.3 mmHg standing (P less than 0.01/P less than 0.01); twice daily dosage appeared satisfactory. Subjective side effects were similar in the ketanserin and placebo groups. Ketanserin is an effective antihypertensive drug of moderate potency when given twice daily, with no orthostatic effect.
PMCID: PMC2418322  PMID: 3161013
4.  Letter: Infections in asplenic adults. 
British Medical Journal  1974;3(5925):254-255.
PMCID: PMC1611964  PMID: 4546489
5.  Acute renal failure with ACE inhibition in aortic coarctation. 
Postgraduate Medical Journal  1994;70(830):927-929.
A 43 year old man with inoperable aortic coarctation and severe hypertension requiring near maximal anti-hypertensive treatment was admitted in severe heart failure. After 2 weeks of treatment the heart failure and blood pressure were incompletely controlled and angiotensin converting enzyme (ACE) inhibitor was started. Serum creatinine was normal before starting the ACE inhibitor and on discharge from hospital. The patient was re-admitted a week later with gross fluid retention and in renal failure. In the absence of alternative causes, a diagnosis of ACE inhibitor-induced renal failure was made and treatment was stopped. The patient required haemodialysis for 2 days and within 1 week the renal function had reverted to normal and has remained so for 1 year. We propose that the renal haemodynamics in severe aortic coarctation are similar to those in bilateral severe renal artery stenosis and advise caution in the use of ACE inhibitors for adults with aortic coarctation.
PMCID: PMC2398015  PMID: 7870644
8.  The association between haemospermia and severe hypertension. 
Postgraduate Medical Journal  1991;67(784):157-158.
The association between haemospermia and hypertension was examined in a case-control study comparing 5 hypertensive patients with haemospermia to 20 age-matched hypertensive men. Patients with haemospermia had much higher blood pressures than hypertensive controls (200/131 mmHg vs 147/90 mmHg; P less than 0.0005/P less than 0.0001), higher left ventricular voltage on ECG (P less than 0.02), and higher concentrations of serum creatinine, proteinuria and renovascular disease (all P = 0.06 vs controls). Haemospermia is associated with severe uncontrolled hypertension. It is not, however, associated with hypertension per se, as the prevalence of hypertension in published series of patients with haemospermia is no higher than that expected in the general population. Men presenting with haemospermia should have their blood pressure measured carefully as they may require antihypertensive treatment urgently.
PMCID: PMC2398961  PMID: 2041846
9.  Local confidential inquiry into avoidable factors in deaths from stroke and hypertensive disease. 
BMJ : British Medical Journal  1993;307(6911):1027-1030.
OBJECTIVE--To audit avoidable deaths from stroke and hypertensive disease. DESIGN--Details of care before death were obtained from general practitioners and other doctors, anonymised, and assessed by two experts against agreed minimum standards of good practice for detecting and managing hypertension. SETTING--Health authority with population of 250,000. SUBJECTS--All patients under 75 years who died of stroke, hypertensive disease, or hypertension related causes during November 1990 to October 1991. MAIN OUTCOME MEASURES--Presence of important avoidable factors and departures from minimum standards of good practice. RESULTS--Adequate information was obtained for 88% (123/139) of eligible cases. Agreement between the assessors was mostly satisfactory. 29% (36/123, 95% confidence interval 21% to 37%) of all cases and 44% (36/81, 34% to 55%) of those with definite hypertension had avoidable factors that may have contributed to death. These were most commonly failures of follow up and continuing smoking. Assessment against standards of minimum good practice showed that care was inadequate but not necessarily deemed to have contributed to death, in a large proportion of patients with definite hypertension. Common shortcomings were inadequate follow up, clinical investigation, and recording of smoking and other relevant risk behaviours. CONCLUSIONS--This method of audit can identify shortcomings in care of patients dying of hypertension related disease.
PMCID: PMC1679247  PMID: 8251776
12.  Systemic Weber-Christian disease with reversible bilateral ureteric obstruction. 
Postgraduate Medical Journal  1989;65(764):410-416.
It has been proposed that idiopathic retroperitoneal fibrosis may be a consequence of 'healed' retroperitoneal lesions of systemic Weber-Christian disease. However ureteric obstruction which is the hallmark of idiopathic retroperitoneal fibrosis, has not been described in systemic Weber-Christian disease. We report a patient with systemic Weber-Christian disease who, during a relapse, developed bilateral ureteric obstruction which resolved when the Weber-Christian disease remitted. The radiological appearances were consistent with a diagnosis of idiopathic retroperitoneal fibrosis, but the clinical course was slightly atypical in that the ureteric obstruction resolved completely and rapidly. Ureteric obstruction can complicate systemic Weber-Christian disease and this observation gives support to the hypothesis that idiopathic retroperitoneal fibrosis is related to systemic Weber-Christian disease.
PMCID: PMC2429349  PMID: 2608584
15.  beta blockade and intermittent claudication: placebo controlled trial of atenolol and nifedipine and their combination. 
BMJ : British Medical Journal  1991;303(6810):1100-1104.
OBJECTIVE--To determine the effects of the beta 1 selective adrenoceptor blocker atenolol, the dihydropyridine calcium antagonist nifedipine, and the combination of atenolol plus nifedipine on objective and subjective measures of walking performance and foot temperature in patients with intermittent claudication. DESIGN--Randomised controlled double blind four way crossover trial. SETTING--Royal Hallamshire Hospital, Sheffield. SUBJECTS--49 patients (40 men) aged 39-70 with chronic stable intermittent claudication. INTERVENTIONS--Atenolol 50 mg twice daily; slow release nifedipine 20 mg twice daily; atenolol 50 mg plus slow release nifedipine 20 mg twice daily; placebo. Each treatment was given for four weeks with no washout interval between treatments. MAIN OUTCOME MEASURES--Claudication and walking distances on treadmill; skin temperature of feet as measured by thermistor and probe; blood pressure before and after exercise; subjective assessments of walking difficulty and foot coldness with visual analogue scales. RESULTS--Atenolol did not significantly alter claudication distance (mean change -6%; 95% confidence interval 1% to -13%), walking distance (-2%; 4% to -8%), or foot temperature. Nifedipine did not alter claudication distance (-4%; 3% to -11%), walking distance (-4%; 3% to -10%), or foot temperature. Atenolol plus nifedipine did not alter claudication distance but significantly reduced walking distance (-9%; -3% to -15% (p less than 0.003)) and skin temperature of the more affected foot (-1.1 degrees C; 0 to -2.2 degrees C (p = 0.05)). These effects on walking distance and foot temperature seemed unrelated to blood pressure changes. CONCLUSIONS--There was no evidence of adverse or beneficial effects of atenolol or nifedipine, when given singly, on peripheral vascular disease. The combined treatment, however, affected walking ability and foot temperature adversely. This may have been due to beta blockade plus reduced vascular resistance, which might also explain the reported adverse effects of pindolol and labetalol on claudication.
PMCID: PMC1671261  PMID: 1747577
17.  Prolongation of the QT interval by ketanserin. 
Postgraduate Medical Journal  1988;64(748):112-117.
In hypertensive patients single doses of ketanserin 40 mg prolonged the corrected QT interval (QTc) for at least 8 hours, with a maximal increase of 35 ms (P less than 0.001, n = 6) after 2 hours. During chronic dosing (20 and 40 mg b.d.) the QTc was further prolonged, by 46 and 45 ms respectively. QTc prolongation after treatment with a mean dose of 73 mg/day for 7 weeks (n = 26) was significantly related to body weight (r = -0.58, P less than 0.01), and to the dose of ketanserin corrected for body weight (r = 0.63, P less than 0.01), but not to plasma concentrations of ketanserin, ketanserinol, potassium or calcium. High doses of ketanserin (mean dose 167 mg/day, n = 9) increased the QTc by 40 ms (P less than 0.001), with prolongation of up to 80 ms in individual patients. Treatment with ketanserin at doses proposed for clinical use (40-80 mg/day) may carry a risk of ventricular arrhythmias.
PMCID: PMC2428798  PMID: 3050936
24.  The lupus syndrome induced by hydralazine: a common complication with low dose treatment. 
The true incidence of the lupus syndrome induced by hydralazine was determined in a longitudinal study of 281 patients consecutively starting hydralazine for hypertension over a 51 month period. Data on the duration of treatment and the maximum dose achieved were examined using life table analysis. After three years' treatment with hydralazine the incidence of the lupus syndrome was 6.7% (95% confidence limits 3.2-10.2%). The incidence was dose dependent, with no cases recorded in patients taking 50 mg daily and incidences of 5.4% with 100 mg daily and of 10.4% with 200 mg daily. The incidence was higher in women (11.6%) than in men (2.8%). In women taking 200 mg daily the three year incidence was 19.4%. Hydralazine is an effective antihypertensive drug that has come to be used in restricted dosage (not more than 200 mg daily) because of its risk of inducing the lupus syndrome. This study shows that the true incidence of the syndrome is still unacceptably high even when the drug is prescribed according to current recommendations.
PMCID: PMC1442447  PMID: 6432120

Results 1-25 (59)