Cautions see notes above; also hepatic impairment; interactions: histamine H₂-antagonists and notes above

Side-effects see notes above; also alopecia; very rarely tachycardia, galactorrhoea, interstitial nephritis

Dose

• 400 mg twice daily (with breakfast and at night) or 800 mg at night (benign gastric and duodenal ulceration) for at least 4 weeks (6 weeks in gastric ulceration, 8 weeks in NSAID-associated ulceration); when necessary the dose may be increased to 400 mg 4 times daily; INFANT under 1 year 20 mg/kg daily in divided doses has been used; CHILD 1-12 years, 25-30 mg/kg daily in divided doses; max. 400 mg 4 times daily

Maintenance, 400 mg at night or 400 mg morning and night

• Reflux oesophagitis, 400 mg 4 times daily for 4-8 weeks

• Prophylaxis of stress ulceration, 200-400 mg every 4-6 hours

• Gastric acid reduction (prophylaxis of acid aspiration; do not use syrup), obstetrics 400 mg at start of labour, then up to 400 mg every 4 hours if required (max. 2.4 g daily); surgical procedures 400 mg 90-120 minutes before induction of general anaesthesia

• Short-bowel syndrome, 400 mg twice daily (with breakfast and at bedtime) adjusted according to response

• To reduce degradation of pancreatic enzyme supplements, 0.8-1.6 g daily in 4 divided doses 1-1 ½ hours before meals

Cimetidine * (Non-proprietary)

Tablets, cimetidine 200 mg, net price 60-tab pack = £1.96; 400 mg, 60-tab pack = £2.30; 800 mg, 30-tab pack = £1.99

Oral solution, cimetidine 200 mg/5 mL, net price 300 mL = £14.24

Excipients may include propylene glycol (see Excipients)

* Cimetidine can be sold to the public for adults and children over 16 years (provided packs do not contain more than 2 weeks’ supply) for the short-term symptomatic relief of heartburn, dyspepsia, and hyperacidity (max. single dose 200 mg, max. daily dose 800 mg), and for the prophylactic management of nocturnal heartburn (single night-time dose 100 mg)

Tagamet® (Chemidex)

Tablets, all green, f/c, cimetidine 200 mg, net price 120-tab pack = £19.58; 400 mg, 60-tab pack = £22.62; 800 mg, 30-tab pack = £22.62

Syrup, orange, cimetidine 200 mg/5 mL. Net price 600 mL = £28.49

Excipients include propylene glycol 10%

Current pharmacotherapy for Benign Prostatic Hyperplasia (BPH) is based on agents that relax the smooth muscles of prostatic urethra and stroma and those that deprive acinar cells of androgen.

Various agents have been tried in the treatment of BPH (Table). They may be broadly grouped into those affecting the dynamic component of urethral obstruction, namely the smooth muscle and prostatic stroma, and those affecting the glandular elements by androgen deprivation. The mechanism of action of many agents claimed to be useful in Benign Prostatic Hyperplasia is not clearly understood.

Caine has suggested that obstruction due to Benign Prostatic Hyperplasia occurs because of two factors: a dynamic component is thought to occur as a result of the contraction of smooth muscles of the prostate and prostatic urethra and is mediated mostly by adrenergic receptors; and a mechanical component of obstruction is related to the presence of a mass of hyperplastic acinar or stromal tissue that compresses and narrows the urethral lumen. There is some evidence that the presence and density of stromal content in BPH may relate to the severity of obstruction.

Current understanding of the biologic mechanisms of obstruction is limited and does not extend to two common clinical facts. The first is that the size of the prostate does not always correlate with the severity of symptoms or objective signs of obstruction. The second is the discrepancy between the histologic changes of BPH and the presence and severity of symptoms. From a physiologic standpoint, five conditions in patients with symptoms of “BPH” may exist singly or in combination. These are prostatic urethral obstruction, impaired detrusor contractility, detrusor instability, sensory urgency, and primary vesical neck obstruction. All these conditions likely result from varying combinations of prostatic enlargement and subtle neurologic dysfunction, all due to age-related central nervous system degeneration. Alternatively, a hyperplastic prostate during growth may disrupt normal sphincteric function. Thus, it is not surprising that prostatectomy fails to relieve symptoms of prostatism in about 20% of patients because the symptoms may be caused by poorly understood deficits in neurosensory pathways regulating micturition and sphincteric function.

Transurethral prostatectomy is the most common surgical procedure currently performed for the treatment of Benign Prostatic Hyperplasia. Outcome analyses have questioned the results of transurethral resection of the prostate (TURP). Patients undergoing TURP have been reported to be at greater risk from cardiovascular death than patients undergoing open prostatectomy. Recently these findings were disputed, and it was reported that transurethral resection for BPH does not increase long-term mortality and that comorbid illnesses and older age probably account for the apparent increase in long-term mortality after TURP. The morbidity of the procedure remains unchanged, however. In a review in 1962, the morbidity after transurethral resection of the prostate was reported to be 18% and the mortality 2.5%. More recently, the American Urological Association (AUA) cooperative study of 3,885 patients after the procedure revealed an overall complication rate of 18% and 0.2% mortality. Thus, the search for alternative therapies has been prompted by patients’ preferences for less invasive forms of treatment without prohibitive side effects. Apart from pharmacotherapy, other methods undergoing trials for the treatment of Benign Prostatic Hyperplasia include laser ablation, microwave hyperthermia, and prostatic stents. Ultimately, the role of surgical treatment and newer modalities must be based on relative effectiveness, cost, morbidity, effect on quality of life, expectations, and treatment preferences of patients.