Blood, semen, and an innocent man

Abstract

In August, 2007, a 30-year-old doctoral student, from Nigeria but living in London, noticed bright red blood in his ejaculate. The problem persisted for 2 months, so he went to see his general practitioner. There was no history of injury to the genitals or the prostate; the patient had used barrier contraception with his current and previous two girlfriends. The patient was not physically examined, but was advised to attend a walk-in genitourinary clinic. When he did so, 3 days later, his blood pressure was 244/170 mm Hg. He was given 5 mg amlodipine, and sent to hospital. There, repeated measurements, with a manual sphygmomanometer, gave a blood pressure of around 239/141 mm Hg, in both arms. The patient’s blood pressure had last been measured 10 years before, when he had been told it was “a little high”. He had never taken antihypertensive drugs. He had been feeling entirely well, although, on close questioning, he described having had a nosebleed and headache 2 months before noticing the blood in his ejaculate. He had no other relevant medical history, and was a lifelong non-smoker. Inspection showed no signs of Cushing’s syndrome, acromegaly, or systemic sclerosis. Physical examination, including neurological, genital, and rectal examination, showed nothing abnormal— notably, radiofemoral delay and renal bruits were absent, and the patient scored 10/10 on the abbreviated mental test score. Dipstick testing of urine showed much protein, but not blood. Urine microscopy showed no casts. Blood tests showed nothing abnormal: notably, concentrations of calcium, creatinine, C-reactive protein, autoantibodies, and prostate-specifi c antigen were normal. Serological and immunological testing showed no evidence of HIV or tuberculosis, respectively. Microscopy and culture of urethral swabs showed no evidence of syphilis, chlamydia, or gonorrhoea. An electrocardiogram showed severe leftventricular hypertrophy; radiography of the chest showed no evidence of aortic coarctation. Fundoscopy showed bilateral papilloedema, but no haemorrhages. Ultrasonography showed kidneys of normal size, without cysts. CT of the abdomen showed nothing abnormal— and specifi cally, no adrenal masses. The patient’s blood pressure was lowered gradually, over several days, with amlodipine, ramipril, and intravenous glyceryl trinitrate; meanwhile, we took three 24-h urine collections: after the collections were done, we started treatment with atenolol, having stopped the glyceryl trinitrate. Urinary concentrations of catecholamines were normal, confi rming that the patient did not have a phaeochromocytoma. Retinal photography showed resolution of the papilloedema, but many cotton-wool spots and nerve-fi bre-layer (“fl ame”) haemorrhages (fi gure)—consistent with grade 3 hypertensive retinopathy. The plasma renin:aldosterone ratio is awaited. The diagnosis is essential hypertension or hyperaldosteronism. The patient was discharged 10 days after admission. When last seen by us, in late November, 2007, his blood pressure was around 150/96 mm Hg; he continued to feel well, and had no blood in his semen. Haematospermia is most commonly caused by infection or injury—including iatrogenic injury from taking biopsy samples of the prostate. Other causes include stones, cysts, vascular abnormalities—and severe hypertension, which causes an estimated 5% of cases. Malignant hypertension is defi ned as blood pressure over 180/100 mm Hg, with papilloedema or retinal haemorrhage. Although malignant hypertension can occur in essential hypertension, causes of secondary hypertension should always be sought. Apart from haemato spermia, our patient was asymptomatic—as are around 10% of people with malignant hypertension. Nonetheless, leftventricular hypertrophy, proteinuria, and retinopathy indicated pronounced end-organ damage, consistent with severe, longstanding hypertension.