1216 ceftriaxone daily over 5 days. On the 7th postoperative day clinically significant bleeding occurred from the abdominal drainage area, with normotest levels below 5%. The patient had received no antibiotic apart from ceftriaxone and there was no evidence of disseminated intravascular coagulation. The defect was rapidly corrected by vitamin K; the normotest result was 105% after oral substitution of 20 mg vitamin K twice daily for 2 days. Hypoprothrombinaemic bleeding after use of third-generation cephalosporins and latamoxef is usually attributed to disturbance of vitamin-K-producing bacteria in the gut by drug eliminated in the bile. Our patient had renal insufficiency, and this causes a compensating increase in biliary excretion of the new cephalosporins. Normotest results should be closely monitored in patients receiving cephalosporins which are substantially eliminated in the bile. 1 It has been suggested that the development of hypoprothrombin- aemic bleeding might be related to the presence of a methylthiotetrazole side-chain at position 3 of the cephalosporin molecule.2 This side-chain is responsible for disulfiram reactions, the side-chain and disulfiram being structurally similar. Ceftriaxone is said to be free of this adverse effect because the methylthiotetrazole side-chain has been replaced by a triazine ring.3 3 The "methylthiotetrazole hypothesis" is not substantiated by this case. 1st Medical Clinic, University of Vienna, A-1090 Vienna, Austria ALEXANDER HAUBENSTOCK PAUL SCHMIDT JAN ZAZGORNIK PETER BALCKE HERBERT KOPSA HYPOTENSION AND THE PENTOLINIUM SUPPRESSION TEST SIR,—DR Channer and colleagues (April 30, p 988) describe a patient who experienced transient hypotension 30 min after the administration of pentolinium as a test for phaeochromocytoma. The 2 - 5 mg dose of pentolinium originally proposed for outpatient tests was chosen because it is adequate to cause a measurable fall in sympathoadrenal activity without causing appreciable or prolonged hypotension. We have done over 130 pentolinium tests and have experienced no problems with hypotension. Last year, blood pressure was measured systematically every 10 min in 41 consecutive patients (32 males, 9 females, mean age 42±13 years) who had this test. Mean blood pressure before pentolinium was ‘ 138±25/90±15 mm Hg, and this fell by 7±12/0-4±7 at 10 min, 7±9/-0.6±7 at 20 min, and 8± 10/ -1 - 7±8 mm Hg at 30 min. The reduction in pressure after pentolinium, as with other antihypertensive drugs, correlated with the height of the pretreatment levels (r = 0’ 5, p<0. 001). No patient in this series had ,hypotension as severe as that reported by Channer et al. We are surprised that their patient became hypotensive 30 min after drug administration without an earlier fall in pressure. All of our patients who had appreciable blood pressure reduction did so within 20 min of the injection. It is also unusual for supine patients to have such profound symptoms of hypotension and we wonder if they can be attributed solely to pentolinium. Finally, the report does not warrant a change in our policy of using this test on an outpatient basis. Patients should remain supine for 60 min after the injection, to avoid postural hypotension. Blood pressure has usually returned to normal, as in the patient reported, by this time. Department of Clinical Pharmacology, Royal Postgraduate Medical School, Hammersmith Hospital, London W 12 0HS MICHAEL B. MURPHY ROGER CAUSON 1. D’Elia JA, Kaldanay A, Miller DG, Yoburn DC, Kaye WA. Moxalactam, bleeding, and renal insufficiency. JAMA 1983; 249: 1565. 2. Neu HC. The new beta-lactamase-stable cephalosporins. Ann Intern Med 1982; 97: 408-19. 3. Daldrup T, Böhm E. Zur Frage der Interaktion zwischen dem Cephalosporin Ceftriaxon und Alkohol. Vortrag, Hahnenklee-Symposium (Sept 9 and 10, 1981). CATECHOLAMINE SUPPRESSION TESTING IN PATIENT WITH PHAEOCHROMOCYTOMA AND NORMAL PLASMA CATECHOLAMINE LEVELS SIR,—Although the catecholamine suppression test, with either clonidine or pentolinium, appears to be a safe, effective tool for the diagnosis of phaeochromocytoma in patients with raised plasma catecholamines,I,2 its usefulness in patients with normal catecholamine levels has not yet been determined. We describe here a patient with a phaeochromocytoma who had normal resting noradrenaline (NA) and adrenaline levels but persistently abnormal plasma NA responses to acute clonidine administration. A 44-year-old man was admitted to the Baltimore Veterans’ Administration Medical Center in July, 1979, with palpitations, nausea, and right flank pain. Blood pressure was 126/80 mm Hg on hydrochlorothiazide, 50 mg twice daily. He had a history of hospital admission with similar symptoms in 1977; diastolic BP at that time was as high as 120 mm Hg. The symptoms resolved spontaneously but a 24 h urine collection showed a vanillylmandelic acid (VMA) level of 12 - 4 mg (normal <6’ 8 mg) and free catecholamines of 450 µg (normal <135 lAg). Repeat urine collections showed normal catecholamines and borderline increases in VMA and metanephrine. The patient was lost to follow-up until April, 1981, when resting plasma catecholamines were normal (NA <650, adrenaline <75 pg/ml) but did not suppress appropriately after 0 - 3 mg clonidine hydrochloride by mouth (figure). Prazosin 2 mg/day and hydrochlorothiazide 50 mg/day had been stopped 1 week before testing. In all of twelve other patients with normal catecholamine levels, but without phaeochromocytoma, plasma NA fell at least 3407o from baseline after clonidine, with a maximum decrease at 3-4 h. Adrenaline levels generally paralleled NA levels but occasionally showed no decline. In January, 1982, before surgery, plasma catecholamines were again normal and did not decrease with clonidine (figure). Abdominal exploration revealed a 2 x 2 cm nodule in the left adrenal gland and a large right adrenal tumour invading the kidney and inferior vena cava. Bilateral adrenalectomy and right nephrectomy were done but part of the tumour surrounding the inferior vena cava was unresectable. Pathological examination of both masses was consistent with phaeochromocytoma. The patient made an uneventful recovery and has remained normotensive on prazosin and replacement doses of cortisone acetate. A third clonidine test in March, 1982, showed normal baseline NA and’ adrenaline levels and absence of normal suppression (figure). Prazosin 2 mg/day had been continued to 24 h before each of the last two clonidine tests. The usefulness of adrenergic suppression testing in detecting phaeochromocytoma has been demonstrated only in patients with raised plasma catecholamine concentrations. In the twenty-eight patients given clonidine or pentolinium by Bravo et all and Brown and colleagues,2 basal values of either NA or adrenaline were increased and failed to decrease into the normal range, thus indicating an autonomous catecholamine source. When we did serial clonidine suppression tests in a patient with ’phaeochromocytoma, plasma NA was not suppressed appropriately, even though basal catecholamine levels were normal. In the tests done on April 6, 1981, and March 31, 1982, shortlived falls in NA greater than 35% were noted 1 or 2 h post-clonidine. Whether this resulted from spontaneous changes in tumour NA release, from transient peripheral adrenergic suppression, or a com- bination of both factors is not known. Serial catecholamine measurements, including several baseline samples, were helpful in demonstrating the abnormal NA responses by 3-4 h. Blood pressure decrements after clonidine were comparable to those noted previously. 1 The failure of clonidine to suppress NA in this patient could be a result of several factors. Since the adrenal glands produce only 2% 1. Bravo EL , Tarazi RC, Fouad FM, Vidt DG, Gifford RW Jr. Clonidine-suppression test. a useful aid in the diagnosis of pheochromocytoma N Engl J Med 1982, 305: 623-26. 2. Brown MJ, Jenner DA, Allison DJ, Lewis PJ, Dollery CT Increased sensitivity and accuracy of phaeochromocytoma diagnosis achieved by use of plasma-adrenaline estimations and a pentolinium-suppression test Lancet 1981; i 174-77