1456

gland, which regressed completely in 3 days after cimetidine wasstopped. Then in 1983, after a resumption of cimetidine at the samedosage, bilateral parotitis had appeared on the 5th day; this

regressed totally in 5 days after the treatment was stopped.Gastroduodenal fiberoptic endoscopy revealed congested

mucosa with no haemorrhagic lesion. No abnormalities were foundon X-ray tomography of the parotid lobes or sialography, or onbuccopharyngeal examination. 10 days after the acute episode,ranitidine (150 mg morning and evening) was given with thepatient’s informed consent. Bilateral parotitis recurred 7 days later,and regressed several days after the treatment was stopped.The sequence of events suggests that Hz receptor antagonists

(cimetidine and ranitidine) caused recurrent parotitis. Thisundesirable effect is reminiscent of the rare cases of pancreatitis2-4that have been reported in response to H2 receptor antagonists.

Medicine and Nephrologyand Medicine and Gastroenterology Services,

CHR Thionville,57100 Thionville, France;

and Department of Clinical Pharmacology,CHU Nancy

PL. CARAMANP. NETTERA. M. SEMIN-COSSONB. PARROTP. TRECHOTE. AZOULAY

1. McGuigan JE. A consideration of the adverse effects of cimetidine. Gastroenterology1981; 80: 181-92.

2. Arnold F, Doyle PJ, Bell G. Acute pancreatitis in a patient treated with cimetidine.Lancet 1978; i: 382-83.

3. Wilkinson ML, O’Driscoll R, Kiernan TJ. Cimetidine and pancreatitis. Lancet 1981;i: 610-11.

4. Joffe SN, Lee FD. Acute pancreatitis after cimetidine administration in experimentalduodenal ulcers. Lancet 1983; i: 383.

ANTI-IgM SCREENING FOR HIV

SIR,-Dr Parry and Dr Mortimer (Oct 25, p 979) report an IgMpositive, IgG negative phase lasting no more than 8 weeks in a seriesof high-risk patients during the initial stages of HIV infection. Thelonger IgM positive, IgG negative periods reported by us (Sept 6,p 570), might, in their view, justify, if confirmed by reliablemethods, a wider application of tests specifically aimed at detectinganti-HIV IgM. In nearly all cases reported by Parry and Mortimer,anti-HIV IgM was already present by the time they were firstsought, which makes it impossible to get an accurate figure for theirtrue duration. Patients in our series, however (to whom a few casesof post-tranfusion HIV infection can now be added), were

confirmed IgM positive, IgG negative for periods lasting up tosome months (tables I and II). Similar data have been reported byothers. 1-5

TABLE I-SEROLOGICAL PATTERNS IN INITIALLY HIV

SERONEGATIVE (IgM AND IgG) DRUG ADDICTS WHO CONVERTEDTO IgM SEROPOSITIVITY

*AJ1 drug addicts at an assistance centre (1-5) or in an mfectious diseases umt (6-13).

TABLE 11-SEROLOGICAL PATTERNS IN THREE INITIALLY HIV

SERONEGATIVE (IgM AND IgG) SUBJECTS TRANSFUSED WITHBLOOD SUBSEQUENTLY FOUND HIV POSITIVE

We think that the test we have developed is specific and quitesensitive, being more suitable for screening than for diagnosticpurposes; its sensitivity gave us the opportunity to detect, withexcellent reproducibility, frequent IgM positivities, even very closeto the cut-off, which were subsequently confirmed both by westernblot IgM and by IgM-IgG switch. The possibility of detecting HIVinfection even only a few weeks before this can be done by othermethods, seems to justify the routine use of an anti-HIV IgMscreening test, at least for blood donors.

Immunohaematology and Transfusion Service,Infectious Diseases Unit,Ospedale Maggiore di Lodi,Milan, Italy

G. BEDARIDAG. CAMBIE’F. D’AGOSTINOM. G. RONSIVALLEE. BERTOM. E. GRISIP. R. CROCCHIOLO

Immunohaematology Service,Ospedale di Tradate, Varese E. MAGNI

1. Alter HJ, Eichberg JW, Masur H, et al. Transmission of HTLV III infection fromhuman plasma to chimpanzees: an animal model for AIDS. Science 1984; 226: 549

2. Joller-Jemelka HI, Muller F, Joller PW, et al. Quantitation of early manifestations ofHTLVIII/LAV infections. Contribution to International Conference on AIDS(Paris, June, 1986).

3. Melioli G, Varnier OB, Merli A, Schito G. Detection of specific anti-LAV/HTLVIIIIgM antibodies during sero-conversion using enzyme-linked immunosorbentassay. Contribution to International Symposium on AIDS and Blood Transfusion(Turin, June, 1985).

4. Valguarnera G, Martinengo P, Amico A. Ricerca degli anticorpi IgM-IgGanti-HTLVIII in donatori di sangue occasionali. Transfus Sang 1986; 31: 75

5. Varnier OE. Diagnostica serologica dell’infezione da HTLVIII. Simposio di

aggiornamento su AIDS e sindromi correlate (Rapallo, March, 1986).6. Bedarida G, D’Agostino F, Ronsivalle MG, et al. La ricerca di anticorpi di classe IgM

anti HTLVIII/LAV in soggetti a rischio risultati negativi in ELISA anti

HTLVIII/LAV IgG: Risultati preliminari. Riv Emotera Immunoematolo 1985; 32:397.

FLUID RETENTION WITH NIFEDIPINE INANTIHYPERTENSIVE THERAPY

SiR,—Your Nov 8 editorial indicated that fluid retention may beseen after nifedipine. Three lines lower down you indicated thatminoxidil may also cause fluid retention. It might be supposed thatnifedipine and minoxidil have similar effects. However, the ankleoedema that sometimes results after nifedipine is not caused by fluidretention but is an entirely local phenomenon. Patients treated withnifedipine (10 mg four times daily) had an increased foot

volume-average baseline foot volume 1246 ml, average volumeduring treatment 1568 ml (p < 0-01). Body weight did not increase.Nifedipine has diuretic qualities,2 so the cause of the increased footvolume is not clear but may be related to arteriolar without venulardilatation on during nifedipine therapy. The addition of captopril, acombined arteriolar and venous dilating agent, returned theincreased foot volume to normaL1 However, frusemide (80 mgdaily) did not decrease nifedipine-induced ankle oedema.3 Whencompared with prazosin, nifedipine caused significantly less weightgain (1 ’41 kg for prazosin, 0-01 kg for nifedipine, p < 0-05).There is no appreciable reason except custom and cost why

calcium antagonists should not be considered along with otheragents including diuretics, (3-blockers and ACE inhibitors as

first-line therapy for hypertension. As a third-line agent, nifedipinecompares well with prazosin and hydralazine.4Heart Research Unit and Hypertension Clinic,Department of Medicine,Medical School,Cape Town, South Africa LIONEL H. OPIE

1. Guazzi MD, De Cesare N, Galli C, et al. Calcium-channel blockade with nifedipineand angiotensin converting enzyme inhibition with captopril in the therapy ofpatients with severe primary hypertension. Circulation 1984, 70: 279-84.

2. Leonetti G, Cuspidi C, Sampieri L, et al. Comparison of cardiovascular, renal, andhumoral effects of acute administration of two calcium channel blockers innormotensive and hypertensive subjects. J Cardiovasc Pharmacol 1982; 4: S319-24

3. Guazzi MD, Fiorentini C, Olivari MT, et al Short- and long-term efficacy of acalcium-antagonistic agent (nifedipine) combined with methyldopa in thetreatment of severe hypertension. Circulation 1980; 61: 913.

4. Ramsay LE, Latham LV. Comparison of nifedipine, prazosin and hydralazine asstep-three drugs for hypertension. J Hypertension 1985; 3 (suppl 3): S555