LOWERING BLOOD PRESSURE

LOWERING BLOOD PRESSURE

1380 longer detectable and they again. have not been observed in her blood We later received a blood sample from a male homosexual with advanced ...

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1380

longer detectable and they again.

have

not

been observed in her blood

We later received a blood sample from a male homosexual with advanced and well-established AIDS. The specimen was received in the laboratory during the evening, and on examination the next morning, the blood film showed numerous homogeneous basophilic bodies identical to those seen in the first, case (figure). There were 20 such bodies per 100 white cells (white cell count 21 x 10’’/1, 75% neutrophils) and the bodies were easily distinguished from leucocytes. No clearly intermediate forms between these basophilic bodies and intact white cells were seen. A further specimen taken the day after admission did not reveal any such bodies. Additional blood films made from the man’s original specimen 18 h after receipt, in which the basophilic bodies showed degenerative changes such as decreased density of staining, were stained with periodic acid-Schiff (PAS) and the Feulgen reaction. The PAS reaction was weakly but consistently positive while the Feulgen stain showed a positive reaction with a different hue from that seen in the nuclei of "healthy" leucocytes. The nature, origin, and significance of these bodies are unknown. We think that they represent degenerating nuclei of damaged cells. However, none of us, with a total of more than 80 years’ experience of examining blood films, has seen this before. To see these bodies in two severe cases of AIDS in such a short space of time suggests that it is a new and possibly significant observation. P. H. PINKERTON T. A. HARPER M. C. QUANTZ S. KRAKOWER A. RACHLIS

Department of Laboratory Haematology, Sunnybrook Hospital, Toronto, Ontario, Canada

LOWERING BLOOD PRESSURE

SIR,—Dr Cruickshank and his colleagues (May 16, p 1154) attribute the excess mortality they found in patients with low attained diastolic pressures to antihypertensive therapy. We have divided the patients in the treatment group of our trial’ according to the mean of all the attained diastolic pressures (excluding pretreatment readings) and have calculated the rate of fatal plus non-fatal myocardial infarction and the total death rate in each band. The table shows that there is a J-shaped curve, with the lowest rates at 80-90 mm Hg. INCIDENCE

(/1000 PATIENT-YEARS) OF FATAL PLUS NON-FATAL

MYOCARDIAL INFARCTION AND TOTAL DEATHS BY ATTAINED DIASTOLIC BLOOD PRESSURE

BRAIN DEATH

SIR,-From time to time, doubts are expressed about the validity of the concept of brain death and criteria for its diagnosis as defined by the Conference of Medical Royal Colleges and their Faculties in 1976,1 with a further memorandum in 1979.2 The conference, it is claimedshould have given more attention to information obtainable in intensive care units. I have examined personal records of 146 head-injury patients managed between Jan 1,1970, and Dec 31, 1978, in the respiratory care unit of Manchester Royal Infirmary. There were records of whether or not the patient was able to breathe spontaneously and of the state of the pupils in all these cases. Soon after admission, 67 patients had no spontaneous respiration (hypocapnia being absent) and had unreactive pupils, either partly or fully dilated. A further 28 developed these signs one to eight days after admission. None of these 95 patients survived. These results offer no support to those who question the Conference criteria, which demand much more extensive tests of brainstem function. University Department of Anaesthesia, Manchester Royal Infirmary, Manchester M13 9WL

Royal Colleges and their Faculties. Diagnosis of brain death Lancet 1976; ii: 1069-70. 2. Conference of Medical Royal Colleges and their Faculties. Diagnosis of death. Lancet 1979; i: 261-62. 3. Sunday Times Dec 7, 1986. 1. Conference of Medical

HYPERCHOLESTEROLAEMIA IN NEWBORN BABIES

SIR,—Dr Asami and Dr Sakai (May 2, p 1038) identified hypercholesterolaemia (above the 90th percentile) in 9-0% (44 of 490) babies 5-7 days old born in Niigati, Japan. This frequency of hypercholesterolaemia is similar to the 10% (5/52) found in newborn babies in this part of Argentina. However, unlike Asami and Sakai, we did fmd a correlation, between the babies (cord blood) and their mothers, for both serum total cholesterol (TC; ’Precimat’ enzymatic method, Boehringer) and the atherogenic index defined as TC minus high density lipoprotein cholesterol (HDLC) all divided by HDLC. TC and atherogenic index in the newborn babies (96-0 [12.6] mg/dl and 2-74) of mothers with high TC levels (273-6 [10-0] mg/dl and 3-86) were significantly higher (p < 0-001) than those observed in newborn babies (79-0 [4-5] mg/dl and 2-19) of normocholesterolaemic mothers (181-8 [16-0] mg/dl and 3-15). Serum lipid levels in the fathers were not measured. It has been suggested that infants with high TC levels may continue to have raised TC levels.’Such infants are at increased risk of cardiovascular complications in early adulthood.2 We agree with Asami and Sakai on the importance of early detection of hypercholesterolaemia, so that intervention can start as soon as possible. Paediatricians should be aware of the importance of measuring serum lipid levels in newborn babies, especially in countries such as Argentina, where coronary heart disease ranks as the first cause of death.3 Hypertension Research Centre,

This corresponds to the findings of Cruickshank et al and of the HAPPHY study. However, a similar analysis of our controls; who were not on any antihypertensive therapy, also reveals a J-shaped curve, the lowest incidence of heart attack and of all deaths being 10 mm Hg higher. Since the mean fall in diastolic pressure on treatment was 11 mm Hg the corresponding group of patients in the treatment group would be shifted one column to the left. It follows that treatment is unlikely to have affected the incidence of cardiac infarction or mortality, irrespective of the fall of diastolic blood pressure, and that it is not the cause of the J-shaped curve. The Waterhouse,

Bollington, near

1.

Macclesfield SK10 5JL

JOHN COOPE THOMAS S. WARRENDER

Coope J, Warrender TS. Randomised trial of treatment of hypertension in elderly patients in primary care. Br Med J 1986; 293: 1145-51.

ANDREW HUNTER

Paediatrics Service, and Central Laboratory, Hospital Zonal 9 de Julio, Araoz 2379, Argentina

J. H. HAUGER KLEVENE C. GAGO E. A. NUÑEZ M. HAYES

1. Clarke

WR, Schrott HG, Leaverton PE, et al. Tracking of blood lipids and blood pressure in school age children: the Muscatine study. Circulation 1978; 58: 626-34 2. Orchard TJ, Donahue RP, Kuller LH, et al. Cholesterol screening in childhood Does it predict adult hypercholesterolemia? The Beaver County experience. J Pediatrics 3.

1983; 103: 687-91. Hauger Klevene JH, Balossi EC. Coronary heart disease mortality and coronary nsk factors in Argentina Cardiology 1987; 74: 133-40.

MECHANISM OF MEMBRANE DAMAGE MEDIATED BY EOSINOPHIL MAJOR BASIC PROTEIN

SIR,-Dr Tai and colleagues (March 21, p 643) suggest that eosinophil granule proteins are involved in cardiac injury in patients with eosinophilic endomyocardial disease. The basic granule proteins were mainly deposited within the areas of acute tissue