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HYPERTENSION AND HYPERURICÆMIA

CALUM N. MCFARLANE.

SIR,-I find myself in slight disagreement with some ofDr. Breckenridge’s findings and conclusions (Jan. 1), althoughmost of them accord with those which I reported in 1963 1 onserum-uric-acid levels in pregnancy, particularly when thiswas complicated by hypertension.

Dr. Breckenridge believes that hyperuricsemia in hyper-tensives does not necessarily prevail in the severe hypertensive,and in this respect he disagrees with some other workers. Myfindings in the pregnant patient (which I agree are not strictlycomparable) showed that those with " essential " hypertension(88) had normal levels of serum-uric-acid, even fractionallylower than in non-hypertensive patients (65 random controls)-mean 3-64 mg. as against 3.80 mg. per 100 ml. In pre-eclamptic toxaemia hypertensives (244) the level is significantlyraised-so much so that I concluded that the raised serum-uric-acid level could be taken to differentiate the pre-eclamptictoxaemia case from the " essential " hypertension case.

In pregnancy one is dealing with a selected group of youngwomen in whom " essential " hypertension has usually existedfor no more than a few years. The serum-uric-acid level tendsto rise in the elderly, even in non-hypertensives. I believe the

hyperuriceemia indicates tubular damage in the kidney, andthat the excessive reabsorption which raises the serum level isthe direct result of vascular disease at the site-temporary inpre-eclamptic hypertensives, but permanent in other hyper-tensives. I maintain that it is less misleading to base theseverity of hypertension on its effects on the patient-e.g.,raised uric-acid level due to kidney damage-than on a

I sphygmomanometer reading. Consequently, the raised serum-uric-acid level should suggest severe disease, and in the majoritythis will occur in the older longstanding hypertensives. Araised serum-uric-acid level is certainly not a feature in theyounger pregnant hypertensive woman, unless she has pre-eclamntic toxaemia.

MEDICAL RECORDS

J. H. MITCHELL.

Nuffield Provincial Hospitals Trust,Medical Records Research Group,

Western Infirmary,Glasgow, W.1.

SIR,-This Group is investigating all aspects of the composi-tion and handling of case-records in both hospital wards andoutpatient clinics; and also considering possible means ofcoping with the increasing strain on storage facilities for theserecords. Recent correspondence regarding the TunbridgeReport on the standardisation of case-sheets indicates thatthere is a widespread interest in the whole subject, and thatwidely differing opinions on it are held. I should, therefore, beglad to receive any such views, and should also welcomeinformation concerning the present position in other centres.

TREATMENT OF ZOLLINGER-ELLISON

SYNDROME

SIR,-Dr. Bank and Dr. Marks (Jan. 1) make the followingmisrepresentations of my paper. At no point did I state orimply that my patient was a case of the Zollinger-Ellisonsyndrome, nor did I infer that this syndrome can be expectedto respond to ganglion-blocking or anticholinergic drugs. I am

very well aware that " significant acid hypersecretion " is farfrom being synonymous with the Zollinger-Ellison syndrome.

Nonetheless, such hypersecretion rightly raises a strongsuspicion that an islet-cell tumour may be present, and I believethat anticholinergic drugs should always be tried in thesepatients. The response may be very gratifying, as in the patientdescribed by Dr. Bank and Dr. Marks in their letter. Toooften this interesting group of hypersecretors is deprived of

1. McFarlane, C. N. J. Obstet. Gynœc. Br. Commonw. 1963, 70, 63.2. Dean, A. C. B. Lancet, 1965, ii, 769.

the benefit of anticholinergic drugs because of the erroneousimpression that the Zollinger-Ellison syndrome never respondsto this treatment, and despite the evidence that an islet-celltumour will not be discovered in more than a small proportionof them.

A. C. B. DEAN.Department of Surgical Service,

University of Edinburgh.

FORTIFICATION SPECTRA

ELSPETH STANFORD.

SiR,—I wonder if any doctor, unfortunate enough to haveseen fortification spectra, could furnish me with facts aboutthis odd symptom which I have often had. I think these

spectra are only seen: (1) in a bright light, and on looking up;(2) early on in an attack, which they often herald; (3) and onlyby a person with long sight whose focal point lies behind the retina.

I believe that fortification spectra may be caused by a suddenreflection of the rods and cones of the retina, for the symptomis accompanied by oedema of the eye-I know of a lady whoseattacks are heralded by the watering of an eye. The excessfluid, together with a sudden dramatic rise in blood-pressure,causes tension in the eye, and a reflection of the retina wouldbe possible in a bright light under these conditions. Dr.C. W. M. Whitty (Oxford) has told me that Gowers, eightyyears ago, thought fortification spectra were connected withthe rods and cones of the retina.Once you have seen the spectra you cannot easily forget

them, for they are such a neat, bright vision-I am temptedto think it is what Paul saw on the Damascus Road, and thatmigraine was his " thorn in the flesh ".

ARTERIAL DISEASE: AN INTERNATIONAL SEARCH

SIR,-In your annotation (Jan. 15) you suggest that fluoro-scopy of the coronary arteries should be applied in populationsurveys to estimate the extent of arterial disease among the

living. This method has various technical difficulties. Oliveret al.1 pointed out that necropsy findings and postmortemradiology clearly indicate that the prevalence of calcificationdetected by fluoroscopy during life is probably underestimated.Jorgens et awl.2 found calcification of coronary arteries in 83% ofthose who came to necropsy, whereas cinefluorographyrevealed calcification in only 25% of live hospital patients. Theyascribe this wide variation to the limitations of the cinefluoro-

graphic method. Whatever the merits of this method for thedetection of more advanced calcified lesions in the coronaryarteries, I do not think that it has a place in population surveysof the extent of arterial disease among the living.You do not mention radiography of the abdominal aorta-a

method which I have used in thousands of patients to detectatherosclerosis during life. A calcified plaque about 1 cm. indiameter can usually be seen in the lateral projection on radio-graphs of this large artery. The detection of atherosclerosis inthe abdominal aorta usually indicates more widespread athero-sclerosis, not only in the branches of the abdominal aorta butalso in the coronary and other large arteries. This methodrevealed a sex difference in the incidence and severity of calcifiedlesions in the abdominal aorta,3 and an association of athero-sclerosis in the central blood-supply of the stomach with gastriculcer in the aged.4 5 This method has also been used as avaluable aid in the radiological differential diagnosis betweenbenign and malignant lesions of the stomach.6 In the 30-49-year age-group, a distinct relation has been reported betweenthe incidence and severity of calcifications in the abdominalaorta and occlusive or complicated lesions of the coronaryarteries. 7

1. Oliver, M. F., Samuel, E., Morley, P., Young, G. B., Kapur, P. L.Lancet, 1964, i, 891.

2. Jorgens, J., Boardman, W. J., Damberg, S. W., Kinney, W. N., Kundel,R. R. Am. J. Roentg. 1965, 95, 667.

3. Elkeles, A. Lancet, 1957, ii, 714.4. Elkeles, A. Am. J. Roentg. 1950, 70, 797.5. Elkeles, A. ibid. 1964, 91, 744.6. Elkeles, A. Br. J. Radiol. 1949, 12, 280.7. Eggen, D. A., Strong, J. P., McGill, H. C. Archs Path. 1964, 78, 575.