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to their organisation being run by paid helpers, enablingthe extra work involved with correspondence, &c., dueto the colostomy members, to be dealt with. Whilst ourAssociation consists entirely of voluntary helpers, andremains so, much help for the colostomies and ileal-bladders remains out of the question; but we shoulddo well to remember that ten years ago the possibilitiesof success for an ileostomy group seemed just as remote.

The Drove, Kempshott, L. F. KINGSTON

Basingstoke, Hants. Editor, I.A. Newsletter.L. F. KINGSTON

Editor, I.A. Newsletter.

LEAD POISONING IN MENTALLY

SUBNORMAL CHILDREN

GRACE E. WOODSRUTH M. WALTERS.

Hortham Hospital,Almondsbury,near Bristol.

SIR,-An article by Sir Alan Moncrieff and hiscoworkers on lead poisoning in children 1 prompted us toinvestigate the levels of blood-lead in selected children atthis hospital. They found that the

" levels were frequentlyhigher in an unselected series of mentally retarded

children, and those with behaviour disorders than inothers ". Out of 100 child patients here, we selected 20children who, the staff said, "

put everything in theirmouths "; 10 children in whom there was a history ofearly normal development followed by mental deteriora-tion and often epilepsy; and 5 children with cerebralpalsy who had never been able to put anything into theirmouths and had been in the hospital for some years. Theaverage level of blood-lead in these 5 children was 13 &mgr;g.(range 21-5 &mgr;g.) per 100 ml. Of the others, 12 had a levelabove 40 &mgr;g. considered high by Great Ormond Streetstandards. Among these were 3 children in whom therewas a strong suspicion that lead poisoning may have beenthe primary cause of the mental deficiency.A boy, now aged eighteen years, was said to have developed

normally until about the age of eighteen months. He had hadwords of speech, had walked, and has begun to feed himselfand to use a pot. He then deteriorated fairly rapidly. For atime he refused to walk; speech eventually ceased, and he hadnot spoken since the age of five years. He had had two pro-longed periods at specialised units for psychotic children beforehis parents reluctantly agreed to admission to a hospital for thesubnormal. There were no abnormal physical signs: he lookeda normal boy. In February, 1964, he began to have epilepticfits, which were confirmed by electroencephalography (E.E.G.).A routine blood-lead examination in April, 1964, gave a level of68 &mgr;g. per 100 ml.; after treatment with penicillamine, thisdropped to 39 p.g. On further questioning of the parents themother stated that the father was a chemist and had been soconcerned about the child’s tendency to chew the cot as a babythat the cot was repainted with two coats of lead-free paint.The parents have recently chipped paint off this old cot (allcoats) and have sent the scrapings for analysis. The resultsshow 6-76% lead as metal, suggesting that merely painting thecot was insufficient, and that to get rid of lead entirely the oldpaint should have been removed. The mother is unable to saywhether the boy began to chew paint after she suspected he wasabnormal or before.The second patient, a girl now aged twelve years, is the

only abnormal child among 8 siblings in a working-class family.The birth was normal, and there was no concern until shebegan to have salaam attacks while sitting in her pram. Shechewed objects as a baby-i.e., pram, cot, &c. She is now a

normal-looking little girl with no abnormal physical signs, butsevere epilepsy and a very abnormal E.E.G. All biochemical

investigations were negative, except her blood-lead which was60 ug. per 100 ml. in March, 1964, and, after a month’s treat-ment with penicillamine, 16 fLg. The mother cannot rememberwhether the fits started before or after the excessive chewing.Her behaviour and epilepsy have improved since treatmentwith penicillamine.1. Moncrieff, A. A., Koumides, O. P., Clayton, B. E., Patrick, A. D.,

Renwick, A. G. C., Roberts, G. E. Arch. Dis. Childh. 1964, 39, 203.

A boy, now aged nine years, had a normal birth and earlydevelopment. From the time he could handle toys he put themin his mouth and his mother remembers that he chewed paintedbricks. He began to walk at eighteen months and was oftenfound chewing painted window-ledges. By two years of agehe had some words of speech and was learning more words-e.g., names of articles of dress. After an attack of influenza attwo and a half years he began to deteriorate. He lost his speechand chewed more, and fits began at three years. He was firstdiagnosed as a psychotic mentally defective child. Leadencephalopathy was suspected at four years, and at this timehis haemoglobin was 77% with no punctate basophilia. The

X-ray report of knees and hands was: " the dense line of boneshown in metaphysis is wide but still within normal limits.This would be consistent with a diagnosis of plumbism madeon clinical and haematological grounds ". The E.E.G. was

abnormal. Subsequent urinary-lead estimation revealed noexcretion of lead in one twenty-four hour sample. He wasadmitted to this hospital for the mentally subnormal at the ageof six and a half years. He is a well-grown boy, with no abnormalphysical signs, apart from epilepsy. He is hyperactive, andpicks up and chews anything. He has no speech and limitedrecognition of people. His blood-lead in March, 1964, wasfound to be 137 jjLg. per 100 ml. Within a month of treatmentwith penicillamine this had fallen to 37 Vg. His pica wasuncontrollable, and the blood-lead rose to 80 &mgr;g. by June.A search of his environment revealed that he was eating puttycontaining red lead around a w.c., and when this source oflead was removed his blood-lead level began to decline again.Subsequently his behaviour was noted to be quieter than usual.These findings might suggest a higher incidence of lead

poisoning as a cause of mental deficiency among ourhospital child-population than the 1 per 100 ml. per 1000that Berg and Zapella found.2 Might not further cases bediscovered if a blood-lead estimation was routinely per-formed in the investigation of any child who exhibitsunexplained epilepsy, mental deterioration, or psychoticbehaviour (whether or not pica is recorded) ? The easewith which children can absorb lead from building andhousehold materials must need further consideration.

SKIN PIGMENTATION FOLLOWING

CHLORPROMAZINE TREATMENT

SiR,ńThe finding described in your annotation 3-skinpigmentation in patients who received up to 1.5 g. chlor-promazine daily-was predicted by us in 1961.4 We

reported then the melanophore-dispersing activity of

reserpine and continued as follows:" This is in conformity with our hypothesis for the mechanism

of the endocrine effects obtained with phenothiazine deriva-tives.5 Following suppression of the hypothalamus, a secondaryimpairment of pituitary and peripheral glands occurs. Withregard to part of the pituitary tropins (FSH, LH, TSH, ACTH) thissuppression becomes balanced according to the push and pullprinciple, which applies readily to the tropins producingsecondary peripheral hormones (’balanced tropins ’). Withregard to those pituitary hormones which are not held inabeyance by the feed-back mechanism of their secondaryperipheral hormones (LTH, ADH and MSH), an overshoot is to beexpected. This would classify LTH, ADH and MSH as

’ unbalanced tropins ’."

Thus, the mechanism of the chlorpromazine pigmentationseems clear. Still, there remains the need to study whetherthese patients really have high melanophore-stimulating-hormone levels in their blood. This can be easily deter-2. Berg, J. M., Zapella, M. J. ment. Defic. Res. 1964, 8, 44.3. Annotation, Lancet, 1964, i, 1206.4. Khazan, N., Sulman, F. G. Proc. Soc. exp. Biol., N. Y. 1961, 107, 282.5. Sulman, F. G. Arch. int. pharmacodyn. 1959, 118, 298.

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mined with our technique. 6 Alternatively, study of thepigmentation under ultraviolet light should revealwhether photosensitivity is also involved. The latter

possibility is quite possible.

F. G. SULMAN.

Department ofApplied Pharmacology,School of Pharmacy,Hebrew University,Jerusalem, Israel.

TOXIC EFFECTS OF MONOAMINE-OXIDASEINHIBITORS

E. R. TALLETT.Burnley General Hospital,Burnley, Lancs.

SIR,-Dr. Blackwell (July 18) suggests that patients onmonoamine-oxidase inhibitors should be provided witha card so as to lessen the hazards of polypharmacy andpoor communications between doctors. Such a card is

already in use in this group, and is routinely given tooutpatients and inpatients who are leaving the hospitalwith supplies of these drugs.The card is similar in size and layout to the card issued by

the Ministry of Health for patients on corticosteroids andexactly fits the film sleeve provided to protect these cards. Thecard in use in this group bears the words " I am a patient onM.A.O. Inhibitor Treatment " in bold type on the front, andprovides space for details of names and addresses of patient,general practitioner, hospital, and consultant, together withdetails of the treatment. The back of the card bears instructionsto the patient regarding the need to avoid cheese and tomention these drugs to any doctor from whom treatment isreceived.Abbott Laboratories, which market Eutonyl’ in this

country, also issue a card with similar information and

warnings on it.Could I plead for the invariable mention of all brand

names when the approved names of drugs are quoted?Tranylcypromine is followed by Parnate ’ in Dr. Black-well’s letter, but not by’ Parstelin’, in which it also occurs.

LONG-ACTING SULPHONAMIDES ASSOCIATEDWITH STEVENS-JOHNSON SYNDROME

JOHN BEVERIDGEMICHAEL HARRISGRAHAME WISELESLIE STEVENS.

Department of Pædiatrics,Prince Henry Hospital andPrince of Wales Hospital,

Randwick, New South Wales.

SIR,-May we draw your attention to 9 cases of childrenwith Stevens-Johnson syndrome admitted to our unit soonafter the administration of long-acting sulphonamides ?Of these children 3 have died and 1 has been gravelydisabled. A further child under the care of a generalpractitioner has also died.

3 patients were admitted in February, 1962, all ofwhom had received sulphamethoxypyridazine, and ofthese 1 died; 1 survived with transverse myelitis of thespinal cord. A 4th patient was admitted in July, 1962,after receiving sulphamethoxypyridazine and also died.A 5th patient admitted this month will probably survive.

3 patients admitted in October, 1963, June, 1964, andJuly, 1964, had sulphamethoxydiazine shortly beforedeveloping Stevens-Johnson syndrome. Of these, 1

patient died, and the other 2 have survived.A fatality in a patient with the Stevens-Johnson

syndrome who had received sulphadimethoxine has beenreported. 7

It seems to members of this unit that there may begrave risks associated with the administration of long-acting sulphonamides to children.

6. Sulman, F. G. Lancet, 1952, i, 1161.7. Jarkowski, T. L., Martmer, E. E. Amer. J. Dis. Child. 1962, 104, 669.

HEALTH VISITING AND GENERAL PRACTICE

PATRICK A. LAWRENCEK. JULIE HAYES.

J. BUTTERWORTHV. P. MCDONAGH.

SIR,-May we endorse from our eight years’ enjoyable(and unfinished) health-visitor attachment the commentsof Dr. Fry and his colleagues (Sept. 5).We feel there is only one sound way of working in

family practice in the dawn of the Hospital Plan, and thisis to aggregate small numbers of doctors with a combinedlist of say 10,000 with the appropriate number of healthvisitors, midwives, district nurses, and physiotherapistsand an adequate administrative staff, so that families areserved medically and socially by an integrated team.These Leeds theories make no sense to our partnership

of four. The instigator of the experiment in 1956, ourM.O.H., Dr. J. F. Warin, is so convinced of the benefitsthat all his health visitors are now attached to practices.

PATRICK A. LAWRENCE

Oxford. K. JULIE HAYES.

SIR,-The investigation described by Miss Akester andDr. MacPhail (Aug. 22) seems to be based on the outworntheory of routine door-to-door visiting by the healthvisitor. It apparently assumes that the health visitor’smethod of working cannot and must not change and thengoes on to search for evidence to prove this thesis. Surelywe must deploy our limited forces in accordance with therequirements of today.

In the light of our experience of a liaison scheme in a smallborough, we should like to comment on the " statistical evi-dence " put forward in this article, much of which we feel to beirrelevant. Firstly, in practice we have found that the difficultyof several doctors to one family is invariably solved by theapplication of a little common sense and basic case-workprinciple.

Table ill is of interest to us since we believe that it does infact emphasise the need for the attachment of health visitors togeneral practitioners. It is obvious that the majority of thesecases would be of interest to the modern general practitioner;nor do we agree with direct referral to either chest physician orpaediatrician without reference to the family doctor,’who has afundamental responsibility in these cases. Naturally we en-visage that the larger cities will present difficulties that we havenot encountered.

J. BUTTERWORTHKeighley. V. P. MCDONAGH.

PLASMA FIBRINOLYTIC ACTIVITY ANDMENSTRUAL CYCLE IN WOMEN

SIR,-Smith and Smith and Willson and Munnell 2

reported that the fibrinolytic activity in the circulatingblood of women was higher during menstruation than inthe intermenstrual period. Since then, knowledge regard-ing the fibrinolytic enzyme system has advanced consider-ably, and methods of estimating fibrinolytic activity havebeen improved. Yet there have been no studies in recentyears on fibrinolytic activity in relation to menstrual cycle.

In the course of our studies of possible factors underlyingspecies and sex differences in susceptibility to atherosclerosis,the fibrinolytic activity in the circulating blood of fourteenhealthy young women, whose ages ranged between 22 and 33years, was studied at two points in the menstrual cycle-close tothe 14th and the 28th day of their cycles. In some the samplesof blood were actually collected during the menstrual period.Fibrinolytic activity was estimated as euglobulin lysis-timeaccording to the method of Von Kaulla and Schultz.3The results showed that the differences in activity during the

intermenstruum and the premenstruum were not statisticallysignificant. Similarly, the circulating fibrinolytic activity during1. Smith, O. W., Smith, G. V. S. Science, 1945, 102, 253.2. Willson, J. R., Munnell, E. R. Proc. Soc. exp. Biol., N.Y. 1946, 62, 277.3. Von Kaulla, K. N., Schultz, R. L. Amer. J. clin. Path. 1958, 29, 104.