1298

wanted to see these data published.In December, 1979, while in Mounana (Gabon), I prepared blood

smears from five patients infected with Plasmodium falciparum,who were 14-28 months old, had primary attacks of malaria, andhad not been treated when the blood films were made.One patient’s peripheral blood smear indicated a 37%

parasitaemia and displayed engulfment or digestion of parasitisedred blood cells by numerous monocytes (see photographs). Bloodsmears from two other patients (0 - 04-13% parasitaemia) showedonly rare phagocytosis of parasitised erythrocytes by peripheralmonocytes. Smears from the two remaining patients (2 - 5-2’ 9%parasitaemia) were negative for monocyte phagocytosis. I have

recently reproduced this phenomenon in vitro, using peripheralblood monocytes from P. falciparum infected chimpanzees.These data indicate that human and primate peripheral

monocytes may participate in host defence mechanisms against P.falciparum infection.

I would like to thank Dr Andraut and his coworker for their help during mystay in Mounana, Dr Languillat and his colleagues for assistance during mystay at the C.I.R.M.F., and Lieutenant M. Pappas for helping me in thepreparation of this communication.

Department of Immunology,Walter Reed Army Institute of Research,Walter Reed Army Medical Center,Washington, D.C.,20012, U.S.A. ALAIN VERNES*

*Present address. INSERM Unit 42, Domaine du C.E.R.T.I.A., 369, rue J. Guesde Flers,59650-Villeneuve d’Ascq, France.

MASTECTOMY WITH PRIMARY RECONSTRUCTION

SIR,-We were interested in Mr Timmons’ comments (Nov. 22,p. 1131) on our Nov. 1 letter. May we first of all assure him aboutstaging. This was done by F. C., independently of G. T. W. Thecomparison is thus not prejudiced by G. T. W.’s ignorance forwhich he apologises. Furthermore, the results from other centreswhich were cited have been adjusted to make them comparable toours-we have not simply transcribed their figures.G. T. W. also regrets that his earlier writing did not make clear

what was meant by "selection". This was the elimination ofadvanc-ed cases (stages III and IV), but they are not relevant here. We do ad-mit to selection in that where the procedure would threaten the pa-tient’s future because of other considerations, such as car-

diovascular disease, we have not contemplated reconstruction; wewould, however, assume that those carrying out the procedures inthe other series cited would do the same. Otherwise the reason forexclusion has been the patient’s own wish. Although superstitionrelates cancer to unhappiness, we have no knowledge of any scien-tific support for an influence of psyche on tumour growth. Nor dowe know of any way in which one can select patients in stages I andII who will do well or badly in their future. If Timmons knows howto do so we (and, probably, most other surgeons) would like to knowhis secret. In delayed reconstruction the situation is very differentsince time selects those who have more rapid disease. In these casescomparison is of very limited value. We shall shortly present ourresults with this procedure but it may be of interest to record herethat, of the 88 patients on whom a delayed reconstruction was car-ried out in the same decade, only 2 have died and 4 showed recur-rence.

Timmons disapproves of our not doing routine node biopsies,since he believes that all cases where this is positive should haveroutine radiotherapy. Random biopsy is unreliable. Even totalclearance of the axilla and the internal mammary nodes can be

misleading. Perhaps Timmons believes this should always be doneand a super-radical mastectomy carried out. If he practises such aclearance where does he irradiate and why?Nipple recurrence was an initial but unfounded fear. We have

been preserving the nipple for nearly two decades. Has Timmonsdone this, and, if so, in how many cases and was histological studydone at the time of operation?We do not feel we can easily comment on the suggestion that

results can be poor or good. We can only report our own experience.In any new procedure some surgeons will obtain good results andothers bad until all have learned which technique gives the best

results. This is not an argument against the method, only againstsome ways of carrying it out. The cosmetic results vary with manyfactors, especially in secondary reconstruction where the surgeonperforming the initial ablation may not have been considering thepossibility of future reconstruction. Nevertheless, it is often possi-ble to give great comfort to patients by using the more modernplastic surgery techniques. In primary reconstruction the patient’sfigure can often be better than before the operation if one is

prepared to treat defects in the other breast such as ptosis, and poordevelopment.We realise that our series is small and would have preferred a

larger one. We are hoping that others will be encouraged to producefurther data. It is, however, as far as we know, the only publishedreport of primary reconstruction performed over a decade that hasbeen presented so far. Also it records cases operated upon by onesurgeon in the same operating theatre, and from the same ward. Wehope that this may balance the problems encountered when produc-ing a larger series with several surgeons, sometimes in differenthospitals with varying techniques. Large series have been inevidence since the 1930s when Keynes had the audacity to challengeradical mastectomy as the only treatment for breast cancer.

Although Timmons has been able to select a clearcut line of treat-ment, most of us are still uncertain-hence the continuing series,large and small. Most surgeons however, appear to be veeringtowards less and less radical procedures regardless of these series.Timmons does not say precisely where he stands or why. We arequite prepared to discover that we may be wrong but hope that atleast we have shown that primary reconstruction now merits con-sideration as a suitable treatment for this disease.

General Hospital,Birmingham B4 6NH

Regional Cancer Registry,Queen Elizabeth Hospital,Birmingham

G. T. WATTSF. CARUSO

J. A. H. WATERHOUSE

FATAL HEPATIC FAILURE AND SODIUMVALPROATE

SiR.—Dr Ware and Dr Millward-Sadler (Nov. 22, p, 1110) reportfive cases of acute liver disease after treatment with sodium

valproate. In his review of this drug Brownel mentioned fourteendeaths due to liver failure in patients taking valproate. ByNovember, 1980, the number of fatal cases of hepatic failure inpatients on sodium valproate which had been reported to themanfacturers had reached twenty-one; only ten, including Ware andMillward-Sadler’s case, have been published.2-7We recently saw a 17-year-old girl who presented in acute hepatic

failure probably related to sodium valproate. At 3 years of age, thispreviously normal girl had started to have absence seizures (petitmal) and was treated with ethosuximide and trimethadione. As theabsence seizures increased these two drugs were stopped, and onOct. 28, 1979, sodium valproate (20 mg/kg daily) was startedassociated with phenobarbitone (100 mg daily). Seizure activitydramatically decreased until the end of 1979, when absence seizuresbecame more frequent (about 10 per day), and, 1 week beforeadmission, the girl complained of weakness and vomiting. Therewas no history of viral hepatitis or toxic exposure.On admission (Feb. 16, 1980) she was conscious and subicteric.

There was no portal hypertension, ascites, or hepatic and splenicenlargement. Laboratory studies revealed: aspartate aminotrans-

1. Browne TR. Valproic acid. N Engl J Med 1980; 302:661-66.2. Donat JF, Bocchini JA, Gonzalez E, et al. Valproic acid and fatal hepatitis. Neurology

1979; 29: 273-74.3. Gerber N, Dickinson RG, Harland RC, et al. Reye-like syndrome association with

valproic acid therapy J Pediatr 1979; 95 142-44.4. Suchy FJ, Balistreri WF, Buchino JJ, et al. Acute hepatic failure associated with the use

of sodium valproate: Report of two fatal cases N Engl J Med 1979; 300: 962-66.5. Jacobi G, Thorbeck R, Ritz A, et al. Fatal hepatotoxicity in child on phenobarbitone

and sodium valproate. Lancet 1980; i. 712-13.6. Young RSK, Bergman I, Gang DI, Richardson EP. Fatal Reye-like syndromes

associated with valproic acid. Ann Neurol 1980; 7: 389.7. Addison GM, Gordon NS. Sodium valproate and acute hepatic failure. Devel Med Child

Neurol 1980; 22: 248-49.