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acute phase, while with oc-globulins it decreased considerably.0,-globulin, on the other hand, increased notably duringhealing (see accompanying figure).

It was interesting to compare these results with thoseof the flocculation methods, modified in our departmentfor investigation of the serum-proteins of rabbits. Theincrease in the a-globulin and pg-globulin fractionsmanifested itself by an increase in the acid-precipitableglobulin (A.P.G.) test (modified after Greenspan). Thedecrease of y-globulin in the acute phase was evidentnot only on electrophoresis, but even in our modificationof the cadmium-sulphate test (Pospisil, personal com-munication). On the other hand, flocculation of totallipoids in the original modification of the thymol test,carried out in pH 4-2,2 showed lowered values when

oc-globulin and (32-globulin increased, thus raising thequestion of the importance of lipoids for the changes inthese fractions in rabbits.

Department of Experimental Pathology,Masaryk University, Brno,

Czechoslovakia. D. WIEDERMANN.

THE "L.E.-CELL" PHENOMENON IN ACTIVECHRONIC VIRAL HEPATITIS

SIR,-The report by Dr. Joske and Dr. King (Sept. 3)prompts me to mention a similar case in which L.E. cellswere found in association with liver disease and in theabsence of lupus erythematosus.A man, aged 50, was first seen in July, 1953, with a purpuric

eruption on the legs. There were also transient tender noduleson the legs which may have been due to an existing footringworm. He had a recent history of loss of appetite, dislikeof fatty foods, and pale stools. He had never been jaundiced,had never received a blood-transfusion, and had never beenexposed to occupational poisons.On admission to hospital the relevant abnormalities were

facial telangiectases, liver enlargement (4 finger-breadths),spleen just palpable, no jaundice.Plasma-albumin was 3-3 g. per 100 ml., plasma-globulin

5’0 g. per 100 ml., serum-bilirubin 0-8 mg. per 100 ml., alkalinephosphatase 18 units, thymol turbidity 16 units, colloidal gold5 units, cephalin-cholesterol 4 units.

L.E. cells were found in large numbers in the blood. In viewof this, particular care was taken to search for clinical signsof lupus erythematosus, but there were none ; the whiteblood-cell count ranged from 14,700 to 4500 per c.mm. ; the

erythrocyte-sedimentation rate was normal ; the bloodWassermann reaction was negative.The patient was discharged from hospital and readmitted

a month later under the care of Prof. Alan Kekwick with

increasing jaundice and intermittent abdominal pain andvomiting of a week’s duration. At this time there was alsoconsiderable ascites. The white blood-cell count was 15,000per c.mm. and again L.E. cells were found in the blood. Hiscondition rapidly deteriorated and he died within two daysof admission.Post-mortem examination confirmed the diagnosis of multi-

lobular cirrhosis with terminal acute necrosis of the liver.Particular attention was directed to the possibility of systemiclupus erythematosus, but no evidence of this was found. Thebone-marrow contained a diffuse infiltration with plasma-cellscompatible with a diffuse type of myelomatosis.We concluded from this case that, although the finding

of L.E. cells in the blood usually indicates disseminatedlupus erythematosus, a positive finding is not pathogno-monic. Since it is known that the serum L.E. factor islinked with y-globulin, it seems possible that, as Joskeand King suggest, in our patient the reaction was relatedto the high globulin levels. The unexpected post-mortemfinding of myelomatosis in our case may also have beenpartly responsible for the production of the L.E.

phenomenon.It is important that the finding of L.E. cells in a particu-

lar case should not be taken to indicate that the diagnosticproblem is completely solved.Middlesex Hospital,

London, W.1. F. RAY BETTLEY.

2. Pospíšil, M. Vnitřní lékarství, 1955, 1, 30.

REGISTRARS

SiR,-Last week’s letters on the registrar problem seemto overlook an important factor concerning the entryinto general practice. This factor is age. There are atpresent many N.H.S. practices which support senior

partners of 70 plus, and in some cases 80. Surely it wouldbe reasonable for the Ministry to set a retiring age of 70,There would then be many more vacancies in generalpractice.

EX-REGISTRAR GENERAL PRACTITIONER.

CHLORPROMAZINE : A SEROTONINANTAGONIST ?

SiR,-Some years ago I pointed out that severalanti-histamines inhibited the amines tyramine, trypta-mine, and phenylethylamine.1 On the basis of these

findings I suggested that more potent 5-hydroxy-tryptamine (serotonin) antagonists could be found amongdiamines of R2 : N.(CH2)3.N : R2 structure. When chlor-promazine became available therefore we investigated itsanti-serotonin action. -

A new interest was added to this question whenGaddum 2 discovered that lysergic acid diethylamidewas the most active anti-serotonin agent hitherto known.The possible role of serotonin and its importance inmental disturbances have also been discussed.1 4 Itseemed rational to investigate the anti-serotonin actionof chlorpromazine, although its effect in psychiatric casesis not the same as that of L.S.D.

In spinal cats we found that the vasopressor effect of20-40 g. per kg. serotonin (expressed as serotonin creati-nine sulphate) was nearly completely blocked by 1.0 mg.per kg. chlorpromazine. On isolated rat uteri the effectof serotonin (0.05-1,0 ;j<.g. per ml. of bath) was completelyinhibited by the same concentration of chlorpromazine.

These preliminary results suggest that chlorpromazineis one of the most potent anti-serotonin drugs. Its effectin both experiments was long-lasting.

Further investigations will be necessary to prove thehypothesis that the mental effects of some drugs arerelated to their anti-serotonin effect. The striking anti-serotonin effect of chlorpromazine, on the other hand,may explain why this drug so effectively counteractsvarious shock symptoms in which serotonin might beinvolved, 5

Department of Pharmacology,Research Institute of thePharmaceutical Industry,

Budapest, Hungary. L. GYERMEK.

GASTRIC SECRETION IN SIMMONDS’S DISEASE

SiR,-In a review of 595 cases of Simmonds’s disease,Escamilla and Lisser 6 found that gastric acidity waslow or absent in 85% of those patients in whom thediagnosis had been confirmed by pathological examina.tion. More than half of these patients had gastro-intestinal symptoms. The following case is of interestbecause the secretion of acid and the gastric mucosaappear to have been restored to normal during hormonetreatment for hypopituitarism.A housewife, aged 51, was admitted in March, 1953, for

investigation following attacks of vomiting over a periodof four months. She had had a severe postpartum haemor-rhage 22 years previously, which was followed by amenor-rhaea and loss of pubic and axillary hair. She was thin andappeared disinterested in her condition. The blood-pressurewas 120/55 mm. Hg, pulse 100 per min., Hb 12-3 g. per 100ml..and 17-ketosteroid excretion nil. Gruel and histamine(0-5 mg.) test-meals showed absence of free gastric acid.

1. Gyermek, L. Acta physiol. Acad. Sci. Hung. 1953, 4, 323.2. Gaddum, J. H. J. Physiol. 1953, 121, 15.3. Gaddum, J. H. Ciba Foundation Symposium on Hypertension.

London, 1954.4. Page, I. H. Physiol. Rev. 1954, 34, 563.5. Page, I. H. Amer. Heart J. 1948, 38, 1.6. Escamilla, R. F., Lisser, H. J. clin. Endocrin. 1942, 2, 65.