97

plastic changes suggest that some normal stimulus,probably hormonal, is reaching the gland in excessivequantity owing to impaired inactivation in the liver. Thisis the current explanation of the gynaecomastia in theclosely similar circumstances of malnutrition and hepaticcirrhosis. There is strong evidence that such breast

enlargement is produced by the excess of oestrogensresulting from reduced intrahepatic inactivation that hasbeen demonstrated both in cirrhosis and in malnutrition.5 5

No hormone can at present be blamed for parotid enlarge-ment with such confidence as can the oestrogens for gynxco-mastia. But the parotid enlargement in some patients withdiabetes mellitus 6 provides some support for the viewthat disturbed hormonal activity is fundamentallyresponsible.

5. Biskind, M. S., Biskind, G. R., Biskind, L. H. Surg. Gynec. Obstet.1944, 78, 49.

6. John, H. J. J. Amer. med. Ass. 1933, 101, 184.7. Beattie, C. P. Trans. R. Soc. trop. Med. Hyg. 1957, 51, 96; see Lancet,

1959, i, 869.8. Paterson, M. W. Scot. med. J. 1960, 5, 467.9. Callahan, W. P., Russell, W. O., Smith, M. G. Medicine, Baltimore,

1946, 28, 343.10. Hall, E. G., Hay, J. D., Moss, P. D., Ryan, M. M. P. Arch. Dis. Child

28, 117.11. Lelong, M., Alison, F., Desmonts, G., Fontaine, M., Michelin, J. Arch.

franç. Pédiat. 1959, 15, 1.12. Morris, D., Levin, B., France, N. E. Lancet, 1955, ii, 1172.

TOXOPLASMOSIS

TOXOPLASMA infection is believed to be very common;serological surveys indicate that by adult life a quarter to ahalf of the population of this country have been infected.’By contrast, illness due to toxoplasma appears to be rare;but there may be more of it than we think, and thereforereports of its varied manifestations are of value. Such a

report has come from Glasgow. s It describes 11 con-

genital cases and 1 acquired case.As in other series choroidoretinitis was the commonest

sign in the congenital cases, being present in 8. Micro-

phthalmos and intracranial calcification were found in 6;microcephaly and mental deficiency in 4; and hydro-cephalus, hepatosplenomegaly, and neonatal purpura eachin 3. Neonatal purpura is not as well known as the other

manifestations, but it has been previously reported.9-12In 1 of the Glasgow cases it was ascribed retrospectivelyto toxoplasmosis after an accident, at the age of 11 months,which led to radiological examination and the demonstra-tion of intracranial calcification. A dye test for toxo-

plasmosis showed antibodies present to the high titre of1 : 1900. It was then remembered that at birth the babyhad had severe neonatal purpura. Apart from the intra-cranial calcification, the only remaining sign of toxo-

plasmosis was microphthalmos of one eye. Surprisinglythere was no choroidoretinitis. Choroidoretinitis is thecommonest sign of congenital toxoplasmosis. It is not

unlikely that in the majority of cases it is the only one, forit is estimated that in 25-35% of cases of choroidoretinitisthe cause is toxoplasmosis. This sign may not be noticedtill school age or even adult life; and diagnosis in individualcases may be difficult or impossible since antibody titreswill have fallen to levels common in the generalpopulation.The 1 acquired case in the Glasgow series was of a boy

of 10 who had a swelling in his neck. Histological examina-tion raised the differential diagnoses of lymphoblastoma,lymphosarcoma, or toxoplasmosis. High dye-test titres(1 : 640 rising to 1 2560) and complement-fixationtitres (1 : 80 rising to 1 : 160) made the diagnosis of toxo-plasmosis virtually certain, and this was supported by thefavourable outcome. Although the Glasgow series in-

cludes only this single case of acquired glandular toxo-plasmosis, such cases outnumber severe congenitalillnesses. Many cases are so mild that they do not reachhospital, and the patients are treated, if at all, by thefamily doctor. In the very rare cases of severe acquiredtoxoplasmosis, predominating features have been meningo-encephalitis, myocarditis, and pneumonitis; pericarditis,pleurisy, myositis, skin rashes, and liver and kidney dam-age have also been noted. In this country Potts andWilliams 13 reported a fatal case of myocarditis in whichtoxoplasma was isolated from the heart. Although sug-gestive evidence, this was not conclusive; for the antibodytitres were not high, and toxoplasma has been found in theheart-muscle of patients who died of unrelated causes. Ina recent case in an adult,14 six weeks of paroxysmal, drycough was followed by bilateral pleurisy, basal pneu-monitis, and pericarditis. A month later the patientseemed to be recovering but he died suddenly, apparentlyof pulmonary embolism. The subsequent finding of toxo-plasma antibodies to the very high titres of 1 : 32,000 inthe dye test and of 1 : 32 in the complement-fixation testin a specimen of serum taken during the illness madetoxoplasmosis a highly probable diagnosis.

13. Potts, R. E., Williams, A. A. ibid. 1956, i, 483.14. Ludlam, G. B. Personal communication.15. Dupuytren, G. Lancet, 1834, ii, 222.16. Skoog, T. Acta chir. scand. 1948, 96, suppl. 139.17. Larsen, R. D., Posch, J. L. J. Bone Jt Surg. 1958, 40A, 773.18. Larsen, R. D., Takagishi, N., Posch, J. L. ibid. 1960, 42A, 993.

DUPUYTREN’S CONTRACTURE

ALTHOUGH Dupuytren’s contracture was first describedwell over a hundred years ago,15 and although it is by nomeans rare, remarkably little is known of its pathogenesis.As the standard treatment has for many years involvedexcision of the incapacitating sclerotic tissue, our ignorancecannot be attributed to lack of opportunity to examine thelesion.

In 1948 Skoog 16 showed quite clearly that the histologi-cal changes in Dupuytren’s contracture were characteristicbut varied with the stage of its evolution from an ill-defined richly cellular nodule of fibroblasts to a poorlycellular band of extremely dense fibrous tissue. He alsocalled attention to the presence of collagen fibres thatended abruptly in the vicinity of the cellular nodules, andto fine grains of haemosiderin within these nodules; andhe regarded these two features as evidence that traumawas an important factor in the development of thedisease.

In 1958 Larsen and Posch 17 reported a study of 61 sur-gically removed specimens of Dupuytren’s contracture;and, although they identified hxmosiderin granules in 9 ofthem, evidence of rupture of collagen fibres was notobtained. An investigation by Larsen et al.18 of a further69 specimens, in which special care was taken in theorientation and sectioning of the specimens, has been moresuccessful. Of the 69 specimens 45 were in the nodularstage of the disease, and of these 45 hasmosiderin wasfound in 19. Furthermore, several examples of abruptlyterminating fibres were found in association with thesenodules, together with others which passed uninterruptedlythrough them. These findings therefore strongly supportSkoog’s original contention that microrupture of thefibres of the palmar aponeurosis is an important factor inpathogenesis.

Larsen et al. attempted to confirm this hypothesis byreproducing the disease in 12 monkeys. Both the palmar