EMPTY-SELLA SYNDROME

EMPTY-SELLA SYNDROME

574 reattend) and the healing-times are shown in the accompanying figure. For all 43 abscesses (fucidin 20, caviject 23) the mean healing-times were ...

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574

reattend) and the healing-times are shown in the accompanying figure. For all 43 abscesses (fucidin 20, caviject 23) the mean healing-times were fucidin 6-6 days, caviject 4.4; for up to 1 in. cavities, fucidin 5-6 days, caviject 3’9 for 1-2 in. cavities, fucidin 7-6 days, caviject (P<0-01); 4-9 (p < 0-001). Our results show that with caviject there is more rapid healing of abscess cavities than with a fucidin wick and that this is especially so with larger cavities. Overall the mean healing-time with caviject is about two-thirds of fucidin wick. This accords with the work of has other advantages: it is compact, introduce, and obviates the need to change wicks.

that with Ritchie.!

a

Caviject

easy to We gratefully

acknowledge the help of Mr D. Annis, consultant surgeon, Liverpool Royal Infirmary, and Mr M. C. K. Tweedie, statistician, Department of Medicine, Liverpool University-

I.en T ahnratnrifs kindlv <:)]r)n1)p

Liverpool Royal Infirmary, Pembroke Place, Liverpool L3 5PU.

effect

on

chromosomes.

National Institute of Nutrition, Indian Council of Medical Research, Tarnaka, Hyderabad 500007, India.

G. SADASIVAN T. C. RAGHURAM.

the materials.

A. FRANKLIN R. F. CALVER.

CHROMOSOMAL ABERRATIONS IN MALNUTRITION

SIR,-Reports on the effects of malnutrition on chromosomal damage have, so far, been few and controversial. While Armendares et al. found that chromosomal aberrations were six times commoner in malnourished children than in normal children, Thorburn et awl. and Khouri et awl. reported that malnutrition per se may not influence chromosomal abnormalities. Even in the data of Armendares et al. it is difficult to assess the extent to which malnutrition per se had contributed to the increased incidence of chromosomal anomalies, since environmental factors, such as radiation, chemical agents, and viral infections, are also known to produce chromosomal aberrations. From the data obtained in a human situation, it will, therefore, be hard to establish the precise role of malnutrition in inducing chromosomal aberrations. An investigation was therefore undertaken in experimental animals, in which genetic and environmental variables had been controlled, to determine the role of malnutrition in chromosomal changes. Female albino rats (Wistar strain) receiving stock diet were used. From the day of successful’mating, half the animals were fed a low-protein diet (9%) and the other half a high-protein diet (23%) of mixed vegetable and animal protein. After the birth of the offsprings, 6 young ones were allowed to suckle each mother. On the 21st day, weanling rats were sacrificed and chromosomal preparations made from bone-marrow, after two hours’ in-vivo colchicine treatment (1 mg. per kg. body-weight). Flame-dried smears were stained with Giemsa and examined for chromosomal aberrations. Breaks and terminal deletions were scored as aberrations, while gaps were only recorded. A group of rats on 23% protein-diet treated with cyclophosphamide served as positive controls. The results were:

The incidence of chromosomal abnormalities

was

clearly

Ritchie, I. C. Br. med. J. 1972, ii, 381. Armendares, S., Salamanca, F., Frenk, S. Nature, 1971, 232, 271. Thorburn, M. J., Hutchinson, S., Alleyne, G. A. O. Lancet, 1972, i, 591. 4. Khouri, F. P., McLaren, D. S. Abstracts of short communications, IX International Congress of Nutrition, Mexico, 1972, p. 31.

1. 2. 3.

in rats whose mothers had had low-protein diets pregnancy and which continued to receive lowprotein diets till the 21st day of life. It is, however, significant that breaks and deletions were the only abnormalities detected. This observation is in contrast to that of Armendares et al., who found all types of aberrations, including acentrics and dicentrics, in malnourished children. It is possible that this difference may be due to the severity of malnutrition, since in the rats studied here only a moderate degree of malnutrition was induced. These results do indicate that malnutrition per se has a deleterious

higher during

EMPTY-SELLA SYNDROME

SIR,-In the letter from Dr Faglia and others (July 21’ p. 149) which recorded twelve patients with probable " primary " empty-sella syndrome, no mention is made of the presence or absence of visual-field defects. Since there is a feeling in some quarters that the primary empty-sella syndrome is not accompanied by visual-field defect, I would be most interested to know if the group in Milan have information about visual-field function in the aforementioned twelve patients. Division of

Ophthalmology, University of Utah Medical Center, Salt Lake City, Utah 84112, U.S.A.

* ** We showed this letter follows.-ED. L.

HENRY J. L. VAN DYK. to

Dr

Faglia, whose reply "

"

SIR,-One of our twelve patients with primary empty-sella had a detectable visual impairment consisting of right optic-nerve atrophy and slight defect in the left eye, while in the other patients no visual-field abnormalities were

demonstrated.

2nd Medical Clinic, Endocrine Unit, University of Milan, 20122 Milan, Italy.

GIOVANNI FAGLIA.

CEPHALOSPORINS

SIR,-In your editorial (Aug. 18, p. 364) you omitted to mention that cephradine is now available in an injectable as well as an oral form and is therefore unique among cephalosporins in this regard. The intramuscular injection is not unduly painful and for severe infections it can be administered intravenously. As you indicated, the cephalosporins differ more in their degree than in their spectrum of activity and also their route of administration. Mention is also made of the variability in protein binding, and in this respect cephradine compares most favourably with other cephalosporins in that only 6%is bound, a greater percentage therefore being available in an active form. It is incorrect to say that no useful clinical data were available when cephradine was released. However, with delays in publication of clinical papers sometimes amounting to over a year, it is quite impracticable to wait for publication of large numbers of clinical trials. Since cephradine has been made available, there have been more than 30 publications on its clinical use. As it was thought that changes in medicines legislation might cause delay in its eventual release, we elected to do our clinical research in other countries and use that data