851 We thank Dr. J. Uriel for having directed our research and for providing the antiserum required for this study. Department of Internal Medicine, Hospital de la Seguridad Social, Zaragoza. Instituto de Investigaciones Ulta, Zaragoza, Spain.
J. R. MUÑOZ G. GUILLEN. F. P. TORIBIO.
ALPHA-FETOPROTEIN: A POSSIBLE FACTOR NECESSARY FOR NORMAL DEVELOPMENT OF THE EMBRYO
Sm,—After the screening of 850 necropsy sera, at the University College Hospital, Ibadan, in 1970, an association
was
found between the presence of various types of
congenital anomalies causing death within 24 hours of birth and the absence of serum a-fetoprotein using the Ouchterlony technique by methods already described.1 Serum a-fetoprotein, as detected by this technique, usually persists up to six weeks of life. The function of the protein has so far not been elucidated. To test the hypothesis that a-fetoprotein may be necessary for normal organogenesis, an attempt was made to neutralise the protein with its antibody in developing chickens and rats. 0-2 ml. of monospecific rabbit antiserum to chicken a-fetoprotein, prepared according to the method of Gitlin and Kitzeswas injected via the yolk sac into 62 fertile eggs which
were then incubated. Control materials non-immune normal rabbit serum and rabbit antiserum to chicken fibrinogen. 2-0 ml. of rabbit antiserum to rat a-fetoprotein, prepared according to the method of Masopust et al.,3 was injected intraperitoneally into 15 pregnant rats. Controls were as for the chicken experiment. One injection only was given because the half-life of rabbit y-globulin is about 28 days, and the normal gestation period of chickens and rats is 21 days. Congenital abnormalities, failure of development in the case of the fertilised eggs, death, and abortions in the rats occurred only in the experimental group. 50% of the chickens developed various congenital abnormalities, including rachischisis partialis, omphalocele, absence of palpebral fissures, and ruffled feathers. 10% of the newborn rats had meningomyeloceles. 40% of the eggs were dead and undeveloped, while 10% hatched to give normal poults. There was a 6% maternal mortality, 20% abortions and stillbirths, and 70% normal newborns in the rat experimental group. As these results did not occur in controls, it seems improbable that they are due to a non-specific antigen-antibody effect on embryogenesis. It is very likely, therefore, that one of the physiological functions of a-fetoprotein is a role in the normal structural development of the organism.
injected
were
A detailed report will be
published later.
Department of Pathology, University of Ibadan, and University College Hospital, Ibadan, Nigeria.
J. A. SMITH.
STILLE INFUSION CANNULA IN SUPRAPUBIC CYSTOSTOMY
SIR,-Dr. Sinha (Nov. 20, p. 1160) and Professor Tinckler (Dec. 25, p. 1422) discuss simplified methods for suprapubic drainage of the bladder. At the urological department of this hospital we have used the disposable so-called infusion cannula (see accompanying figure) with 1. 2. 3.
an outer
diameter of 1-45-2-20
mm.
Smith, J. A., Francis, T. I., Edington, G. M., Williams, A. Br. J. Cancer, 1971, 25, 337. Gitlin, D., Kitzes, J. Biochem. biophys. Acta, 1967, 147, 334. Masopust, J., Kithier, I. C., Radl, J., Koutechky, J., Kotal, Int. J. Cancer, 1968, 3, 364.
O.
and a luer lock connection. At the tip of the catheter we have made six side holes to prevent obstruction to the flow. It is inserted under local anaesthesia. The instrument which has the biggest diameter is very useful when temporary cystostomy is required for adequate preoperative examination. We have used the technique in examination of the pressure-flow functions of the bladder where the patient has made 12-15 micturitions, and we had no difficulties such as slipping out of the catheter or leakage, as described by Professor Tinckler. We have here used the cannula with outer diameter of 1 ’45 mm. A third use of this cystostomy is to secure a radiograph of the urethra when the urographic contrast is too thin for a micturating urethrogram and the meatus is deformed, so that the instrumentation normally suitable for urethrograms cannot be used. We think the Stille infusion cannula is a safe, simple, and atraumatic instrument for temporary acute cystostomy. The instrument is made by A. B. Stille-Werner, Bondegatan 21, 102 61 Stockholm 4. Diameters: outer/inner 145J100; 175/130; 2-20/1-60 mm. Length 17 cm. Price 5 SCr (40p).
Department of Urology, Karolinska Hospital, 104 60 Stockholm, Sweden.
DIABETES WITH LIVER FAILURE
SiR,—Within one month, three alcoholic patients, two with surgically created portal-systemic shunts, have been seen with the combination of uncontrolled diabetes mellitus and hepatic coma. Possible causes for hepatic encephalopathy in the presence of uncontrolled diabetes mellitus include the effects of recent acute alcoholic debauch, the acute stress of the uncontrolled diabetic state, and inadequate perfusion of organs, including the liver, in the presence of dehydration and hypovolxmia. However, in light of recent work, other mechanisms seem worth exploring. The kidney may be an important gluconeogenetic organ, and, in starvation or the presence of a badly damaged liver, may produce as much glucose as the liver.1 Renal gluconeogenesis is apparently very sensitive to changes in potassium homreostasis and starvation, and is stimulated by metabolic acidosis. Thus, in chronic metabolic acidosis, there is increased renal production of ammonia, and the deaminated aminoacids are converted to glucose.2 The increased renal formation of glucose from glutamate and alpha-ketoglutarate in acidosis and potassium deficiency is directly related to the increase in renal ammonia production observed in these conditions. Therefore, one of the contributing factors in the development of hepatic encephalopathy in patients with severe liver disease and uncontrolled diabetes mellitus may be a large increase in renal ammonia production. This may be due to the systemic acidosis and potassium depletion which develop in the course of ketoacidosis (or lactic acidosis) and to the increase in renal gluconeogenesis engendered by the uncontrolled diabetic state. Owen, O. E., Felig, P., Morgan, A. P., Wahren, J., Cahill, G. F., Jr. J. clin. Invest. 1969, 48, 574. 2. Goodman, A. D., Fuisz, R. E., Cahill, G. F., Jr. ibid. 1966, 45, 612. 1.
L.
BODO VON GARRELTS CLAES R. NYMAN.