131I TREATMENT FOR THYROTOXICOSIS

131I TREATMENT FOR THYROTOXICOSIS

1035 jaundice, petechise on her limbs, and redema; blood-pressure was 160/110 mm. Hg, blood-urea nitrogen 132 mg. per 100 ml., serum-creatinine 7.2 m...

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1035

jaundice, petechise on her limbs, and redema; blood-pressure was 160/110 mm. Hg, blood-urea nitrogen 132 mg. per 100 ml., serum-creatinine 7.2 mg. per 100 ml., creatinine clearance 4,7 ml. per minute, hæmatocrit 16%, hxmoglobin 5-07 g. per 100 ml.; the blood-film showed poikylocytosis and schistocytosis, platelet-count was 120,000 obvious

per c.mm., and reticulocytes 6%. Fibrinogen-degradation products were 45 µg. per ml. (normal 0-7 µg. per ml.) 1; serum-bilirubin was 4-2 mg. per 100 ml. A renal-biopsy specimen showed some fibrinoid thrombi occluding the arterioles, and segmental necrosis of arteriolar

walls. The glomerular loops were shrunken. Immunofluorescence microscopy revealed deposits of fibrin on the arteriolar walls and the glomerular loops. On July 7, we began treatment with heparin (300 mg. daily by subcutaneous injection) and dipyridamole (425 mg. daily). On July 26 we stopped heparin because of a large haematoma on her left arm, and the creatinine clearance, which had risen to 23 ml. per minute, fell to 15 ml. per minute. 7 days later we resumed heparin treatment and the creatinine clearance rose to 38 ml. per minute. On Aug. 14, heparin treatment was stopped, but she was kept on dipyridamole and started on phenindione. Her creatinine clearance is now 39 ml. per minute, blood-urea-nitrogen 19 mg. per 100 ml., hæmatocrit 30%, haemoglobin 10.3 g. per 100 ml., platelet-count 240,000 per c.mm., and blood-pressure

births. The mother of the infant born in February, 1970, was 24, and the mother of the infant born in July, 1970, was 29. The above observations may not be significant because they encompass two relatively small populations. It will be interesting, and perhaps important, to learn whether other investigators, in nearby as well as distant locations, have made similar observations. This work was supported by a grant from the Birth Defects Institute, New York State Department of Health.

Cytogenetics Laboratory, Mental Retardation Research Unit, Letchworth Village, Thiells, N.Y. 10984.

LAWRENCE R. SHAPIRO.

131I TREATMENT FOR THYROTOXICOSIS

SIR,-Since 1311 therapy

introduced for the treatresults have been assessed by several groups.3-10 Professor Werner and his colleagues (Oct. 3, p. 681) have now reported their experience with 1251 in New York and Amsterdam. The incidence of hypothyroidism and problems of management seem to be similar to those with 131I. We have analysed all patients

ment of

was

thyrotoxicosis, 1,2 the

170/110 mm. Hg. This case is similar to that of Dr. Luke and his colleagues, except that our patient was never given oxytocic substances. The clinical findings were not strikingly different from those in M.H.A. arising during pregnancy or immediately after delivery.2 The fact that clinical symptoms arose a few days after delivery does not exclude the possibility that the condition was caused by an intravascular coagulation process which began during pregnancy or delivery. In fact the rise in fibrin-degradation products in late normal pregnancy probably depends on the commonly present lesions of the placenta.3 In rare cases, possibly, the process of intravascular coagulation may evolve slowly, and cause a hamiolytic-uraemic syndrome several days after expulsion of the placenta. We thank Dr. P. M. Mannucci (Institute of Medical Pathology, of Milan) for coagulation studies.

University

CLAUDIO PONTICELLI Department of Urology, Section of Nephrology, University of Milan, Italy.

ENRICO IMBASCIATI ANTONIO TARANTINO GIORGIO GRAZIANI.

Relationship between gland size, dose in mCi, and results of treatment.

TRISOMY 18

SIR,-Dr. Kardon and her colleagues (Oct. 10, p. 782) report an apparent 7-8 fold increase in the occurrence of trisomy 18 in the newborn service of Mount Sinai Hospital, New York City, from February to July, 1970. They found 5 cases of trisomy 18 with an incidence of about 1 in 600 live births, and the maternal ages of three of their cases were under 30. During the same six-month period from February to July, 1970, we diagnosed 2 cases of trisomy 18 confirmed by chromosome analysis. These were the first cases of trisomy 18 noted by us since the establishment of our laboratory in 1968. Rockland County, New York, is a suburban area north of New York City in which 2959 live births were recorded for 1969. For the six-month period from February to July, 1970, 1544 live births were recorded with an incidence of trisomy 18 of about 1 in 774 live Woodfield, D. G., Cole, S. K., Allan, A. G. E., Cash, J. D. Br. med. J. 1968, iv, 665. 2. Brain, M. C., Baker, L. R. I., McBride, J. A., Rubenberg, M. L., Dacie, J. V. Br. J. Hœmat., 1968, 15, 603. 3. Devi, B., Jennison, R. F., Langley, F. A. J. clin. Path. 1968, 21, 322. 1.

treated with 13’1 in the South-West Wales area from January, 1965, to June, 1969, with a view to identifying factors responsible for persistent thyrotoxicosis and hypothyroidism. A total of 183 patients (148 females and 35 males) were treated with an initial calculated dose of 5000 rads.3 Results of the first radioactive iodine therapy were:

euthyroid, 59%; hypothyroid, 14% ; persistent thyrotoxicosis, 25%; not assessed, 2%. Using the x2 test of statistical significance, the outcome was not significantly affected by age, family history, previous treatment, duration of the illness, or precipitating factors such as the death of a spouse 1. 2. 3.

4. 5. 6. 7. 8. 9. 10.

Hertz, S., Roberts, A. J. clin. Invest. 1942, 21, 624. Hamilton, J. G., Lawrence, J. H. ibid. p. 624. Blomfield, G. W., Eckert, H., Fisher, M., Miller, H., Munro, D. S., Wilson, G. M. Br. med. J. 1959, i, 63. Beling, U., Einhorn, J. Acta radiol. 1961, 56, 275. Dunn, J. T., Chapman, E. M. New Engl. J. Med. 1964, 271, 1037. Green, M., Wilson, G. M. Br. med. J. 1964, i, 1005. McGirr, E. M., Thompson, J. A., Murray, I. P. C. Scott. med. J. 1964, 9, 505. Crooks, J. Current Topics in Thyroid Research (edited by C. Cassano and M. Andreoli); p. 1208. New York, 1965. Nofal, M. M., Beierwaltes, W. H., Patno, M. E. J. Am. med. Ass. 1966, 197, 605. Staffurth, J. S., Young, J. J. clin. Endocr. 1967, 27, 1062.

1036 CÆSAREAN SECTION UNDER LOCAL ANÆSTHESIA

TIME OF PEAK UPTAKE IN RELATION TO OUTCOME OF THERAPY

p. 719), describing the section under local anxsthesia in

SiR,-Mr. Hai-Kahn (Oct. 3,

performance

domestic worries. Neither was it related to peak uptake, biological half-life of the tracer dose, nor the dose administered in terms of mCi of 131I. Gland size was significantly correlated to outcome at the 5% level. As gland size increased, the incidence of subsequent hypothyroidism fell. No case was recorded with a gland size over 80 g. There was a lower incidence of persistent thyrotoxicosis in patients with small glands, being 20% in those with glands of 70 g. or less and 43% in those with glands over 70 g. The accompanying figure shows the distribution of dose in mCi in relation to gland size and outcome. The mean dose and the standard deviation in each of the three groups of gland size is indicated. The time at which the peak uptake occurred, as estimated by plotting the neck uptake, was significantly correlated with the outcome at the 1 % level (see accompanying table). The earlier the peak uptake in hours after administration of the tracer, the lower the subsequent incidence of hypothyroidism and the higher the incidence of persistent thyrotoxicosis. 46 patients had persistent thyrotoxicosis after their first radioactive-iodine therapy. 30 received two treatments with 1311, 6 had a third dose, and one required a fourth dose. The overall incidence of hypothyroidism was 12% at one year and 17% at two years. The incidence of hypothyroidism will undoubtedly increase with time. In two cases, hypothyroidism followed a second treatment of 2500 rads. The importance of gland size has been emphasised previously.3,9,10 The relationship to the time of the peak uptake relates the results of treatment in some way to iodine turnover. This may in turn be related to the iodine content of the diet and other geographic factors postulated by Professor Werner to account for the differences between patients in New York and Amsterdam. Another source of indeterminate variation in the results is that the use of the Sheffield formula to calculate the dose assumes uniform uptake of the radioiodine by the thyroid gland. But this has been shown not to be "the case.ll,12 Thus a predictable " partial thyroidectomy with radioactive iodine is unlikely to be possible.13 Since surgical treatment 14 is associated with significant hypothyroidism and recurrent thyrotoxicosis, and drug therapy ’5 with a tendency to relapse after cessation of therapy, the inevitable conclusion must be that successful management of thyrotoxicosis depends as much on continuous follow up of cases, as on the therapeutic agent employed. or

We wish

J. Ivey and the staff of the medical Singleton Hospital, Swansea, and the department of medical photography at Llandough Hospital, to

thank Dr.

physics department

at

Cardiff.

Llandough Hospital, Penarth, Glamorgan. Singleton Hospital, Swansea.

IVOR SURVEYOR.

J. N. HARRIS-JONES.

of

caesarean

debilitated women, says that " the peritoneum was not anaesthetised ". This surprises me. In a similar situation in my native country (Colombia), I found that the main drawback to this procedure was difficulty in anaesthetising the peritoneum. Traction on this membrane produces severe pain, and some of my patients went into shock. I was able to prevent this by spraying the parietal and visceral peritoneum with 2% xylocaine viscous. In spite of this the patients suffered intense pain and the procedure was not easy.

Washington University, Barnes Hospital, St. Louis, Missouri.

HECTOR J. RODRIGUEZ.

GAMMA-GLUTAMYL TRANSPEPTIDASE AS A DIAGNOSTIC AID

SIR,-Dr. Zein and Dr. Discombe (Oct. 10, p. 748) conclude that, since increased levels of gamma-glutamyl transpeptidase (G.G.T.P.) have been reported in cholestatic jaundice and liver neoplasia as well as in some cases of acute hepatitis, chronic hepatitis, and liver cirrhosis,I-6 a raised level of the enzyme in serum is not specific for any type of liver disease. Our results are at variance with this conclusion. In 512 patients with various liver diseases, a significant correlation was found between G.G.T.P. (measured by Szasz’s method ’) and alkaline phosphatase (A.P.) in all the diseases studied. A significant correlation was also observed between G.G.T.P. and leucine aminopeptidase (L.A.P.) in patients with chronic hepatitis and cholestatic jaundice. No correlation was observed between G.G.T.P. and transaminases in any disease. These data have also been experimentally confirmed in rats after bileduct ligation and after chronic carbon-tetrachloride poisoning. Moreover, the increases in serum-G.G.T.P. levels observed in acute hepatitis, chronic hepatitis, and liver cirrhosis were always accompanied by histological evidence of intrahepatic cholestasis. G.G.T.P. is therefore strictly correlated with cholestasis. As a diagnostic index, G.G.T.P. shows advantages over A.P. and L.A.P.: normal G.G.T.P. levels have never been found in patients with increased serum levels of A.P. or L.A.P. However, some patients showed high G.G.T.P. levels with normal values of A.P. or L.A.P. This is in agreement with the results given by others. 6-10 In addition, the increase of G.G.T.P. is higher than that of A.P. and L.A.P.: 70% of the G.G.T.P. increases were more than twice the normal values; but only 20% of the A.P. and L.A.P. increases were more than twice the normal values. G.G.T.P. estimation seems also to have great prognostic value in chronic hepatitis. We observed that in patients who later made a good recovery the enzyme levels were 1. 2. 3. 4.

Szczeklik, E., Orlowski, M., Szewczuk, A. Gastroenterology, 1961, 41, 353. Goldbarg, J. A., Pineda, E. P., Smith, E. E., Friedman, O. M., Rutenburg, A. M. ibid. 1963, 44, 127. Rutenburg, A. M., Goldbarg, J. A., Pineda, E. P. ibid. 1963, 45, 43. Gibinski, K., Szaton, R., Maraszek, J. Gastroenterologia, 1963, 99, 237.

11. Levene, M. B., Andrews, G. A., Kniseley, R. M. Am. J. Roentgen. 1955, 73, 88. 12. Sinclair, W. K., Abbatt, J. D., Farran, H. E. A., Harriss, E. B., Lamerton, L. F. Br. J. Radiol. 1956, 29, 36. 13. Philp, J. R., Harrison, M. T., Ridley, E. F., Crooks, J. Lancet, 1968, ii, 1307. 14. Hedley, A. J., Flemming, C. J., Chesters, M. I., Michie, W., Crooks, J. Br. med. J. 1970, i, 519. 15. McLarty, D. G., Alexander, W. D., Harden, R.McG., Clark, D. H. ibid. 1969, iii, 203.

5. 6. 7. 8. 9. 10.

Aronsen, K. F., Hanson, A., Nosslin, B. Acta chir. scand. 1965, 130, 92. Villa, L., Dioguardi, N., Agostoni, A., Idéo, G., Stabilini, R. Enzymol. biol. clin. 1966, 7, 109. Szasz, G., Rosenthal, P., Fritsche, W. Schweiz. med. Wschr. 1969, 99, 606. Idéo, G., Morganti, A., Dioguardi, N. Digestion (in the press). Lukasik, S., Richterich, R., Colombo, J. P. Schweiz. med. Wschr. 1968, 98, 81. Szasz, G., Rosenthal, P., Fritsche, W. Dt. med. Wschr. 1969, 94, 1911.