Admiraal, J.

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854HYPOTHYROIDISM IN CONGENITAL RUBELLASIR,&mdash;Several manifestations of intrauterine rubella maydevelop months or years after birth. This late-onset diseasemay be due to direct action of the persisting infection or to animmunopathological process.’ 1A small-for-dates girl was born by spontaneous breech at 40weeks menstrual age in May, 1972. Birthweight 2.0 kg andocciputofrontal circumference 30 cm. Rubella-antibody titrewas 1/256, but there were no signs of congenital rubella. Atage 2 years she was still small but bone age was normal. Overthe next year her growth velocity slowed further and she wasadmitted for investigation. Her height was 80.4 cm and weight8.2 kg, both below the third centile. Her skin was dry and sca-ly ; there was no goitre. Fundoscopy showed evidence of rubellaretinopathy.Thyroxine 37 mmol/1 (normal 59-138); serum thyroid-sti-mulating hormone >64 &micro;U/ml (normal 10-35); thyroglobu-lin (tanned-red-cell) titre 1/2560; thyroid microsomalheemagglutination-titre 160;2 rubella antibody 1/320 (aged 3years 11 months); bone age 2 years 2 months (chronologicalage 3 years 4 months). She became biochemically euthyroid(T.S.H.<1.0 &micro;U/ml) on L-thyroxine 0.05 mg three times daily.Her height has increased by 9.4 cm in 10 months.The very rare association of poor intrauterine growth andjuvenile hypothyroidism in this patient has been emphasised ata recent clinical meeting of the Royal Society of Medicine,Pxdiatric Section. Two recent reports2 3 from overseas ofthe association between hypothyroidism and congenital rubellahave prompted this letter. The raised thyroid-antibody titresshowed evidence of a thyroiditis caused by continuing rubellainfection acquired in utero. Cooper reported a case of hypo-thyroidism in congenital rubella and one other case in theUnited Kingdom is known.5If growth and development are slower than expected inchildren with congenital rubella, thyroid function should beassessed, but in such a clinical state other endocrine disordersmay be responsible, such as growth-hormone deficiency.6I thank Dr W. C. Marshall for his encouragement and advice inwriting this report, and Dr David Harvey for his permission.Department of Child Health,St George’s Hospital Medical SchoolLondon SW17 0QT TESSY K. HANIDFATAL INHALATION OFMETHYLFLUOROSULPHATESIR,&mdash;Methylfluorosulphate (CH3OS02F) is used in manylaboratories as a methylating agent. A fatal accident in thedepartment of chemical technology at this university high-lights the hazard of inhaling only a minute quantity of thisvery toxic substance.On March 25, 1976, at 11.30 A.M. a 25-year-old chemistspilt a few millilitres of a fluid containing methylfluorosul-phate on his laboratory coat and pullover. He immediatelytook off the coat and cleaned his pullover with water. Althoughhe had no complaints, the man was sent to hospital at about1 P.M. No abnormality was found, and he was allowed to gohome. At 5 P.M. the man began to cough a little and had somedifficulty with deep breathing. At 7 P.M. he was admitted tohospital in a moribund state due to pulmonary cedema. Hedied the next day despite intensive treatment.1. Marshall, W. C. in Intrauterine Infection (Ciba Symp. ser. 10); p. 3. Amster-dam, 1973.2. Comas, A. P., Bentances, R. E. J Pediat. 1976, 88, 1065.3. Nieburg, P I., Gardner, L. I. ibid. 1976, 89, 156.4. Cooper, L Z. in Infections of the Fetus and the Newborn Infant (Progr. clin.biol. Res. vol. III) (edited by S. Keriyman, and A. Gershin); p. 1. Liss,1975.5. Grant, D G. Personal communication.6. Marshall, W C. B J. clin. Pract. 1976, 30, 56.Protein denaturation seems to be the major contributor tothe development of pulmonary oedema. Moreover, hydrogenfluoride and sulphuric acid are generated when methylfluoro-sulphate makes contact with water.This case should be a serious warning to everyone workingwith methylfluorosulphate. Immediate administration of corti-costeroids should be considered if this or other alkylatingagents is thought to have been inhaled. Continuous closeobservation during the first 24 h is necessary.Medical Department,Technical University Twente,Ensched&eacute;, Netherlands J. ADMIRAALASCORBIC ACID AND PARAQUAT TOXICITYSIR,&mdash;Paraquat is extremely toxic, and even the mostvigorous treatments may not be able to prevent death afterexposure to the chemical.’ Paraquat toxicity seems to be dueto the ability of the reduced form of this compound to generatethe superoxide radical,2-4 which can undergo several reactionsleading to lipid peroxidation and tissue damage. The enzymesuperoxide dismutase catalyses the breakdown of the superox-ide radical,s and attempts have been made to use this enzymeto treat paraquat-poisoned animals. Promising results in pre-liminary experiments6 have not been confirmed, and the lackof effect of superoxide dismutase seems to be due to its inabilityto penetrate cells.’ What is therefore required is a compound,transported into lung tissue, which can react with superoxide,Such a compound is ascorbic acid. 9 It enters the lung fromthe blood and appears to accumulate in the fluid lining the airspaces, and its reaction with superoxide has been directlydemonstrated.9 The toxicity of hyperbaric oxygen seems to bedue to increased formation of superoxide, 10 and in rats exposedto hyperbaric oxygen prior administration of ascorbic acid les-sened the toxic effects. 11Since massive doses of ascorbic acid do not seem signifi-cantly harmful to man,12 it might be possible to use this treat-ment in paraquat poisoning.Department of Biochemistry,King’s College,London WC2R 2LS B. HALLIWELLBLAST-CELL TRANSFORMATION CHRONICGRANULOCYTIC LEUK&AElig;MIASIR,&mdash;Howes and Emerson" described a patient having blas-tic crisis in chronic granulocytic leukaemia with features sug-gesting lymphoblastic rather than myeloblastic transfoma-tion.We have seen a 38-year-old man who was admitted after afall which caused a massive hasmatoma of his leg without boneinjury. Hb 6.8 g/dl, white-cell count 200 x 109/1 with granuto-cytes at all stages of maturation, and platelets 800 x 109/l.The neutrophil alkaline-phosphatase score was 7 and Philadel-phia chromosome was demonstrated in the peripheral blood,The spleen was enlarged.1. Goulding, R., Volans, G. N., Crome, P., Widdop, B. Br. med. J. 1976, i, 422. Bus, J. S., Aust, S. D., Gibson, J. E. Biochem. biophys. Res Comm 1974,58, 749.3. Bus, J. S., Aust, S. D., Gibson, J. E. Res. Comm. chem. Path. Pharmac.1975, 11, 31.4. Fisher, H. K., Clements, J. A., Wnght, R. R. Am. Rev. resp. Dis. 1973, 107,246.5. Halliwell, B. New Phytol. 1974, 73, 1075.6. Autor, A. P. Life Sci. 1974, 14, 1309.7. Huber, W. in Proceedings of the EMBO Workshop on Superoxide andSuperoxide Dismutase (edited by A. M. Michelson) (In the press8. Willis, R. J., Kratzing, C. C. Biochim. biophys. Acta, 1976, 444, 1089. Nishikimi, M. Biochem. biophys. Res. Comm. 1975, 63, 463.10. Crapo, J. D., Tierney, D. F. Am. J. Physiol. 1974, 226, 140111. Jamieson, D., van den Brenk, H. A. S. Biochem. Pharmac 1964. 13, 15912. Cameron, E., Campbell, A. Chem.-Biol. Interac. 1974, 9, 28513. Howes, D., Emerson, P. Lancet, 1975, ii, 1302.

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Fatal inhalation of methylfluorosulphate

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Fatal inhalation of methylfluorosulphate

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