UNIVERSITY CLINICAL ACADEMIC STAFF

UNIVERSITY CLINICAL ACADEMIC STAFF

1192 of the higher medical degrees which -would continue to denote academic distinction. Nor would it alter the place of the M.R.C.P. and similar qual...

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1192 of the higher medical degrees which -would continue to denote academic distinction. Nor would it alter the place of the M.R.C.P. and similar qualifications which would, as now, be the gateway to advanced training for specialist work. GEORGE

JOHNSON.

UNIVERSITY CLINICAL ACADEMIC STAFF SIR,-An Association of University Clinical Academic Staff has been formed.l Membership of this Association is open to all academic, medical, and dental staff holding honorary The Association was formed in contracts with the N.H.S. response to growing dissatisfaction among clinical academic staff with the present rates of remuneration and the failure of the Government to include any recommendation for clinical academic staff in the recent pay award made to N.H.S. doctors. Representative meetings are being organised in each medical school and postgraduate institution; in the meantime anyone wanting further information or wishing to join the Association should contact me. IAN A. D. BOUCHIER Royal Free Hospital, temporary secretary, Gray’s Inn Road, London W.C.1.

Association of University Clinical Academic Staff.

THYROCALCITONIN-EXCESS SYNDROME SIR,- The importance of thyrocalcitonin in human physiology is now strongly supported by the finding that this hypocalcaemic principle is active in man1 and is present in the human thyroid.23 Furthermore it has been shown 4 that the thyroid gland is also essential in the control of hypercalcxmia in man. Therefore it seems justified to consider thyrocalcitonin as a possible factor in abnormal conditions with deranged calcium metabolism, and to postulate the existence of syndromes due to deficit or excess of this principle. We describe here a case which seems to show the existence of a syndrome due to thyrocalcitonin excess. A

39-year-old, normally intelligent, mother of two children admitted with a history of tetany and diffuse non-toxic goitre since adolescence. She was not from a goitre area. At the time of admission repeated determinations showed persistent hypocalcaemia, with an average of 8-1 mg. calcium per 100 ml. blood, and an average blood-phosphorus level of 3’6 mg. per 100 ml. Serum-alkaline-phosphatase level was 3 Bodansky units per 100 ml. Urine calcium and phosphorus levels were 130 and 590 mg. per 24 hours respectively. Blood-urea level was 19 mg. per 100 ml. There was diffuse moderate enlargement of the thyroid. Radioiodine uptake was 89% and 87% at the 6th and 24th hours respectively. Basal metabolic rate was --10 %, and serum- protein-bound-iodine level was 4’9Ilg. per 100 ml. There was no steatorrhoea and no X-ray evidence was

CLASSIFICATION OF FATAL PERICARDITIS

SiR,ņThe way in which advances in medical practice outrun the classification of causes of death laid down by the International Statistical Classification of Diseases, Injuries, and Causes of Death (I.C.D.) is illustrated by Dr. Rose in his article (Oct. 15, p." 851), in which he suggests "that many deaths reported as active rheumatic pericarditis (l.c.D. no. 401.0) are unlikely to be in fact rheumatic. It is now possible to provide evidence substantiating his statement. In 1964 there were 41 deaths assigned to this category,2 the youngest deceased person being 22 years old, as follows:

Auricular fibrillation was mentioned as associated with 1 of the 18 deaths due to acute pericarditis in the age-group 60 and over. The pericarditis was specified as rheumatic in only 1 patient, but a variety of other conditions were mentioned that could be of setiological importance, as follows:

One death from acute pericarditis was associated with a burst abdominal wound, and one from acute fibrinous pericarditis with infected varicose veins. Some of these deaths could have been coded to other underlying causes if the information had not been relegated to part n of the death certificate, or if the tenuous wording (such as " associated with ") had been replaced by a forthright " due to ". As the rules of classification stand, there is no choice but to assign these deaths to the same group as rheumatic

Biopsy

I, table 17.

a

one normal-sized parathyroid gland was identified and left in situ apparently undamaged. After the

1. 2. 3.

Wales, 1964, part

about

justified. At operation

WILLIAM A. WILSON.

1. See Lancet, Nov. 19, 1966, p. 1121. 2. Registrar General’s Statistical Review of England and

to

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of metabolic bone-disease. A 4-hour calcium-tolerance test showed 55% of calcium retention and 16% decrease of phosphaturia on the day of infusion. The Ellsworth-Howard test with controlled glomerular filtration-rate gave a normal threefold increase in phosphaturia. Known causes of chronic hypocalcxmia being ruled out, we considered the possibility of latent tetany due to thyrocalcitonin excess. Thyroid biopsy was therefore performed for thyrocalcitonin bioassay and microscopic features. This showed the coexistence of large and small follicles with many epithelial cells which appeared to be interfollicular in the tissue-section (see accompanying figure). The hypocalcaemic activity was 1100 units per g. thyroid tissue; our values for normal thyroid are 0-80 units per g., which agree closely with those obtained by Aliapoulios et awl. Total thyroidectomy therefore appeared

pericarditis.

General Register Office, London W.C.2.

specimen. (Modified Mallory staining; reduced 1150.)

half from

4.

Foster, G. V., Joplin, G. F., MacIntyre, I., Melvin, K. E. W., Slack, E. Lancet, 1966, i, 107. Aliapoulios, M. A., Voelkel, E. F., Munson, P. L. J. clin. Endocr. Metab. 1966, 26, 897. Milhaud, G., Moukhtar, M. S., Bourichon, J., Perault, A. M. C. r. Acad. Sci., Paris, 1965, 261, 4513. Mazzuoli, G. F., Terrenato, L., Coen, G. in Excerpta Medica Foundation, International Congress series no. 120, 1966.