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Tertiary Hyperparathyroidism 17 August 1968 British Medicine in Australia-Rieger ,B~ff 395 We in Australia, after 15 years of running repairs and alter- doubt have exhorted us to continue our efforts to achieve a ations, have a vehicle in need of a major overhaul. Like you national registration board. Lister would have experienced Br Med J: first published as 10.1136/bmj.3.5615.395 on 17 August 1968. Downloaded from in Britain, our difficulties are basically those of finance, how great satisfaction in the progress of surgery. Osler would best to obtain and apply this to provide all members of the doubtlessly have regarded our progress in the control of medical community with complete cover. practice with " equanimity." It has become apparent that our ideas on the basic philosophy All three would assuredly survey the advances of science and of national health care are again approximating, and that our technology with amazement, and we trust they would approve paths, at present as antipodean as our countries, are converging. the progress made towards maturity, and promised in our Both our countries can gain much from each other in their " vigorous infancy," of " British Medicine in Australia." efforts to provide, on a national scale, readily available medical When the time arrives for your return to your homes we care of the highest standard. This we shall both achieve if all hope that you will take with you many happy memories of concerned approach the task with open minds, actuated by your stay in this land of Australia, new friendships, and an the highest motives, basing their decisions on facts and dili- enhanced knowledge and appreciation of our country, its gently pursuing one common purpose. people, and their way of life. What would have been the reaction of those distinguished We, for our part, shall long cherish this occasion and treasure gentlemen who attended that 65th Annual Meeting if they the wisdom you bring with you, as well as the great personal could perchance be with us this week ? Roddick would no pleasure we have in this meeting with you. Tertiary Hyperparathyroidism D. R. DAVIES,* F.R.C.S.; C. E. DENT,* F.R.C.P.; LYAL WATSON,* F.R.A.C.P. Brit. med. ., 1968,3, 395-399 Sunmary: In our first 200 caqt. of pr y hyperpara- Dent (1962) presented further evidence that autonomous thyroidism confirmed by operation 12 were also shown hyperparathyroidism with adenoma formation may have to have a long history either of a malabsorption syndrome developed from a background of secondary parathyroid hyperd or of chronic renal-glomerular failure. We consider that plasia both in malabsorption syndromes and in chronic renal- they first went through a phase of secondary hyperpara- glomerular failure. Other reports followed. The Case Records thyroidism, during which one or more of the glands of the Massachusetts General Hospital (1963) reported the case became autonomous adenamata. This then produced the of a patient with a long history of progressive chronic pyelo- biochemical changes of " primary " hyperparathyroidism, nephritis who gradually developed hypercalcaemia. At operation necessitating excision of the adenoma.' This condition is a parathyroid adenoma was removed and this patient was con- http://www.bmj.com/ best described as " tertiary " hyperparathyroidism. The sidered to be the first case of secondary hyperparathyroidism transition from secondary to- tertiary hyperparathyroidism developing under biochemical observation into primary hyper- occurred in four of the 12 patients while under our parathyroidism in the way that Davies et al. (1956 had postu- observation. We think the same process can be traced lated retrospectively in their patient. During the discussion of retrospectively in the other eight cases. The concept of the case Dr. Walter St. Goar suggested the use of the term tertiary hyperparathyroidism may help to explain the high " tertiary " hyperparathyroidism to describe such cases in which incidence of other diseases i assoon with primary autonomous parathyroid adenomata causing hypercalcaemia hyperparathyroidism. apparently developed from a background of reactive (or on 25 September 2021 by guest. Protected copyright. secondary) parathyroid hyperplasia. Though the term is not The behaviour of the parathyroid glands provides a ideal we think it is the best available. valuable model for the investigation of tumour formation in man. All states occurred in our patients with Other cases of supposed tertiary hyperparathyroidism have primary from normal through since been described by McPhaul et al. (1964), Golden et al. hyperparathyroidism. (1965), and Ludwig et al. (1967). In addition Glanville and hyperplasia to adenoma formation and finally to para- Bloom (1965) described one of our patients with adult-present- thyroid carcinoma. ing " vitamin D resistant " osteomalacia who developed hyper- calcaemia under observation and from whom we then removed ntroduction a parathyroid adenoma. Among our first 200 patients with In 1956 Davies, Dent, and Willcox described the case of a hyperparathyroidism confirmed at operation there are 12 prob- patient with steatorrhoea and osteomalacia (their Case 2). She able cases of tertiary hyperparathyroidism and two possible appeared to have suffered from lifelong coeliac disease, but her cases. Only three of these 14 cases arose on the basis of long- plasma calcium level was persistently raised even before treat- standing renal failure, a situation presenting particular ment with vitamin D, and there was only a partial response difficulties in retrospective diagnosis, and in interpretation of of the osteomalacia when vitamin D treatment was given. After plasma electrolyte levels. two parathyroid adenomata were later removed at operation the patient was cured of her hypercalcaemia and then responded normally to vitamin D. Davies et al. concluded: "In some Case MaterWial cases of steatorrhoea a parathyroid hyperplasia occurs which is reversible with vitamin D treatment. In other cases, however, The 12 probable cases of tertiary hyperparathyroidism are presumably of longer duration, one or more adenomata will listed in Table I. Five of these have been reported elsewhere develop." (as shown in the Table), three as such and two others in papers dealing with other clinical aspects of hyperparathyroidism. * University College Hospital, London W.C.l. Short case reports of the remaining seven are included in this BDC sN 396 17 August 1968 Tertiary Hyperparathyroidism-Davies et al. MEDICINE JOURNL TABLE I.-Details of Patients with Tertiary Hyperparathyroidism IV Br Med J: first published as 10.1136/bmj.3.5615.395 on 17 August 1968. Downloaded from Representative Evidence of Bone Disease Preoperative Chemical Findings* Operative Case Age end Y ra IP_. Findings Aetiological Factor Previously Reported NO. Ca P Fase Osteo- HPTt Operation (mg./100 ml.) (mg-/ (K.A. malacia S.G. in Parentheses lOOml.) Units) 2-5 63 None X-ray Adenoma Gluten-sensitive Dent and Garretts 5 64 F 1951 14-5 9-5 g. enteropathy (1960) 69 X-ray X-ray 2 adenomata Gluten-sensitive Davies et at. (1956 11 41 F 1955 114 20 150 mg. and 1 g. enteropathy 9 X-ray Adenoma Renal glomerular Dent (1962§ F 10-0 3-9 None 57 60 1960 (1024) 1-8 g. failure 12-7 2-0 31 X-ray X-ray Adenoma 4-5 g. Polycystic kidneys 59 48 M 1960 15 None None Adenoma Gluten-sensitive 91 59 F 1963 10-9-+12-6 2 2 1-5 g. enteropathy (1028) 28 X-ray None Adenoma Vitamin-D-resistant Glanville and Bloom 107 46 M 1964 9-6-10-8 1-8 1-2 g. osteomalacia (1965) (1028) 17 X-ray X-ray Adenoma Postgastrectomy 138 67 F 1965 10-4 2 8 800 mg. (1025-6) 13 Biopsy X-ray Adenoma Gluten-sensitive Smith and Stern 144 46 F 1965 11-6 19 2-4 g. enteropathy (1967) (1025-6) None Adenoma Postgastrectomy F 1965 9-3-+10-7 2-0 33 X-ray 146 65 (1021) (1024) 500 mg. 1-4 37 X-ray. X-ray. Adenoma Gluten-sensitive 147 47 F 1966 9 6--11 7 Biopsy Biopsy 3-1 g. enteropathy (1025-6) (1026-7) 131 Biopsy X-ray. Adenoma Gluten-sensitive 158 28 F 1966 9-7(+10-3225 Biopsy 2 g. enteropathy (1024) (1024) 9 None Adenoma Postgastrectomy F 11-3 2-2 X-ray. 1 185 72 1967 (1024) Biopsy g. * Arrows indicate rises observed while under follow-up. t Osteitis fibrosa generalisata. had significant hypercalcaemia before diagnosis paper. Data from three of these latter patients are plotted in All patients 107 has been redrawn from the was finally established at operation. In four cases (Nos. 146, Figs. 1-3. The chart of Case developed while the patients original publication (Glanville and Bloom, 1965) and brought 147, 158, and 107) hypercalcaemia our observation, usually while treatment with up to date as Fig. 4. - were under vitamin D was being given for osteomalacia (see Figs. 1-4). In calcium was determined on the Eppendorf Total plasma two of these (146 and 158) the important plasma ionized (normal range 9-10 mg./100 ml. after correc- flame photometer calcium fraction was shown to rise from normal to abnormal to a specific gravity of 1027 as described by Dent (1962)). tion levels (normal range 5-5.8 mg./100 bl.). In a third (Case 107) was determined by the method of Rose (1957), Ionized calcium calcium rose from 5.9 in 1957 (normal range then range 5-5.8 mg./100 ml.). the ionized with minor modifications (normal below 6.2 mg./100 ml.) to 6.4 in 1964 (normal range then below 5.8 mg./100 ml.); this was useful additional informa- Vt.D2 4 tion in establishing the presence of significant hypercalcaemia FsMr.OG .0|. in patients whose plasma total calcium levels were only Forathroldectomy marginally raised. It is likely that the biochemical changes ++ 56 C observed in these four individuals show the course of develop- http://www.bmj.com/ ment of all 12 cases.
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