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THE occurrence of hyperthyroidism and hyperparathyroidism in the same patient is a rarity and presents a specially interesting diagnostic problem since both diseases can cause loss of calcium from the body. Such a problem is presented here; there are 17 previously documented examples i n the literature (Breuer and McPherson, 1966).
CASE REPORTMrs. E. S., aged 32, first presented with acute bronchitis in March, 1967, when hypercalcaemia was detected on routine investigation. There was an additional history of insomnia, weight-loss, loose motions, and irritability. I n June, 1967, she was admitted again with a diagnosis of hyperthyroidism which was confirmed on investigation.Examination revealed a thyroid enlargement estimated at 40 g., firm and with no bruits to be heard. Investigations revealed the following: FBI, 11.1 pg. per IOO ml.(normal 3'5-7'5 pg. per IOO d.); PBI3lI (48 hours), 1.07 per cent (normal 0.1-0.4 per cent); T. index (Russell Fraser), 53.2 (normal 2.8-13.0); 1311 uptake, neck uptake (48 hours), 70.8 per cent; thyroid antibodies, negative; serum calcium, 5.7 mEq. (mean of six estimations) (normal, 4'5-5.5 mEq.). The hypercalcaemia was not suppressed by cortisone administration; her serum calcium values at the end of 10 days (150mg. per day) remained higher than her previous level. Serum inorganic phosphorus was 1.7 mg. (mean of six estimations) (normal 1.6-2.4 mg.); alkaline phosphatase, 9 King-Armstrong units (normal 4-11); strontium space, 19'5 plasma units (normal (18); phosphate excretion index, basal + 0.07, +0.13 (normal *o.og); urinary calcium, 25 mEq. in 24 hours (normal
THE occurrence of hyperthyroidism and hyperparathyroidism in the same patient is a rarity and presents a specially interesting diagnostic problem since both diseases can cause loss of calcium from the body. Such a problem is presented here; there are 17 previously documented examples i n the literature (Breuer and McPherson, 1966).
CASE REPORTMrs. E. S., aged 32, first presented with acute bronchitis in March, 1967, when hypercalcaemia was detected on routine investigation. There was an additional history of insomnia, weight-loss, loose motions, and irritability. I n June, 1967, she was admitted again with a diagnosis of hyperthyroidism which was confirmed on investigation.Examination revealed a thyroid enlargement estimated at 40 g., firm and with no bruits to be heard. Investigations revealed the following: FBI, 11.1 pg. per IOO ml.(normal 3'5-7'5 pg. per IOO d.); PBI3lI (48 hours), 1.07 per cent (normal 0.1-0.4 per cent); T. index (Russell Fraser), 53.2 (normal 2.8-13.0); 1311 uptake, neck uptake (48 hours), 70.8 per cent; thyroid antibodies, negative; serum calcium, 5.7 mEq. (mean of six estimations) (normal, 4'5-5.5 mEq.). The hypercalcaemia was not suppressed by cortisone administration; her serum calcium values at the end of 10 days (150mg. per day) remained higher than her previous level. Serum inorganic phosphorus was 1.7 mg. (mean of six estimations) (normal 1.6-2.4 mg.); alkaline phosphatase, 9 King-Armstrong units (normal 4-11); strontium space, 19'5 plasma units (normal (18); phosphate excretion index, basal + 0.07, +0.13 (normal *o.og); urinary calcium, 25 mEq. in 24 hours (normal
The coexistence of hyperparathyroidism complicating thyrotoxicosis is quite rare. We report the case of one patient who presented with thyrotoxicosis, (total thyroxine of 15.1 micrograms/dl (5-13), free thyroxine index of 18 (4-15) and triiodothyronine by RIA of 305 ng/dl (70-230) and asymptomatic hypercalcemia of 15 mg/dl (8.5-10.6), who was also initially noted to have an elevated (C-terminal) serum immunoreactive parathyroid hormone (iPTH) level of 8,800 pg/ml (50-340). With propylthiouracil and propranolol, however, this patient became normocalcemic with a decrease in iPTH values to 714 pg/ml. As the patient was tapered from medication, after being rendered euthyroid, a recurrence of hypercalcemia with rising iPTH levels occurred. PTH levels should be helpful in defining coexisting hyperparathyroidism in patients with thyrotoxicosis since in the latter iPTH is usually suppressed. Our findings support the recommendation that in patients suspected of having both hyperparathyroidism and hyperthyroidism, a diagnosis of the former can only be made with certainty after the patient has been rendered euthyroid with persistently elevated serum calcium and iPTH levels. While there are no clinical features which permit the easy identification of patients who present with dual lesions, the determination of iPTH values may be the most consistently helpful test initially, whereas other parameters such as vitamin D, serum phosphate are less reliable.
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