Acta Obstet Gynec Scand 54: 281-283, 1975
CASE REPORTS HYPERPARATHYROIDISM AND PREGNANCY Report of a C a s e and Review of the Literature
Niels Thorsgaard Pedersen and Henrik Permin From the Department of Gynaecology and Obstetrics (Heads: Dr H . Lefevre, Dr J . Weber and Dr E. Naver), the Medical Department B (Heads: Dr E. D . Barrels and Dr H . E. Jsrgensen) and the Surgical Department D (Heads: Dr M . Ottsen, Dr P . Ejby Poulsen and Dr 0.Storm). Glostrup Hospital, Copenhagen, Denmark
Abstract. A 28-year-old gravida 111, with a history of two unsuccessful pregnancies, was admitted with hyperemesis gravidarum and was found to be suffering from hyperparathyroidism (HPT). She was treated surgically and was later delivered of a wellformed, premature girl. The literature is reviewed and the histories of 40 females (including the patient of this case report) with a minimum of 93 pregnancies while suffering from HPT shows, that HPT during pregnancy is a serious condition for the fetus as well as for the mother. There was an increased incidence of spontaneous abortion, pennatal death, premature birth and neonatal morbidity. The mothers suffered from increased episodes of renal calculi and hyperemesis gravidarum. The exacerbations nearly always occurred in the first and second trimesters or post partum.
CA SE HISTORY
Hyperparathyroidism (HPT) is reported t o occur
in 4% of the adult Danish population, somewhat more often in women than in men (26), but it is not diagnosed in nearly as many cases. Th e explanation is that the disease may run a fairlq silent course, having exacerbations simulating o th e r diseases e.g. renal calculi, duodenal ulcer ' bone pain, constipation, an d depression. Therefore. a number o f exacerbations usually occur before t h e true nature of the disease is realized. Latent HPT may be provoked and thus become manifest. Provocative factors have been reported t o be bed rest, operation, rough palpation on the neck, dehydration, and infection (3, 32). By means of the present case report and a study of the literature o n HPT in connection with pregnancy, we are trying t o demonstrate that pregnancy, too, may provoke an exacerbation of HPT.
'
Past history. In 1962 the patient, aged 19 years, had experienced isolated episodes of low-back pain and haematuria and had observed passage of calculi. She was pregnant for the first time, and the expected date of delivery was the middle of September 1%5. At the beginning of the pregnancy, however, she developed severe nausea and vomiting, accompanied by weight loss. She was admitted to a hospital elsewhere on 9.2.1%5. The symptoms subsided on conservative treatment. The serum calcium was not determined during this stay in hospital. On 23.7.1%5 the patient was readmitted to the same hospital, as she had now again had nausea and vomiting for 6 days. Between the two admissions she had been feeling perfectly well. After admission no fetal movements were felt. A few days later the patient delivered a stillborn, macerated male fetus, weight I550 g, length 39 cm. Numerous infarcts were found in the placenta. On the 14.6.1966 the patient again was admitted to the same hospital with hyperemesis gravidarum. The size of uterus was found to correspond to 6th-8th week pregnancy. It proved impossible to arrest the hyperemesis, and uterine curettage was performed. Thereafter the patient felt well. The serum calcium was not determined. Present admission. On 23. I I . 1971 the patient. now aged 28 years, and in her third pregnancy, was admitted to Glostrup Hospital with hyperemesis gravidarum. She was in the 9th week of pregnancy. During the past 5 weeks she had had nausea and 4-10 vomits daily, with a total weight loss of 6 kg. The patient was emaciated and dehydrated, weighing 37 kg, height 163 cm and BP 100/80. Gynaecological examination showed no abnormality. The size of uterus corresponded to an 8week pregnancy. Physical examination showed no goitre and no palpable masses on the neck. The total serum calcium was elevated, 170 mg/l (normal 90-105 mg/l), ultrafiltrable calcium 99 mg/l (normal 54-64 mg/l), seActo Obsret Gynec Scond54 (1975)
282
N. Thorsgaard Pedersen and H . Permin
rum phosphate 19 mg/l (normal 20-50 mg/l), serum creatinine 11 mg/l, creatinine clearance 66 ml/min, alkaline phosphatases 6.9 U/ml (normal 3.0-10.0 U/ml), total protein 68 g/l and Hgb 98 g/l. A cortisone suppression test was performed with cortisone acetate tablets, 50 mg 3 times daily for 10 days. Serum calcium remained at an unchanged, elevated level throughout the test. X-rays of the hands revealed a translucency in the distal phalanx of the left little finger. Moreover translucencies were found in both medial malleoli. Somewhat decreased calcium content in the right humerus. Radiography of the chest and dental alveoli showed no abnormalities. After an unsuccessful attempt to find the tumour on 6.12.1971 a new exploration of the neck was made on 29.12. A flat, pedunculated, greyish-red tumour, I x 1 xa cm was found on the right of the upper pole of the thyroid gland. Histological examination: Well-defined adenoma consisting predominantly of fairly large chief cells. Minor accumulation of oxyphilic cells and “waterclear’’ cells. Diagnosis: Parathyroid adenoma. The postoperative course was uneventful. The patient was admitted on 26.5.1972, in the 36th week of gestation, as the waters had passed. Two days later she was delivered of a girl weighing 1910 g, 47 cm in length. The baby thrived well and was discharged on 19.6 in a good general condition. The serum calcium was normal. At an out-patient visit on 3.7.1973 mother as well as infant were in good health and serum calcium was normal.
DISCUSSION According to the past history, this patient has presumably had HPT for 9 years. For long periods, the course has been fairly silent, but there were exacerbations in connection with the pregnancies. During all 3 pregnancies, the patient developed severe nausea and vomiting. A contributary cause of the long course was probably that these symptoms are common complaints also in pregnancies without HPT. ‘Perusing the literature we found reports of 40 pregnant women with HPT (1-2, 4-16, 18-25, 2731), including the patient of this case report. These women went through a minimum of 93 pregnancies while suffering from HPT. Of these pregnancies 39 were complicated by purely maternal complaints, most often renal calculi, skeletal diseases and hyperemesis gravidarum. Thus, 7 patients (7, 15, 19, 25, 30. 31) had hyperemesis without this complaint leading to a diagnosis of HPT. It was characteristic of the present case, that the symptoms appeared at a very early stage of the pregnancy, each time about two weeks after the first missed period. Out of the 39 pregnancies Acto Obstet Gynec Scond 54 (1975)
reported to have shown purely maternal symptoms, we found 22 statements about the time at which the maternal symptoms had set in. In 7 pregnancies the symptoms occurred early (2,7, 15, 19, 21, 28, 31), in 9 cases in the 5th-6th month (4, 8, 13, 18, 21, 28, 31), and in 5 cases post partum (10, 16, 23, 28). In addition to the present patient, yet another one (19) has exhibited symptoms in the 3rd trimester. The symptoms in the first pregnancy of the present patient returned in the 3rd trimester, possibly because of the fall in estriol production caused by intrauterine death of the fetus. The symptoms ceased shortly after the pregnancy ended. There is no explanation why the exacerbations in HPT occurred at the times stated, but the findings are in keeping with Lehr & Krukowski’s observations from experiments on rats (17). These workers found, that in the last trimester of pregnancy rats could tolerate an injected dose of parathyroid hormone (PTH), which was fatal in nonpregnant rats and in rats in the first and second trimesters. The onset of symptoms at the beginning of pregnancy and their disappearance shortly after the first 2 pregnancies had been terminated in our patient appear to show that pregnancy has an adverse influence upon the course of HPT and may provoke an exacerbation. This hypothesis has previously been advanced by Spingarn & Geist (25) and Clerc (7) whose patients had a distinct exacerbation of HPT at the onset of pregnancy. Wagner et al. (28), analysing a series of 23 women having a minimum of 34 pregnancies in the course of their HPT, compared the findings with those in 138 patients making up a consecutive series of HPT. They found the serum calcium level in the pregnant patients to be on average higher than among the non-pregnant patients. They also observed that the mean period from the initial sign of HPT until it was diagnosed was half as long in pregnant women with HPT as in the non-pregnant patients. The comparison showed, moreover, that among pregnant patients there was a somewhat higher incidence of ske:etal changes than in non-pregnant patients. Also, for the fetus, HPT is a serious complication. Among the 93 cases were 21 instances of spontaneous abortion or perinatal death. In a further 16 cases there occurred premature deliveries and neonatal morbidity, especially neonatal tetany.
Hyperparathyroidism and pregnancy T h u s HPT is a serious complication of pregnancy-just as pregnancy is a serious complication of HPT. T h e diagnosis is made in pregnant patients o n the basis of the same criteria as in nonpregnant persons, i.e. primarily by demonstrating an elevated total serum calcium or (better) by demonstrating elevated ultrafiltrable calcium or ionized calcium. For the purpose of differentiating between hypercalcaemia d u e to HPT and hypercalcaemia due t o other causes, a cortisone suppression test was performed in t h e present case. It did not give rise t o side effects in t h e mother or infant. In 1947 Petit & Clark (21) were t h e first t o remove a parathyroid adenoma successfully in a pregnant patient. Since then, this operation has been carried out in 5 cases (8, 12, 16, 18, 22), every time with a good result. Our patient also stood the operation well.
283
12. Goldsmith, R. E., Salme, E. & Weinstein, A. S.: Clinical experience with primary hyperparathyroidism. Acta Endocrinol52: 221, 1966. 13. Hartenstein, H. & Gardner, L. I.: Tetany of the newborn associated with maternal parathyroid adenoma. N Engl J Med 274: 266,1%6. 14. Hunter, D. & Turnbull, H. M.: Hyperparathyroidism. Br J Surg 19: 203, 1931. 15. Hutchin, P. & Kessner, D. M.: Neonatal tetany. Ann Intern Med61: 1109, 1964. 16. Johnstone, R. E.,Kreindler, T. & Johnstone, R. E.: Hyperparathyroidism during pregnancy. Obstet Gynecol40: 580, 1972. 17. Lehr, D. & Krukowski, M.: Protection by pregnancy against the sequelae of acute hyperparathyroidism. Arch Exp Pathol Pharmakol 242: 143, 1961. 18. Ludwig, G . D.:Hyperparathyroidism in relation to pregnancy. N Engl J Med 267: 637, 1%2. 19. McGeown, M. G. & Field, C. M. B.: Asymptomatic Hyperparathyroidism. Lancet 2: 1268, 1960. 20. Mizrahi, A. & Gold, A. P.: Neonatal tetany secondary to maternal hyperparathyroidism. JAMA 190: 155, 1964.
ACKNOWLEDGEMENT Thanks to Dr Herluf Jensen, Medical Department B, Glostrup Hospital, for great help with this case report.
REFERENCES 1. Baehr, G.: Personal communication to Spingarn &
Geist (25). 2. Bevere, L. & Somentino, B.: Contributio allo studio dell'osteite fibro-cistica generalizzata. Riforma Med 48:313. 1932. 3. Boquist, L., Bergdahl, L. & Anderson, A.: Parathyroid adenoma complicated by acute hyperparathyroidism. Ann Surg 173: 593, 1971. 4. Bramley, P. & Dwyer, D.: Primary hyperparathyroidism. Oral Surg30: 464, 1970. 5 . Bruce, J. & Strong, J. A.: Maternal hyperparathyroidism and parathyroid deficiency in the child. Q J Med 24: 307, 1955. 6. Buchs, S.: Congenital hypoparathyroidism in 3 bro:hers following hyperparathyroidism in the mother. Schweiz Med Wschr91: 660, 1%1. 7. Clerc, J . L.: Ein Fall von Osteitis fibrosa generalisata in der Schwangerschaft. Gynaecologia 121: 152, 1946. 8. Findlay, W. S.: Hyperparathyroidism complicating pregnancy. Proc Roy SOCMed62: 835, 1969. 9. Friderichsen, C.: Tetany in suckling with latent osteitis fibrosa in mother. Lancet I: 85, 1939. 10. Frohner, R. N. & Wolgamot. J. C.: Primary hyperparathyroidism: Five cases in one family. A n n Intern Med 40: 765, 1954. 1 1 . Garlock, J . H.:Differential diagnosis of hyperparathyroidism. Ann Surg 108: 347, 1938. 20-752863
21. Petit, D. W. & Clark, R. L.: Hyperparathyroidism and pregnancy. Am J Surg 74: 860, 1947. 22. Rubin, A., Chaykin, L. & Ludwig, G. D.: Maternal hyperparathyroidism and pregnancy. JAMA 206: 128, 1968. 23. Schenker, J. G. & Kqllner, B.: Fatal postpartum hyperparathyroid crisis due to primary chief cell hyperplasia of parathyroids. Obstet Gynecol 25: 705, 1%5. 24. Schlesinger, H. & Goid, E.: Osteitis fibrosa cystica generalisata Rechlinghausen mit intrathyroidalem Epithelkorpertumor. Klin Wschr 12: 784, 1933. 25. Spingarn, C. L. & Geist, S. H.: Hyperparathyroidism and pregnancy. JAMA 113: 2387. 1939. 26. Transbel, 1.: Glandulae parathyreoideae - fysiologi, patofysiologi og klinik. Mdskr prakt kgeg 47: 421, 1967. 27. VanArsden, P. P.: Maternal hyperparathyroidism as a cause of neonatal tetany. J Clin Endocrinol 15: 680, 1955. 28. Wagner, G., Transbel, 1. & Melchior, J. C.: Hyperparathyroidism and pregnancy. Acta Endocrinol 47:549, 1964. 29. Walton, A. J.: Surgical treatment of parathyroid tumours. Br J Surg 19: 285, 1931. 30. Walton, R. L.: Neonatal tetany in two siblings: Effect of maternal hyperparathyroidism. Pediatrics 13: 227, 1954. 31. Whalley. P. J.: Hyperparathyroidism and pregnancy. Am J Obst Gynecol86:517, 1963. Submitted for publication Oct, 23, 1973 Henrik Parmin Kildevaenget 33 2100 Copenhagen 0 Denmark Acta Obstet Gynec Scand 54 (1975)
CASE REPORTS HYPERPARATHYROIDISM AND PREGNANCY Report of a C a s e and Review of the Literature
Niels Thorsgaard Pedersen and Henrik Permin From the Department of Gynaecology and Obstetrics (Heads: Dr H . Lefevre, Dr J . Weber and Dr E. Naver), the Medical Department B (Heads: Dr E. D . Barrels and Dr H . E. Jsrgensen) and the Surgical Department D (Heads: Dr M . Ottsen, Dr P . Ejby Poulsen and Dr 0.Storm). Glostrup Hospital, Copenhagen, Denmark
Abstract. A 28-year-old gravida 111, with a history of two unsuccessful pregnancies, was admitted with hyperemesis gravidarum and was found to be suffering from hyperparathyroidism (HPT). She was treated surgically and was later delivered of a wellformed, premature girl. The literature is reviewed and the histories of 40 females (including the patient of this case report) with a minimum of 93 pregnancies while suffering from HPT shows, that HPT during pregnancy is a serious condition for the fetus as well as for the mother. There was an increased incidence of spontaneous abortion, pennatal death, premature birth and neonatal morbidity. The mothers suffered from increased episodes of renal calculi and hyperemesis gravidarum. The exacerbations nearly always occurred in the first and second trimesters or post partum.
CA SE HISTORY
Hyperparathyroidism (HPT) is reported t o occur
in 4% of the adult Danish population, somewhat more often in women than in men (26), but it is not diagnosed in nearly as many cases. Th e explanation is that the disease may run a fairlq silent course, having exacerbations simulating o th e r diseases e.g. renal calculi, duodenal ulcer ' bone pain, constipation, an d depression. Therefore. a number o f exacerbations usually occur before t h e true nature of the disease is realized. Latent HPT may be provoked and thus become manifest. Provocative factors have been reported t o be bed rest, operation, rough palpation on the neck, dehydration, and infection (3, 32). By means of the present case report and a study of the literature o n HPT in connection with pregnancy, we are trying t o demonstrate that pregnancy, too, may provoke an exacerbation of HPT.
'
Past history. In 1962 the patient, aged 19 years, had experienced isolated episodes of low-back pain and haematuria and had observed passage of calculi. She was pregnant for the first time, and the expected date of delivery was the middle of September 1%5. At the beginning of the pregnancy, however, she developed severe nausea and vomiting, accompanied by weight loss. She was admitted to a hospital elsewhere on 9.2.1%5. The symptoms subsided on conservative treatment. The serum calcium was not determined during this stay in hospital. On 23.7.1%5 the patient was readmitted to the same hospital, as she had now again had nausea and vomiting for 6 days. Between the two admissions she had been feeling perfectly well. After admission no fetal movements were felt. A few days later the patient delivered a stillborn, macerated male fetus, weight I550 g, length 39 cm. Numerous infarcts were found in the placenta. On the 14.6.1966 the patient again was admitted to the same hospital with hyperemesis gravidarum. The size of uterus was found to correspond to 6th-8th week pregnancy. It proved impossible to arrest the hyperemesis, and uterine curettage was performed. Thereafter the patient felt well. The serum calcium was not determined. Present admission. On 23. I I . 1971 the patient. now aged 28 years, and in her third pregnancy, was admitted to Glostrup Hospital with hyperemesis gravidarum. She was in the 9th week of pregnancy. During the past 5 weeks she had had nausea and 4-10 vomits daily, with a total weight loss of 6 kg. The patient was emaciated and dehydrated, weighing 37 kg, height 163 cm and BP 100/80. Gynaecological examination showed no abnormality. The size of uterus corresponded to an 8week pregnancy. Physical examination showed no goitre and no palpable masses on the neck. The total serum calcium was elevated, 170 mg/l (normal 90-105 mg/l), ultrafiltrable calcium 99 mg/l (normal 54-64 mg/l), seActo Obsret Gynec Scond54 (1975)
282
N. Thorsgaard Pedersen and H . Permin
rum phosphate 19 mg/l (normal 20-50 mg/l), serum creatinine 11 mg/l, creatinine clearance 66 ml/min, alkaline phosphatases 6.9 U/ml (normal 3.0-10.0 U/ml), total protein 68 g/l and Hgb 98 g/l. A cortisone suppression test was performed with cortisone acetate tablets, 50 mg 3 times daily for 10 days. Serum calcium remained at an unchanged, elevated level throughout the test. X-rays of the hands revealed a translucency in the distal phalanx of the left little finger. Moreover translucencies were found in both medial malleoli. Somewhat decreased calcium content in the right humerus. Radiography of the chest and dental alveoli showed no abnormalities. After an unsuccessful attempt to find the tumour on 6.12.1971 a new exploration of the neck was made on 29.12. A flat, pedunculated, greyish-red tumour, I x 1 xa cm was found on the right of the upper pole of the thyroid gland. Histological examination: Well-defined adenoma consisting predominantly of fairly large chief cells. Minor accumulation of oxyphilic cells and “waterclear’’ cells. Diagnosis: Parathyroid adenoma. The postoperative course was uneventful. The patient was admitted on 26.5.1972, in the 36th week of gestation, as the waters had passed. Two days later she was delivered of a girl weighing 1910 g, 47 cm in length. The baby thrived well and was discharged on 19.6 in a good general condition. The serum calcium was normal. At an out-patient visit on 3.7.1973 mother as well as infant were in good health and serum calcium was normal.
DISCUSSION According to the past history, this patient has presumably had HPT for 9 years. For long periods, the course has been fairly silent, but there were exacerbations in connection with the pregnancies. During all 3 pregnancies, the patient developed severe nausea and vomiting. A contributary cause of the long course was probably that these symptoms are common complaints also in pregnancies without HPT. ‘Perusing the literature we found reports of 40 pregnant women with HPT (1-2, 4-16, 18-25, 2731), including the patient of this case report. These women went through a minimum of 93 pregnancies while suffering from HPT. Of these pregnancies 39 were complicated by purely maternal complaints, most often renal calculi, skeletal diseases and hyperemesis gravidarum. Thus, 7 patients (7, 15, 19, 25, 30. 31) had hyperemesis without this complaint leading to a diagnosis of HPT. It was characteristic of the present case, that the symptoms appeared at a very early stage of the pregnancy, each time about two weeks after the first missed period. Out of the 39 pregnancies Acto Obstet Gynec Scond 54 (1975)
reported to have shown purely maternal symptoms, we found 22 statements about the time at which the maternal symptoms had set in. In 7 pregnancies the symptoms occurred early (2,7, 15, 19, 21, 28, 31), in 9 cases in the 5th-6th month (4, 8, 13, 18, 21, 28, 31), and in 5 cases post partum (10, 16, 23, 28). In addition to the present patient, yet another one (19) has exhibited symptoms in the 3rd trimester. The symptoms in the first pregnancy of the present patient returned in the 3rd trimester, possibly because of the fall in estriol production caused by intrauterine death of the fetus. The symptoms ceased shortly after the pregnancy ended. There is no explanation why the exacerbations in HPT occurred at the times stated, but the findings are in keeping with Lehr & Krukowski’s observations from experiments on rats (17). These workers found, that in the last trimester of pregnancy rats could tolerate an injected dose of parathyroid hormone (PTH), which was fatal in nonpregnant rats and in rats in the first and second trimesters. The onset of symptoms at the beginning of pregnancy and their disappearance shortly after the first 2 pregnancies had been terminated in our patient appear to show that pregnancy has an adverse influence upon the course of HPT and may provoke an exacerbation. This hypothesis has previously been advanced by Spingarn & Geist (25) and Clerc (7) whose patients had a distinct exacerbation of HPT at the onset of pregnancy. Wagner et al. (28), analysing a series of 23 women having a minimum of 34 pregnancies in the course of their HPT, compared the findings with those in 138 patients making up a consecutive series of HPT. They found the serum calcium level in the pregnant patients to be on average higher than among the non-pregnant patients. They also observed that the mean period from the initial sign of HPT until it was diagnosed was half as long in pregnant women with HPT as in the non-pregnant patients. The comparison showed, moreover, that among pregnant patients there was a somewhat higher incidence of ske:etal changes than in non-pregnant patients. Also, for the fetus, HPT is a serious complication. Among the 93 cases were 21 instances of spontaneous abortion or perinatal death. In a further 16 cases there occurred premature deliveries and neonatal morbidity, especially neonatal tetany.
Hyperparathyroidism and pregnancy T h u s HPT is a serious complication of pregnancy-just as pregnancy is a serious complication of HPT. T h e diagnosis is made in pregnant patients o n the basis of the same criteria as in nonpregnant persons, i.e. primarily by demonstrating an elevated total serum calcium or (better) by demonstrating elevated ultrafiltrable calcium or ionized calcium. For the purpose of differentiating between hypercalcaemia d u e to HPT and hypercalcaemia due t o other causes, a cortisone suppression test was performed in t h e present case. It did not give rise t o side effects in t h e mother or infant. In 1947 Petit & Clark (21) were t h e first t o remove a parathyroid adenoma successfully in a pregnant patient. Since then, this operation has been carried out in 5 cases (8, 12, 16, 18, 22), every time with a good result. Our patient also stood the operation well.
283
12. Goldsmith, R. E., Salme, E. & Weinstein, A. S.: Clinical experience with primary hyperparathyroidism. Acta Endocrinol52: 221, 1966. 13. Hartenstein, H. & Gardner, L. I.: Tetany of the newborn associated with maternal parathyroid adenoma. N Engl J Med 274: 266,1%6. 14. Hunter, D. & Turnbull, H. M.: Hyperparathyroidism. Br J Surg 19: 203, 1931. 15. Hutchin, P. & Kessner, D. M.: Neonatal tetany. Ann Intern Med61: 1109, 1964. 16. Johnstone, R. E.,Kreindler, T. & Johnstone, R. E.: Hyperparathyroidism during pregnancy. Obstet Gynecol40: 580, 1972. 17. Lehr, D. & Krukowski, M.: Protection by pregnancy against the sequelae of acute hyperparathyroidism. Arch Exp Pathol Pharmakol 242: 143, 1961. 18. Ludwig, G . D.:Hyperparathyroidism in relation to pregnancy. N Engl J Med 267: 637, 1%2. 19. McGeown, M. G. & Field, C. M. B.: Asymptomatic Hyperparathyroidism. Lancet 2: 1268, 1960. 20. Mizrahi, A. & Gold, A. P.: Neonatal tetany secondary to maternal hyperparathyroidism. JAMA 190: 155, 1964.
ACKNOWLEDGEMENT Thanks to Dr Herluf Jensen, Medical Department B, Glostrup Hospital, for great help with this case report.
REFERENCES 1. Baehr, G.: Personal communication to Spingarn &
Geist (25). 2. Bevere, L. & Somentino, B.: Contributio allo studio dell'osteite fibro-cistica generalizzata. Riforma Med 48:313. 1932. 3. Boquist, L., Bergdahl, L. & Anderson, A.: Parathyroid adenoma complicated by acute hyperparathyroidism. Ann Surg 173: 593, 1971. 4. Bramley, P. & Dwyer, D.: Primary hyperparathyroidism. Oral Surg30: 464, 1970. 5 . Bruce, J. & Strong, J. A.: Maternal hyperparathyroidism and parathyroid deficiency in the child. Q J Med 24: 307, 1955. 6. Buchs, S.: Congenital hypoparathyroidism in 3 bro:hers following hyperparathyroidism in the mother. Schweiz Med Wschr91: 660, 1%1. 7. Clerc, J . L.: Ein Fall von Osteitis fibrosa generalisata in der Schwangerschaft. Gynaecologia 121: 152, 1946. 8. Findlay, W. S.: Hyperparathyroidism complicating pregnancy. Proc Roy SOCMed62: 835, 1969. 9. Friderichsen, C.: Tetany in suckling with latent osteitis fibrosa in mother. Lancet I: 85, 1939. 10. Frohner, R. N. & Wolgamot. J. C.: Primary hyperparathyroidism: Five cases in one family. A n n Intern Med 40: 765, 1954. 1 1 . Garlock, J . H.:Differential diagnosis of hyperparathyroidism. Ann Surg 108: 347, 1938. 20-752863
21. Petit, D. W. & Clark, R. L.: Hyperparathyroidism and pregnancy. Am J Surg 74: 860, 1947. 22. Rubin, A., Chaykin, L. & Ludwig, G. D.: Maternal hyperparathyroidism and pregnancy. JAMA 206: 128, 1968. 23. Schenker, J. G. & Kqllner, B.: Fatal postpartum hyperparathyroid crisis due to primary chief cell hyperplasia of parathyroids. Obstet Gynecol 25: 705, 1%5. 24. Schlesinger, H. & Goid, E.: Osteitis fibrosa cystica generalisata Rechlinghausen mit intrathyroidalem Epithelkorpertumor. Klin Wschr 12: 784, 1933. 25. Spingarn, C. L. & Geist, S. H.: Hyperparathyroidism and pregnancy. JAMA 113: 2387. 1939. 26. Transbel, 1.: Glandulae parathyreoideae - fysiologi, patofysiologi og klinik. Mdskr prakt kgeg 47: 421, 1967. 27. VanArsden, P. P.: Maternal hyperparathyroidism as a cause of neonatal tetany. J Clin Endocrinol 15: 680, 1955. 28. Wagner, G., Transbel, 1. & Melchior, J. C.: Hyperparathyroidism and pregnancy. Acta Endocrinol 47:549, 1964. 29. Walton, A. J.: Surgical treatment of parathyroid tumours. Br J Surg 19: 285, 1931. 30. Walton, R. L.: Neonatal tetany in two siblings: Effect of maternal hyperparathyroidism. Pediatrics 13: 227, 1954. 31. Whalley. P. J.: Hyperparathyroidism and pregnancy. Am J Obst Gynecol86:517, 1963. Submitted for publication Oct, 23, 1973 Henrik Parmin Kildevaenget 33 2100 Copenhagen 0 Denmark Acta Obstet Gynec Scand 54 (1975)
