2 fetal growth were found adequate. She was diagnosed with pseudohypoparathyroidism 1a and prescribed oral calcium (2.5 gm/day) and active vitamin D (1 µg/day) together with levothyroxine 125 µg daily in empty stomach. She had spontaneous onset of labor at 40 weeks of gestation. Her serum calcium was found very low (1.52 mg/dL) but without any seizures or tetany. She was managed with calcium infusion. Augmentation of labour with oxytocin failed to progress, and emergency cesarean section was done under regional anesthesia for nonprogress of labour. She delivered a healthy baby with a birth weight of 3.2 kg with good Apgar score. Her intraoperative and postoperative course was uneventful. She was discharged in satisfactory condition on fourth postpartum day. 3. Discussion PsHP is a disorder of calcium metabolism resulting from renal resistance to PTH. It is characterized by low serum calcium with elevated serum phosphate and parathormone levels. PsHP type 1a also shows resistance to other peptide hormones like thyroid stimulating hormone, gonadotropins, and gluacgon besides PTH. PsHP type 1a presents with characteristic phenotype, collectively called Albright’s hered- itary osteodystrophy. The constellation of ﬁndings includes short stature, stocky habitus, round face, skeletal anomalies, heterotopic calciﬁcation, and developmental delay. Patients may develop symptoms of hypocalcemia like paresthesias, muscle cramps, tetany, carpopedal spasm, or seizure. Pri- mary hypothyroidism occurs in most patients with type 1a PsHP. Women may have delayed puberty, oligomenorrhea, and infertility. Our patient had normal menarche but scanty ﬂow. There are also increased risks of spontaneous abortion, preterm labor, still birth, and intrauterine growth retardation together with increased risk of tetany during labour. She also had similar morphologic features, history of abortion, and symptoms of hypocalcemia together with hypothyroidism corroborating with type 1a PsHP. Intermittent normocalcemia may occur spontaneously in patients with PsHP [2]. Although the exact mechanism is unknown, this is possibly due to PTH-mediated bone resorption [3]. Calcium metabolism is subtly altered in pregnancy, in relation to albumin levels and increased levels of parathyroid hormone. The eﬀects on calcium homeostasis in PsHP during pregnancy are less clear and have rarely been studied [4]. During pregnancy, fetus avidly draw calcium from maternal circulation via active placental transport predisposing mother to hypocalcemia and its sequel [5]. Most such patient, requires therapeutic calcium and vitamin D supplementation to avoid maternal symptoms while ensuring adequate calcium supply to the fetus. However, some patients may become normocalcemic during pregnancy without ingesting therapeutic calcium and vitamin D. The mechanism by which PsHP improves during pregnancy is unclear. It may include placental secretion of parathyroid hormone-related protein (PHTrP) and calcitriol whose level has been reported to double or triple during second and third trimester of pregnancy in a report of two cases [6]. Case Reports in Obstetrics and Gynecology In pregnancy with PsHP, serum calcium needs frequent monitoring. It should not be allowed to fall below 6.8 mg/dL (1.70 mmol/L) to avoid preterm labor or midtrimester abortion. Hyperventilation during labor may precipitate hypocalcemia and -tetany, thus needs to be discouraged. Labour analgesia may be of some help by giving pain relief. Thyroxin supplementation and frequent monitoring of thyroid function are needed to maintain euthyroid status during pregnancy so as to avoid side eﬀects of hypothy- roidism on fetus. Fetus may also develop transient secondary hyperparathyroidism, leading to skeletal demineralization, subperiosteal bone resorption, osteitis ﬁbrosa cystica, and intrauterine fractures. The eﬀect is usually transient, man- ifests as poor feeding and fractures usually resolved by 7-8 months of life. During lactation, the requirement of calcium changes and needs frequent monitoring. The calcitriol dose should be reduced during lactation. The goal of therapy is to maintain serum total and ionized calcium level within reference range while avoiding hypercalciuria and to suppress PTH level to normal. Rarely elevated PTH levels in PsHP may cause increased bone remodeling leading to hyperparathyroid bone disease. 4. Conclusion The management of PsHP in pregnancy is quite intriguing. It needs regular calcium monitoring throughout pregnancy, labor, and postpartum period together with therapeutic supplementation of calcium and vitamin D as needed. The aim is to keep serum calcium in low normal range as overzealous calcium and vitamin D supplementation can cause hypercalcemia, hypercalciuria, and ectopic calciﬁca- tion. Keeping patients euthyroid with thyroxin supplemen- tation is important for normal fetal development. References [1] D. O’Donnell, J. Costa, and A. M. Meyers, “Management of pseudohypoparathyroidism in pregnancy. Case report,” British Journal of Obstetrics and Gynaecology, vol. 92, no. 6, pp. 639– 641, 1985. [2] N. A. Breslau, D. D. Notman, J. M. Canterbury, and A. M. Moses, “Studies on the attainment of normocalcemia in patients with pseudohypoparathyroidism,” American Journal of Medicine, vol. 68, no. 6, pp. 856–860, 1980. [3] N. A. Breslau, A. M. Moses, and C. Y. C. Pak, “Evidence for bone remodeling but lack of calcium mobilization response to parathyroid hormone in pseudohypoparathyroidism,” Journal of Clinical Endocrinology and Metabolism, vol. 57, no. 3, pp. 638–644, 1983. [4] H. Gershberg and A. C. Weseley, “Pseudohypoparathyroidism and pregnancy,” The Journal of Pediatrics, vol. 56, no. 3, pp. 383– 386, 1960. [5] T. E. Croley, “The intracellular localization of calcium within the mature human placental barrier,” American Journal of Obstetrics and Gynecology, vol. 117, no. 7, pp. 926–932, 1973. [6] N. A. Breslau and J. E. Zerwekh, “Relationship of estrogen and pregnancy to calcium homeostasis in pseudohypoparathy- roidism,” Journal of Clinical Endocrinology and Metabolism, vol. 62, no. 1, pp. 45–50, 1986.