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Abstract: FR-PO600

A Case of Pseudohypoparathyroidism Presenting with Symptomatic Hypocalcemia After Acute Hepatitis Due to Epstein-Barr Virus

Session Information

  • Trainee Case Reports - III
    October 26, 2018 | Location: Exhibit Hall, San Diego Convention Center
    Abstract Time: 10:00 AM - 12:00 PM

Category: Trainee Case Reports

  • 402 Bone and Mineral Metabolism: Clinical

Authors

  • Itayama, Ritsuko, Tokai University School of Medicine, Isehara, Kanagawa, Japan
  • Nakagawa, Yosuke, Tokai University School of Medicine, Isehara, Kanagawa, Japan
  • Isozaki, Yudai, Tokai University School of Medicine, Isehara, Kanagawa, Japan
  • Takahashi, Hiroo, Tokai University School of Medicine, Isehara, Kanagawa, Japan
  • Komaba, Hirotaka, Tokai University School of Medicine, Isehara, Kanagawa, Japan
  • Koizumi, Masahiro, Tokai University School of Medicine, Isehara, Kanagawa, Japan
  • Wada, Takehiko, Tokai University School of Medicine, Isehara, Kanagawa, Japan
  • Fukagawa, Masafumi, Tokai University School of Medicine, Isehara, Kanagawa, Japan
Introduction

Pseudohypoparathyroidism (PHP) type 1b is characterized by isolated resistance to parathyroid hormone without the features of Albright hereditary osteodystrophy (AHO). In PHP type 1b, most cases are sporadic and the timing of development of symptomatic hypocalcemia is quite variable. The initial manifestations of hypocalcemia such as tetany, muscle cramps and convulsion usually occur in childhood or adolescence, but they may be delayed until adulthood. Here, we report a young adult case of PHP type 1b which presenting with hypocalcemic tetany after acute hepatitis due to Epstein-Barr virus infection.

Case Description

A 24-year-old man who had been previously healthy was admitted to the hospital because of nausea and appetite loss followed by tetany for three days. He had been well until two weeks prior to the admission, when he got a febrile pharyngitis with lymphadenopathy. The symptoms were improved by taking some antipyretics and antibiotics, however, general fatigue and appetite loss steadily developed with tetany and weakness. Laboratory test revealed significantly elevated transaminases which indicated acute hepatitis, as well as hypocalcemia, hyperphosphatemia and increased level of intact PTH. Head computed tomography showed bilateral basal ganglia calcification. On the basis of PTH-resistant hypocalcemia without the features of AHO, he was given diagnosis of PHP type 1b and started on calcium and calcitriol. He was symptomatically improved with treatment and his laboratory findings returned to normal range. At the same time, acute hepatitis, which had been proved to be caused by primary Epstein-Bar virus infection, recovered spontaneously.

Discussion

It is unknown what factor triggers symptomatic hypocalcemia in PHP type 1b. In our case, it was considered that decreased synthesis of 25-OH vitamin D in the liver due to acute hepatitis provoked PTH resistance followed by symptomatic hypocalcemia. PHP type 1b might be overlooked and should be taken into account if asymptomatic hypocalcemia is identified.