De novo autoimmune hepatitis associated with PTH(1-34) and PTH(1-84) administration for severe osteoporosis in a liver transplant patient

P. Anagnostis; Z. Efstathiadou; E. Akriviadis; P. Hytiroglou; M. Kita

P133

Prev Next

Section Contents Cite

Endocrine Abstracts (2012) 29 P133

ICEECE2012 Poster Presentations Bone & Osteoporosis (67 abstracts)

De novo autoimmune hepatitis associated with PTH(1–34) and PTH(1–84) administration for severe osteoporosis in a liver transplant patient

P. Anagnostis ¹ , Z. Efstathiadou ¹ , E. Akriviadis ² , P. Hytiroglou ² & M. Kita ¹

Err

Author affiliations

¹Hippokration Hospital of Thessaloniki, Thessaloniki, Greece; ²Aristotle University of Thessaloniki, Thessaloniki, Greece.

Introduction: Recombinant parathyroid hormone 1–34 (PTH(1–34)) and 1–84 (PTH(1–84)) stimulate new bone formation and are associated with significant decrease in the risk of vertebral and non-vertebral fractures. De novo autoimmune hepatitis (AIH) is a rare graft dysfunction occurring in patients having undergone liver transplantation (LT) for causes other than AIH.

Case report: A 61-year old woman was referred to our metabolic bone clinic due to severe osteoporosis (T-score of −2.7 in lumbar spine and −3.2 in femoral neck), 3 years after LT for primary biliary cirrhosis. The investigation for other conditions compromising her bone health revealed only vitamin D deficiency.

Taking into consideration the patient’s severe osteoporosis in need of treatment, along with the impaired renal function that made the use of bisphosphonates rather problematic in addition to the prior use of glucocorticoids, the decision to proceed to teriparatide (PTH(1–34)) administration along with calcium carbonate 1000 mg and cholecalciferol 800 IU/day was made. At 3 month-assessment, asymptomatic hypertransaminasemia (two-fold the upper limit of normal) developed, which normalized after drug discontinuation.

A new flare of transaminases (three-fold the upper limit of normal), along with elevated alkaline phosphatase, was observed, after administration of PTH(1–84), which did not resolve after PTH(1-84) withdrawal. After exclusion of common causes of liver enzyme elevation, a liver biopsy was performed. Histological findings showed de novo AIH, which responded rapidly to treatment with methylprednisolone.

Conclusions: To our knowledge, this is the first case described in the literature involving development of post-LT de novo AIH, following PTH administration for severe osteoporosis. The exact mechanisms linking PTH with AIH are not clarified. However, it can be hypothesized that, since Kuppfer cells in the liver are implicated in PTH degradation, expressing the PTH/PTH-related protein type 1 receptor, they produce interleukin-6 which plays an important role in the pathogenesis of AIH.

Declaration of interest: The authors declare that there is no conflict of interest that could be perceived as prejudicing the impartiality of the research project.

Funding: This research did not receive any specific grant from any funding agency in the public, commercial or not-for-profit sector.