Induction of FGF23-related hypophosphatemic osteomalacia by alcohol consumption

Autor: Seiji Fukumoto, Nobuaki Ito, Noriko Makita, Masaki Katsura, Yuka Kinoshita, Masaomi Nangaku, Minae Koga, Hajime Kato, Yuko Oyama, Naoko Hidaka
Rok vydání: 2021
Předmět:
Zdroj: Bone Reports
Bone Reports, Vol 15, Iss, Pp 101144-(2021)
ISSN: 2352-1872
Popis: Context Fibroblast growth factor (FGF) 23 is a hormone that regulates serum phosphate levels, the excess action of which causes chronic hypophosphatemic rickets/osteomalacia. To date, there are only two identified causes of acquired FGF23-related hypophosphatemic osteomalacia: tumor-induced osteomalacia (TIO) and osteomalacia induced by the intravenous infusion of some forms of iron preparations. In the current study, two cases of FGF23-related hypophosphatemia probably induced by chronic alcohol consumption were first introduced. Case description Case 1 and case 2 had been drinking high amounts of alcohol for more than twenty years until they were admitted to the hospital. Case 1 was a 43-year-old man with progressive worsening multiple pains and muscle weakness who exhibited chronic hypophosphatemia with increased intact FGF23 levels. A week after admission, the serum phosphate level recovered to the reference range, and the intact FGF23 level declined. Case 1 resumed drinking after discharge, and hypophosphatemia concomitant with high intact FGF23 levels recurred. The alleviation of FGF23-related hypophosphatemia was observed each time he temporarily abstained from drinking for a short period. Case 2 was a 60-year-old man with recurrent fractures and exacerbation of pain in multiple joints who also exhibited hypophosphatemia with increased intact FGF23 levels. After admission, the serum phosphate level gradually increased to the lower limit of the normal range. The intact FGF23 level decreased, but it was still higher than 30 pg/ml, and causative FGF23-producing tumors were not identified even with thorough examinations, including somatostatin receptor scintigraphy, fluorine-18-fluorodeoxyglucose-positron emission tomography/computed tomography (18F-FDG-PET/CT) and systemic venous FGF23 sampling. He completely abstained from alcohol after discharge. Along with the serum phosphate level, intact FGF23 was subsequently decreased and had been normalized for 5 months. Both patients had no genetic mutation related to hereditary FGF23-related hypophosphatemic rickets/osteomalacia, including autosomal dominant hypophosphatemic rickets/osteomalacia (ADHR). Conclusion Two cases of FGF23-related hypophosphatemia probably induced by alcohol were first introduced in this study. Identifying this reversible condition among acquired FGF23-related hypophosphatemic osteomalacia is critical to obtain better patient outcomes and save medical resources. This condition is similar to iron infusion-induced FGF23-related hypophosphatemia in terms of the dysregulation of FGF23 due to exogenous factors. Future research to elucidate the precise mechanism of these conditions is warranted.
Highlights • Two adults with acquired FGF23-related hypophosphatemic osteomalacia were studied. • Tumor-induced osteomalacia was suspected initially, but no tumor was identified. • Cessation of alcohol led to recovery from FGF23-related hypophosphatemia. • Alcohol is a well-recognized cause of hypophosphatemia, but osteomalacia is uncommon. • Alcohol-induced FGF23-related osteomalacia is a totally new and distinct phenomenon.
Databáze: OpenAIRE