Successful Superficial Blood Sampling to Localize a Fibroblast Growth Factor-23-Producing Tumor.

BACKGROUND Tumor-induced osteomalacia (TIO) is a paraneoplastic syndrome caused by aberrant fibroblast growth factor-23 (FGF-23)-producing tumors. Early surgical resection is the optimal strategy for preventing TIO progression. Thus, tumor localization is a priority for successful treatment. A simple and safe examination method to identify functional endocrine tumors is essential to achieve better outcomes in patients with TIO. CASE REPORT A 64-year-old Japanese man with recurrent fractures, hypophosphatemia, and elevated alkaline phosphatase and FGF-23 levels (109 pg/mL) was admitted to our university hospital and was diagnosed with FGF23-related hypophosphatemic osteomalacia. Notably, the superficial dorsal vein in the patient's left foot exhibited a high FGF-23 level (7510 pg/mL). Octreotide and ¹8F-fluorodeoxyglucose (FDG) scintigraphy and systemic venous sampling revealed that the tumor in the third basal phalanx of the left foot was responsible for FGF-23 overproduction. Tumor resection resulted in a rapid decrease in serum FGF-23 levels and an increase in serum phosphorus levels. CONCLUSIONS Octreotide scintigraphy, FDG-positron emission tomography, and systemic venous sampling are the standard methods for localizing functional endocrine tumors. However, the limited availability and invasive nature of these examinations hinder effective treatment. Here, we highlight the importance of peripheral superficial blood sampling as an alternative to conventional systemic methods for confirming the presence of FGF-23-producing tumors. Clinicians should consider TIO as a potential cause of acquired hypophosphatemic osteomalacia. Furthermore, peripheral superficial vein blood sampling may be useful for confirming the localization of FGF-23-producing tumors.

Reduction of Proteinuria in a Patient With Primary Aldosteronism by Angiotensin II Receptor Blocker Administration.

The renin-angiotensin-aldosterone system (RAAS) is a major target for treating hypertension and preventing various complications. Mineralocorticoid receptor (MR) antagonists are recommended as specific drugs to ameliorate hyperactive MR signaling, especially for patients with idiopathic hyperaldosteronism. However, the clinical implications of an increased RAAS activity and angiotensin II level induced by MR antagonist administration remain unclear. A 72-year-old Japanese man was referred to our university hospital for refractory hypertension management. He has also had type 2 diabetes mellitus and nephropathy for 8 years. MR antagonists, initiated based on the diagnosis of primary aldosteronism, effectively improved his hypertension. However, proteinuria of 2.5 g/g creatinine, concomitant with an increase in both active renin concentration and plasma aldosterone concentration, occurred. Additional administration of an angiotensin II receptor blocker successfully reduced the plasma aldosterone concentration and proteinuria (<0.3 g/g creatinine). Preserved renal function was confirmed for 1 year thereafter. In conclusion, this case suggests that the angiotensin II receptor is a potential target to treat proteinuria concomitant with primary aldosteronism. RAAS reactivation should be considered when an MR antagonist is initiated for patients with primary aldosteronism, especially idiopathic hyperaldosteronism.