BKV‐HC is a serious complication of allogeneic HSCT. To characterize the incidence, risk factors, and clinical outcomes of post‐HSCT BKV‐HC, we retrospectively analyzed 112 patients who underwent one or more allogeneic HSCTs at our hospital between 2001 and 2017. Twenty underwent second or third HSCT thereafter. Ten patients developed BKV‐HC at a median of 30 days after HSCT. The 100‐day cumulative incidences of grade 0‐4 and grade 2‐4 BKV‐HC were 7.8% and 6.2%, respectively. HSCTs performed in 2011‐2017 associated with significantly higher 100‐day cumulative incidence of grade 2‐4 BKV‐HC (14.0%) than HSCTs performed in 2001‐2010 (1.3%, P = 0.004). On multivariate analysis, second or third HSCT was the only independent significant risk factor for development of grade 2‐4 BKV‐HC (P = 0.015). Serial PCR monitoring of urine and blood BKV load did not predict BKV‐HC. The recent increase in the incidence of BKV‐HC may reflect recent innovations in transplant technologies that facilitate second or third HSCT, which are known to cause prolonged immune deficiency. If safe and effective treatment or prophylaxis becomes available, it could be used to target the high‐risk patients for BKV‐HC.

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Compared to cerebral radiation-induced cavernous hemangiomas (RICHs), little is known about intraspinal RICHs. A 13-year-old male suddenly developed symptomatic spinal hemorrhage eight years after hematopoietic stem cell transplantation using a total body irradiation (TBI) based myeloablative regimen. A solitary small hemangioma was detected on follow-up T2 star weighted magnetic resonance imaging of the spine. His neurological symptoms gradually improved with supportive treatment and rehabilitation, although he experienced rebleeding 2 years later. Intraspinal RICH is very rare but should be recognized as a possible late adverse effect in pediatric patients who received TBI.

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Growing teratoma syndrome is a well-recognized condition associated with both intracranial and extracranial nongerminomatous germ cell tumors (NGGCTs), which mostly manifest as rapid growth of cystic and solid components during or within several months after treatment. Here, we report a patient with NGGCT who experienced slow growth of intracranial growing teratoma syndrome with intraventricular lipid accumulation over 10 years without any clinical symptoms. Considering the clinicopathologic heterogeneity of this syndrome, long-term clinical and radiologic follow-up is required for all patients with intracranial NGGCT.