: Despite observed and theoretical effectiveness and safety in immune thrombocytopenia (ITP), partial splenic angioembolization has not yet been included in clinical practice recommendations. At present, this is the first and only recorded case of partial splenic angioembolization done for chronic ITP in our institution. This case report will add to the growing body of evidence of partial splenic angioembolization as a viable and attractive alternative in treating refractory ITP among patients who refuse or are otherwise unfit for surgery. : We present a 61-year-old female, known chronic ITP unresponsive to steroids, vincristine, rituximab, mycofenolate mofetil, avatrombopag and azathioprine. She refused splenectomy and was offered partial splenic angioembolization. She achieved a durable response at post-procedure days 67, 82, and 130 with platelet count at 50 x 109/L, 85 x 109/L, and 72 x 109/L, respectively, despite continued slow tapering of prednisone and discontinuation of TPO-RA and other immunosuppressive agents. Immune thrombocytopenia (ITP) results from decreased platelet function and increased platelet destruction. About 10% of ITP becomes refractory to treatment within a year. Even among hematologists, the management of refractory chronic ITP remains to be challenging. Splenic artery angioembolization has traditionally been used as an optimization prior to splenectomy of massively enlarged spleens. Its effectiveness in treating ITP remains uncertain. However, current practice endorses it as a rescue therapy in patients deemed unfit for splenectomy.
Human ; Female ; Middle Aged: 45-64 yrs old

: In rare cases with no clinical practice guidelines available, the approach heavily relies on small studies, reports, and professional experience based on sound clinical judgement from available data. : We present a case of a 52-year-old male radiation technologist with a 5-year history of pancytopenia diagnosed with radiation-induced marrow aplasia after presenting with bilateral lower extremity weakness and numbness. MRI revealed spinal EMH along T3 to T12. He was given steroids and radiation therapy (RT) of 18Gy in 10 fractions with improvement in sensory status at 4th session of RT and was discharged with steroid on tapering and maintenance of eltrombopag. BM aplasia following chronic low-level radiation exposure results from the accumulation of cytogenetic abnormalities over time. EMH is a compensatory mechanism for BM aplasia, the diagnosis of which is established by MRI. In spinal EMH, transverse myelopathy occurs from spinal cord compression (SCC). As of writing and with our literature-search, spinal EMH has never been reported in patients with aplastic anemia or radiation-related BM aplasia. With the paucity of available data, there is currently no specific guidelines in managing BM aplasia from radiation and consequent SCC. However, as with most cases of SCC, radiotherapy, steroids, and surgical decompression are viable options. This case report will add to the very small pool of information on EMH from radiation-induced BM aplasia and its approach to management especially in this rare, never-before-reported presentation.
Human ; radiation