Refractory ITP 71-year-old male Afib, PAD, on methotrexate golimumab for psoriatic arthritis presented with thrombocytopenia, IPF fraction was high, thrombocytopenia determined to be in setting of ITP patient given 4 days of 40 mg Dex p.o., 2 days of IVIG, platelet count improved to 36 on day 3 and patient was discharged, 2 to 3 days later the platelet count dropped to 7, methylprednisone 1 mg/kg/day p.o. was restarted along with IVIG in outpatient setting, on day 2 platelet count improved from 7 to 40, IPF decreased from 30-16. Plan was to have him start rituximab from next week, however hepatitis surface antibody and core antibody positive. My question was - Whether you recommend starting him on rituximab or Romiplostin next. Rituximab was help with Psoriatec arthritis as well so technically that is better, given unlikely he will be going back on methotrexate and golimumab, anytime soon. However, we cannot start rituximab until we start him on Entecavir given positive hepatitis B serology, it will take at least 1 to 2 weeks to get entecavir before we can start Rituximab. Romiplostin can be started sooner. 2- How long do we keep on on methylpred and IVIG and concomitantly start Romiplastin and what dose do you start with. 3- If I start Rituximab (can I give it concomitantly with IVIG

Classical Hematology Specialist

Pulse dose steroids and IVIG, while often effective in ITP, often elicit only a transient response, as seems to be the case here. Given the transient response to pulse steroids and IVIG, a more durable therapy must be considered. Rituximab is a reasonable choice as responses, although not universal, are typically durable. Although the patient is HepB core ab positive, rituximab may still be given so long as the patient is maintained on entecavir for HBV prophylaxis throughout and following therapy. Notably, although rituximab is often effective, there is often prolonged time to response, and some patients may take as long as 2 months following initiation of therapy to manifest response. Thus when patients with severe thrombocytopenia start rituximab, they often require a temporary bridging therapy to support plt count until rituximab takes effect. IVIG and pulse dose steroids are not an ideal bridge as responses may only last a few days in some patients (as seems to be the case here) and giving multiple recurrent IVIG infusions and/or multiple pulses of high dose steroids is often not practical. Prednisione starting at 1mg/kg and gradually tapering over 2 months or so is often a sufficient bridge though some patient's will not respond adequately to this. Romiplostim, given its quick onset of action and reliable response rates, is often an effective bridge therapy for rituximab, and may be given until there is evidence of response to rituximab (and then discontinued thereafter). I find that doses of romiplostim < 5mcg/kg are rarely effective. I would start at 5cg/kg administered weekly at rituximab infusion visits (or starting prior to initiaiton of rituximab), and titrating up if inadequate response. Romiplostim is usually not an ideal long-term therapy as it requires frequent clinic visits for administration, and doing this for prolonged periods may prove burdensome to patient (romiplostim must often be given indefintiely to maintain response). If there is preference not to proceed to rituximab, an alternate durable long-term therapy would be an oral tpo mimetic such as eltrombopag or avatrombopag. Responses to these are generally quick (5-10 days) and no bridging therapy would be required. Unlike rituximab (which may typically be discontinued after 4 weekly infusions), oral TPO mimetics most often need to be continued indefinitely to maintain response.