Nplate remission - was there an article??

Hi all

I may well have dreamt this but is there an article about remission AFTER stopping nplate anywhere? I've tried to search this site & google but I'm not having much luck I'm sure I saw one.....

My count is hovering abround 30 at the moment, with IVIG treatment every 3 weeks or so, plus 10mg prednisolone. I'm still trying to decide what to do next and have just found an article about romiplostim (nplate) use in pregnancy (for those who don't know - I have a little girl who is 2 and want another baby, but I'm not responing to prednisolone or IVIG for long so I'm looking for other treatments that might be ok in pregnancy ). The article is called 'successful treatment of severe thrombocytopenia with romiplostim in a pregnant patient with systemic lupus erythematosus' and was pubished in Lupus, Dec 2012.

If anyone has access to either of these articles and would share I would be eternally grateful!!

I'm determined to find a treatment that works for me and allows me to live my life and fulfil my dreams!!!

Here's one:

With the knowledge that the thrombocytopenia in ITP is caused in part by impaired platelet production, TPO-R agonists have recently been used successfully to treat ITP.4,5 Response rates of 70% or higher have been achieved, but only while patients continue on treatment is the effect on their platelets maintained.4,5 As platelet response is driven by TPO-R agonist stimulation of thrombopoiesis, it is not unexpected that drug-induced platelet production thus ceases when the drug is stopped. In this context, the first demonstration of improved Treg activity with TPO-R agonists by Bao and colleagues is surprising and highly significant.1 However, this small cross-sectional study requires confirmation by a much larger longitudinal study, in particular a study which also shows antigen-specific increase in Treg activity (as immunosuppression by Tregs is antigen-dependent2). Nevertheless, the finding1 of Bao et al is still interesting and may explain the sustained platelet response experienced by 7% of ITP patients treated with TPO-R agonists in clinical trials. The unexpected remissions were initially attributed to spontaneous remission which can occur occasionally in chronic ITP, although all these patients had failed several ITP treatments before receiving TPO-R agonist therapy.


It is tempting to speculate that TPO-R agonists may have immune-modulating activity and thus induce sustained remission in ITP patients if given to appropriate patients for an adequate duration. However, immune cells do not have TPO-Rs. If this activity exists, TPO-R agonists must exert this effect via a mechanism independent of TPO-R. Tregs and other less well-studied suppressive T cells2 are probably the key to this activity. ITP occurs because APCs, macrophages, stimulatory Th cells, and B cells (which perpetuate the disease) escape the immune surveillance by Tregs. Tregs exert immune control by modifying the functions and numbers of these cells, and consequently return the immune system to homeostasis and health. For example, Tregs can induce apoptosis of the effector cells or can inhibit their activation and functions.2 These Treg actions are mediated by soluble factors (such as transforming growth factor-β [TGF-β], interleukin-10, perforins, etc) and cell-associated molecules (such as cytotoxic T lymphocyte antigen 4, lymphocyte activation gene-3, LFA-1/CD11a, CD18, CD39, etc).2,3 However, how TPO-R agonists improve Treg activity is still unknown. It may be via a sustained increase in antigen load that induces tolerance or via an increase in anti-inflammatory cytokines such as TGF-β as both antigen and TGF-β can induce Tregs.3 There is no good evidence to support either hypothesis and hence further studies are clearly needed.

bloodjournal.hematologylibrary.org/content/116/22/4388.full?sid=6289f8c7-0a84-4a8d-93cb-7f281787cd36

Here's one about Promacta:

Approximately one-third of patients with immune thrombocytopenia who were treated with a thrombopoietin-receptor agonist maintained adequate platelet counts 6 months after stopping treatment, according to study results.

Researchers conducted the study to evaluate patients with immune thrombocytopenia who had electively discontinued eltrombopag (Promacta, GlaxoSmithKline) without substituting additional therapy. They wanted to observe what impact, if any, this discontinuation would have on platelet counts.

Fifteen patients who had been taking the drug for a minimum of 4 months before the start of the study were included. A platelet count of ≥30,000/mcL and ≥20,000/mcL above initial baseline for 6 months off eltrombopag without intervening treatment (other than rescue) served as the primary endpoint. Being stable off therapy at 4 weeks after discontinuing eltrombopag served as the secondary endpoint.

Five of the patients enrolled in the study demonstrated response for 5 months or longer, while 10 patients were classified as non-responders. The fifth responder discontinued therapy 5 months ago and had platelet counts ≥195,000/mcL.

Two of the responders had undergone splenectomy, and all had three or more previous therapies.

Non-significant factors associated with response included age, duration of immune thrombocytopenia, duration of eltrombopag therapy, splenectomy status, number of prior immune thrombocytopenia treatments, bleeding history and platelet count at the time that eltrombopag was discontinued.

Responders demonstrated a lower absolute immature platelet fraction value when treatment was stopped (P=.022).
Reference:

www.healio.com/hematology-oncology/hematology/news/print/hematology-oncology/%7BB11CEC31-E0A4-4C96-89E0-D441862C9E10%7D/Eltrombopag-maintained-efficacy-after-cessation-in-immune-thrombocytopenia

You're a star sandi - as always!

Glad I could help!

Thank you for sharing! The doc at Cleveland is an expert on this.

I want to bump this thread.