Discussion
In general, SARS-CoV-2 as any viral infection could trigger the immune system to cause thrombocytopenia. Although the development of new-onset ITP in the context of COVID-19 infection has been well discussed in the literature, the chronic ITP has been rarely reported. Our study is addressing the course of chronic ITP in patients who contracted COVID-19 and admitted to the hospital. Also, the study is examining the propensity to relapse among these patients.
The incidence of ITP relapse in chronic ITP patients with COVID-19 infection was 43% in our study which is almost double what was reported before in the literature. de la Cruz –Benito et al published a case series for 8 chronic ITP patients, managed as in-patient and out-patient during the first months of the pandemic in Madrid, Spain. The author reported that 25% of chronic ITP patients had relapses, and 50% developed paradoxical thrombocytosis, including one of the relapsed patients. The author included patients without positive PCR tests and didn’t report blood counts for two patients. The sharp inclining then declining in the platelet count which was reported by the author, makes it questionable if it was false reading or related to other causes of thrombocytosis. In our study, we didn’t observe paradoxical thrombocytosis. Our study included larger sample size, more strict inclusion and exclusion criteria which could explain the difference in the observation between our study and de la Cruz –Benito et al. Onset time of ITP relapse in majority of cases was during the first week from COVID-19 diagnosis which is similar for what we reported in our experience with newly diagnosed ITP during the pandemic.5
From a clinical perspective, ITP relapses could be asymptomatic or could present with bleeding. Among the five patients who developed relapse, 38.5% presented with non-major bleeding symptoms which didn’t require a blood transfusion. Half (50%) of those events were related to G.I bleeding, which is different than what was observed in COVID-19 patients who developed acute ITP, where G.I bleeding reported in 9% - 18% of the patients, while cutaneous manifestations in form of petechiae/purpura/ecchymoses consisted the majority, 46% - 49%.5, 6
Current guidelines recommend systemic steroids as first‐line therapy for COVID‐19‐induced ITP and reserve IVIG as a second line when immediate platelet count elevation is required or if there is failure to respond to steroids. Although there are no data on the use of TPO‐RAs in COVID‐19 positive patients, the risk of hepatotoxicity and the potential for increased thrombosis remain a concern, and experts advice to weigh the risks and benefits before using it.11 In our study, the complete response to ITP treatment has been observed in 80% (4/5) of the patients and 20% (1/5) achieved partial response. Only one patient had steroid failure and required a second-line agent, Romiplostim, which re-emphasis the cornerstone role of steroid in managing COVID-19 related ITP as recommended by expert consensus from the United Kingdom.11 No patient received IVIG in our study. The response rate to treatment close to what reported by de la Cruz –Benito et al in their chronic ITP series, but interestingly this rate is higher than what observed in newly diagnosed ITP induced by SARS-CoV-2 infection; complete response rate 45 - 67% and partial response rate 18% - 27.3%. This might be explained by the fact that chronic ITP patients were already getting treatments for ITP.
Our study has some limitations. First, the study is retrospective in nature. Second, it was difficult to determine whether COVID-19 infections solely triggered relapses in our patients since other comorbidities and even critical illness could have played a role in the ITP course. In conclusion, our study highlights the fact that COVID-19 is associated with an increased risk of flares in patients with chronic ITP within the first week of symptoms and up to three weeks in some cases. A complete response to systemic steroids is expected in the majority of cases.