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.