July 28, 2021
By Erica Kaufman West, MD
Early in the COVID-19 pandemic, there was concern that solid organ transplant (SOT) patients would have worse outcomes based on their immunosuppressed state, their high-risk comorbidities (e.g., hypertension, diabetes), and on the prior experience of outcomes with other respiratory viruses like influenza. Conversely, there was speculation that SOT patients might do better than non-SOT patients because their immunosuppression may dampen the severe cytokine release syndrome (CRS) that COVID-19 precipitated in some patients.
A retrospective, matched cohort study published in Transplant Infectious Disease looked at 30 SOT patients and 60 non-SOT patients. It also looked at cytokine signatures to see how immunosuppression might affect the evolution of COVID-19 and CRS. Of note, at this center, mycophenolate mofetil was discontinued in all SOT patients diagnosed with COVID-19. The majority of the SOT patients (87%) were renal transplant recipients with 70% on tacrolimus and nearly all on less than 5 mg of prednisone daily. SOT and non-SOT patients were matched for hypertension, body mass index, and diabetes, but SOT patients were more likely to have chronic cardiac disease. SOT and non-SOT patients had similar C-reactive protein, ferritin, D-dimer, procalcitonin, absolute lymphocyte count, and lactate dehydrogenase results at baseline. Tocilizumab and steroid use were higher in SOT patients but not significantly so. The groups did remarkably similarly with no statistical difference in critical status (high flow oxygen or above) or mortality. The non-SOT group had a slight advantage in length of stay (9 vs 12 days, P = .47).
The cytokine panel looked at interleukin-6 (IL-6), interleukin-10 (IL-10), and soluble interleukin-2 receptor (sIL2R) and was only done on SOT patients; it would have been interesting to compare these to non-SOT patients’ levels. A future prospective study might include these findings. IL-6 levels were higher in patients with critical disease, and levels rose after tocilizumab administration as has been reported in other studies. IL-10 levels were low, as has been reported in SOT patients with influenza, and rose after tocilizumab only in those requiring less than 3 L/min of oxygen via nasal cannula. sIL2R was elevated, as is normally seen in SOT patients, and also rose after tocilizumab. The authors speculated that these findings indicate that T-cell activation is not really altered by tocilizumab administration. They also found no increase in infections post-tocilizumab, contradicting a prior study that showed more superinfections post-tocilizumab.
These study starts to chip away at the complexity of the immune system and CRS. While remaining speculation, it seems that SOT patients’ immunosuppression does alter the natural course of COVID-19. Their mortality rates should be higher than their non-SOT counterparts, however these authors found no difference at all.