The Sars-Cov-2 virus is responsible for Covid-19, a disease that has impacted the entire world and is blamed for the induction and exacerbation of immunocompromised patients and carriers of autoimmune diseases. (6, 7, 10).
In addition to immunocompromised patients, HSCT recipients are part of a group of patients at greater risk of contracting COVID-19 (11).
Allogeneic and autologous HSCT recipients have increased mortality, morbidity, and clinical complication rates when contracting COVID-19 (8, 12–14). A report on a group of patients undergoing transplantation showed a mortality rate for autologous HSCT of 17%, and for allogeneic HSCT was 21% (8). These data configure the severity to which HSCT recipients are submitted in both modalities. There is a reason for evaluating a group of patients previously submitted to autologous HSCT and its impact on Crohn's Disease.
Crohn's Disease courses with dysbiosis of the digestive system, which is the primary habitat and target of infection by Sars-Cov-2. That is due to a high intestinal expression of angiotensin-converting enzyme-2 (ACE2) and serine transmembrane protease-2 (TMPRSS2) receptors, which are found at high levels at this site (15).
The intestinal microbiome of healthy people, compared to that of people with COVID-19 or Crohn's disease, shows a considerable reduction of anti-inflammatory bacteria (15).
Patients with COVID-19 have gastrointestinal manifestations during the infection, and the Sars-Cov-2 virus is considered to trigger CD in patients predisposed to the disease (16). However, studies on COVID-19 on gut health and inflammation among patients with inflammatory diseases remain uncertain, particularly on the susceptibility and clinical impact of COVID-19 and its impact on the gut microbiota (5).
It is believed that the immune dysregulation caused by COVID-19 can trigger the onset of various autoimmune diseases, including in patients with active CD, and persist after recovery from the infectious episode (17).
COVID-19 shares similarities with autoimmune diseases regarding clinical manifestations, immune responses, and pathogenic mechanisms. In addition, there are reports of several patients with evolution to several autoimmune diseases, such as Guillain Barre Syndrome, lupus, vasculitis, myopathies, and description of isolated cases of multiple sclerosis and Still's Disease (18–20).
In our series of 50 patients with CD, and in the 19 patients who had COVID-19, there was no description of an increase in the morbidity rate or presence of mortality, data that differ from the literature described, (8, 12–14). In the analysis of the series of patients submitted to autologous and allogeneic HSCT, we observed that they had once-hematological diseases submitted to rescue chemotherapy, mobilization schemes with high doses of chemotherapy, and myeloablative conditioning. Our sample differs in using mobilization regimens with low doses of cyclophosphamide and non-myeloablative conditioning regimen. This may explain the low morbidity, describing only one (1) case that required hospitalization but outside the Intensive Care Unit. Another relevant data observed was the absence of deaths.
In our patients, there was no change in DC status in most cases, with only a change from clinical remission to disease recurrence observed in three cases (#40, #43, and #44). These patients had undergone HSCT less than six months before the infectious episode. This data corroborates the information on patients' vulnerability in the first year after autologous HSCT (21).
There are reports that COVID-19 can affect the endocrine system and trigger changes in thyroid function, with clinical and biochemical manifestations and the development of antithyroid antibodies. (22, 23). One of the cases (#40) that recurred after the infectious episode presented endocrinological manifestations of CD, with the presence of anti-TPO.
Post-COVID syndrome is currently recognized as a new disease in the context of Sars-Cov-2 infection. However, its pathogenesis is still not fully understood, with data that acute inflammation may be responsible for this clinical picture (24–27). Of our patients, nine (9) reported clinical manifestations that may be related to the Post-COVID Syndrome. However, only one (1) of the patients had cognitive disorders, and two (2) patients had digestive manifestations and diarrhea and were in a relapse of the CD.
In conclusion, with the observed data, we can say that the patient with CD who submitted to autologous non-myeloablative HSCT has a low morbidity rate and no mortality and that patients in the first year after transplantation have an increased risk of contracting COVID-19 and with probable repercussions on the status of his illness.