DISCUSSION
In our study, high periostin levels were detected in both mild/moderate
and severe cases after the first month of their follow-up. The periostin
level was higher especially in severe cases than in mild cases, and this
was statistically significant. We believe that the periostin level can
be used in the follow-up of disease severity.
In the case of inflammation and/or stress, the release of cytokines such
as IL-4, IL-13, and TGF-β increases from inflammatory cells, and they,
in turn, cause the release of periostin from the airway epithelial cells
(9-11). In our study, although the periostin level was found to be high,
no significant change was found in TGF-β level. This may be because the
regulation of periostin is affected not only by the expression of TGF-β
but also by IL-4 and IL-13 in patients with COVID-19. We believe that
further studies are needed to understand the molecular mechanisms behind
the host response. In addition, we believe that the high level of
periostin in the first month of the disease despite the clinical
improvement may be a guide for complications that may develop in the
future, which can be assessed in a longer follow-up period.
In another study, the proinflammatory factor tenascin C and
extracellular factor mucin-1 in bronchoalveolar lavage and serum samples
were found to be higher in patients with COVID-19 compared to healthy
controls. It has been suggested that these molecules can be used as
potential biomarker candidates or therapeutic targets (14). Based on the
results of our study, we believe that periostin can be used to assess
disease severity in patients with COVID-19; however, we recommend
conducting further studies with a longer duration and a larger number of
cases.
In our study, ferritin level was found to be significantly higher in
severe cases. D-dimer, LDH and CRP levels were also found to be higher.
In another study, lactate dehydrogenase, ferritin, D-dimer, and IL-6
levels were found to be associated with mortality (15). In yet another
study, especially the levels of D-dimer and fibrin degradation products
were found to be higher in patients with COVID-19 who died (16). The
reason for finding higher levels only for ferritin in our study can be
explained by the low number of cases.
In a study analyzing severe cases, lymphopenia was detected in 85% of
the cases with COVID-19 pneumonia (4). Older patients with lower
lymphocyte and platelet counts were found to have a higher risk of
disease and an increased duration of hospital stay (17). A notable
result of our study was that there was a weak but significant negative
relationship between basal levels of lymphocytes and periostin and a
weak, but positive relationship between the basal levels of lymphocytes
and TGF-β. In another study, it was shown that lymphopenia in CD8 + T
cells was an independent predictor for COVID-19 severity and treatment
effectiveness (18). In yet another study, lymphocyte percentage was
proposed as a predictive biomarker for disease severity or recovery
(19). In the light of these results, lymphopenia associated with
COVID-19 has been identified as a key pathological biomarker and a
criterion that marks the severity of the disease. Our data also support
this finding.
Limitations: The limitations of our study included the small
number of cases and short duration of the study. Another limitation was
that only TGF-β level was investigated, although the level of periostin
is affected by many cytokines.