Faculty of Medicine, Universitas Muhammadiyah Prof. DR. HAMKA, Jakarta Indonesia
Wening Tri Mawanti Faculty of Medicine, Universitas Muhammadiyah Prof. DR. HAMKA/Jakarta Islamic Hospital, Pondok Kopi, Jakarta Indonesia
Dewi Martalena Faculty of Medicine, Universitas Muhammadiyah Prof. DR. HAMKA/Jakarta Islamic Hospital, Pondok Kopi, Jakarta Indonesia
Erlin Listiyaningsih Faculty of Medicine, Universitas Muhammadiyah Prof. DR. HAMKA, Jakarta Indonesia
Rizkyana Avissa Faculty of Medicine, Universitas Muhammadiyah Prof. DR. HAMKA, Jakarta Indonesia
Rini Latifah Faculty of Medicine, Universitas Muhammadiyah Prof. DR. HAMKA, Jakarta/Dr. M Goenawan Partowidigdo Pulmonary Hospital, Bogor, Indonesia Indonesia
Wawang S Sukarya Faculty of Medicine, Universitas Muhammadiyah Prof. DR. HAMKA, Jakarta Indonesia
Shinta Dewi Permata Sari(1*), Wening Tri Mawanti(2), Dewi Martalena(3), Erlin Listiyaningsih(4), Rizkyana Avissa(5), Rini Latifah(6), Wawang S Sukarya(7)
(1) Faculty of Medicine, Universitas Muhammadiyah Prof. DR. HAMKA, Jakarta (2) Faculty of Medicine, Universitas Muhammadiyah Prof. DR. HAMKA/Jakarta Islamic Hospital, Pondok Kopi, Jakarta (3) Faculty of Medicine, Universitas Muhammadiyah Prof. DR. HAMKA/Jakarta Islamic Hospital, Pondok Kopi, Jakarta (4) Faculty of Medicine, Universitas Muhammadiyah Prof. DR. HAMKA, Jakarta (5) Faculty of Medicine, Universitas Muhammadiyah Prof. DR. HAMKA, Jakarta (6) Faculty of Medicine, Universitas Muhammadiyah Prof. DR. HAMKA, Jakarta/Dr. M Goenawan Partowidigdo Pulmonary Hospital, Bogor, Indonesia (7) Faculty of Medicine, Universitas Muhammadiyah Prof. DR. HAMKA, Jakarta (*) Corresponding Author
Abstract
COVID-19 is caused by the SARS-CoV-2 infection that attacked the human respiratory system. In severe conditions, it causes pneumonia, kidney failure, acute respiratory distress syndrome (ARDS), and even death. The SARS-CoV-2 infection triggers the immune cells to secrete an excess of pro-inflammatory cytokines lead to cytokine storm. It is believed to become one of the mechanisms that cause the ARDS condition. The level of pro-inflammatory cytokines will differ with each case severity. This study aimed to evaluate the profile of pro-inflammatory cytokines in COVID-19 patients with different severity. Therefore, it could be used as therapeutic approach for cytokine storm conditions. It was a cross sectional study using plasma samples of COVID-19 patients from Jakarta Islamic Hospital, Pondok Kopi and Dr. M. Goenawan Partowidigdo Hospital, Cisarua, Indonesia. The COVID-19 patients with severe (n=20) and mild to moderate (n=25) severity were involved in this study. As negative control plasma sample from healthy subjects (n=13) was used. Plasma IL-6 levels were measured using the ELISA technique and plasma lymphocyte levels were measured using a hematology analyzer. The results showed that no significant difference between severity and gender was observed (p=0.256). Meanwhile, there is a significant difference in IL-6 level between negative control, mild-moderate, and severe categories (p=0.015). The average IL-6 level in severe categories was higher than mild-moderate and negative control categories, with values 105.375, 59.75, and 64.577 pg/mL, respectively. This result becomes supporting evidence that there is a cytokine storm condition in severe COVID-19 patients. Furthermore, the lymphocyte level in the severe group is significantly lower than the mild to moderate group. This result may indicate lymphocytopenia in the severe group.
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