There are both broadly immunosuppressive approaches, such as high-dose corticosteroids, and more novel targeted approaches that go after inflammatory cytokine proteins

There are also a few effective treatments for cytokine storms despite the fact that we still do not know exactly which treatments will ultimately be developed and recommended across the board for COVID-19 related cytokine storms.

Cytokine storms also can be indicated by liver enzyme abnormalities.

Luckily, the tests to diagnose cytokine storms are often cheap and readily available in hospitals.

When your body responds the way it is supposed to, the cytotoxic T-cells will only target infected cells to be killed and move along. Additionally, the immune response also has a chemical indicator that ideally tells overzealous immune response cells to stand down once the threat has been neutralized. It is when we are in the throes of a cytokine storm that those systems start to get overwhelmed and malfunction. In essence, our body’s immune response gets so amped up that it stops differentiating between infected and healthy cells and attacks everything in its path.

In the present study, we also found that markers of inflammatory response, such as C-reactive protein, procalcitonin, and leukocytes, were significantly increased among patients who suffered from cardiac injury. The activation or enhanced release of these inflammatory cytokines can lead to apoptosis or necrosis of myocardial cells.

Third, Huang’s study noted that high concentration of IL-1β, IFN-γ, IP-10 and MCP-1 could be detected in patients infected with 2019-nCoV, which might lead to activated T-helper-1 (Th1) cell responses [4]. Furthermore, they also found that ICU patients had much higher concentrations of inflammatory factors than those non-ICU patients, suggesting that the cytokine storm was associated with disease severity

Other proposed mechanisms of myocardial injury include a cytokine storm triggered by an imbalanced response by type 1 and type 2 T helper cells