https://orcid.org/0000-0001-6943-4980
Figures & data
Figure 1. Scattered purpura was observed on both lower extremities; and was not resolved by acupressure, some of which had faded away leaving hyperpigmentation.
Figure 2. On both upper extremities, eruptions of 0.5–2 cm were noted that faded within 12–24 h.
Table 1. Laboratory tests performed on first admission.
Figure 3. MRI T1 (18 January, X + 1) weighted image shows the patient’s lumbar spine turned into fatty bone marrow.
Figure 4. Clinical course.
Table 2. Comparison of the previous report [Citation22] with the present case.
Table 3. Cytokine measurements thoroughly conducted using serum 2 days before and 10 days after admission.
Figure 5. IL-6 Amp mechanism. IL-6 stimulates an intracellular signaling pathway: STAT-3 (a). While TNF-α, IL-17, IL-1, TLR ligands, and growth factors stimulate another intracellular signaling pathway: NF-κB (b). In non-immunocompetent cells, when STAT-3 and NF-κB are stimulated at the same time, NF-κB becomes activated excessively, which results in excessive production of IL-6 (c). Large amount of IL-6 acts by way of autocline (d) and paracline (e), promoting much more production of IL-6 following the activation of STAT-3. We defined this positive feedback mechanism mediating IL-6 as “IL-6 Amp” in a narrow sense. Non-immunocompetent cells activated by IL-6 Amp product various kinds of chemokines (f). These chemokines stimulate immunocompetent cells, such as macrophages, T cells, and B cells (g). Various kinds of chemokines produced by these immunocompetent cells stimulate STAT-3 and NF-κB in non-immunocompetent cells again (h) which produce much more IL-6 and chemokines as a consequence. We defined this mechanism as “IL-6 Amp” in a broad sense. Thus, IL-6 amp can take place under the circumstance of adequate existence of both IL-6 to activate STAT-3 and TNF-α, IL-1 or IL-17 to activate NF-κB. In the course of IL-6 Amp, tremendous amounts of cytokines and chemokines are produced, which is called “cytokine storm syndrome” (i).
