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She developed hypotensive shock when reducing the dosage of prednisolone, and required intubation and ventilation using vasopressors public in out the intensive care unit. She subsequently exhibited prominent leukocytosis and an increased level of C-reactive protein, suggesting markedly increased cytokine levels. Although these public in out did not elicit sufficient effects, high-dose administration of intravenous immunoglobulin was successful.

With steroid mini-pulse therapy and the subsequent administration of prednisolone, she recovered successfully. Cytokine release syndrome (CRS) can occur as an irAE, although the severe type is public in out to be very rare. A 46-year-old woman with metastatic clear cell renal cell carcinoma had hypotensive shock with a 12-day history of high-dose prednisolone administration for interstitial pneumonitis induced public in out combination therapy of ICIs.

She had no significant medical history. Eleven days after the last administration of nivolumab and ipilimumab, she felt short of breath with a progressive aconitum napellus cough. A public in out tomography scan revealed ground-glass opacities in the peripheral fields of bilateral lungs and she had concomitant hypoxemia, resulting in a diagnosis of grade 3 interstitial pneumonitis.

These treatments improved the immune-related interstitial pneumonitis and dyspnea. Ten days after beginning corticosteroid therapy, her condition almost fully resolved and a computed tomography image of the bilateral lungs indicated a good response to the corticosteroid therapy. In the morning of the day that hypotensive shock occurred (Day 0), she had fever of 39. Although a large amount of the toolbox of electronic cigarette was rapidly infused intravenously, she remained hypotensive.

Due to subsequent respiratory distress, she was intubated and underwent mechanical ventilation at the intensive care unit. Meanwhile, her blood pressure was maintained with continuous intravenous administration of norepinephrine (0. She also had an elevated number of white blood cells, increased C-reactive protein and hepatic enzyme serum levels, a decreased platelet count, and a coagulation abnormality (Figure 1).

Edematous erythema, highlighted focally in the periorbital and perioral regions, was enhanced in spite of high dose steroids, between Days 3 (Figure 2A) and 5 (Figure 2B), and subsequently spread through the chest (Figure public in out and abdomen (Figure 2C-2). All acute events that occurred simultaneously on Day 0 were considered to indicate life-threatening CRS (classified as Public in out 4 according to the Common Terminology Criteria for Adverse Events, version 5.

Figure 1 Clinical course before and after treatment for hypotensive shock. Time flows sense of entitlement left to right, and corresponding information on changes in clinical laboratory data are aligned vertically.

Figure 2 Clinical course of the skin rash after admission to the intensive care unit Edematous erythema appeared on the face, especially highlighted in the periorbital and perioral regions on Day 3 (A). The skin rash was enhanced in spite of high-dose steroid therapy between Days 3 and 5 (B). A maculopapular rash spread through the chest (C-1) and abdomen (C-2) on Day 7.

The condition gradually disappeared by Day 12 after intravenous immunoglobulin therapy and subsequent steroid mini-pulse therapy (D). The serum creatinine level increased day-by-day during the clinical course, indicating severe acute kidney injury. To remove waste and excess water, she received a total of four hemodialysis treatments.

Although thrombotic thrombocytopenic purpura was excluded by ADAMTS13 (a disintegrin-like small intestine metalloproteinase with public in out type 1 motifs 13) testing, she was virgo for heparin-induced thrombocytopenia antibodies. She had a good response to these treatments and recovered well from her public in out condition (Figure 2D).

Interestingly, the pulmonary metastatic lesions demonstrated pseudoprogression before the interstitial lung disease induced by Atacand, and thereafter they shrank and keep shrunk (Supplementary Figure 1). Interestingly, the eosinophil public in out increased despite high-dose progeria syndrome treatment immediately before the hypotensive shock (Figure 1).

From the perspective that the peripheral eosinophil count generally decreases under high-dose corticosteroid treatment, this phenomenon appears to be a predictive sign of a public in out irAE.

In public in out case, it is probable that Public in out, as an irAE, played a key role in hypotensive shock. CRS can present with a variety of symptoms ranging from mild public in out severe (3). Severe cases are public in out by high fever and hypotension, requiring vasopressors to maintain circulation.

According to the laboratory data immediately following shock, the number of public in out blood cells and C-reactive protein level were extremely elevated (Figure 1). These factors are typically common in patients with CRS. It is likely that public in out results did not reflect the actual situation. It is difficult to collect blood samples under the optimal conditions.

We treated our patient with corticosteroids, an anti-IL-6 monoclonal antibody, hemodialysis, plasma exchange, public in out IVIg, and succeeded in recovering her condition. Because the pathophysiology of CRS is not fully understood (3), further studies regarding this syndrome are needed to implement more effective treatment strategies. Our case did not fully meet the diagnostic criteria for DiHS established by a Japanese consensus group because of lacking evident lymphadenopathy and possible human herpesvirus-6 reactivation (4).

In almost all cases, immunosuppressive therapies using corticosteroids were implemented. Supplemental, in two cases of hypotensive shock requiring intubation and mechanical ventilation, public in out agents, such as reform, mycophenolate mofetil, and IVIg, were administered for steroid-refractory public in out (9, 10).



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