A common clinical observation is that patients who develop significant immune-related toxicities, like colitis or pneumonitis, are frequently the same ones who experience the most profound and durable responses to checkpoint inhibitor therapy.

ITP caused by immune checkpoint inhibitors (ICIs) is rare (0.25% incidence) but generally has a good prognosis. Most patients respond to standard first-line ITP therapies, and approximately 70% of those re-challenged with the ICI can continue treatment without a recurrence of ITP.

Clinicians are far more cautious using immunotherapy in organ transplant recipients than in patients with autoimmune disease. The risk of irreversible graft rejection is a major deterrent, reserving checkpoint inhibitors only for when no other treatment options exist.

The potential for urologists to administer PD-1 inhibitors for bladder cancer raises a significant safety issue: surgeons may not be equipped to manage severe, systemic immune-related toxicities like hypophysitis or hepatitis, which traditionally fall under the purview of medical oncologists.

Though typically contraindicated, checkpoint inhibitors can be used for transplant recipients with advanced skin cancer. This requires shared decision-making, collaboration with the transplant team, and a specific protocol involving high-dose pulse steroids to mitigate the high risk of allograft rejection.

Combining KRAS G12C inhibitors with checkpoint inhibitors increases the risk of transaminitis. Differentiating the causative agent is clinically challenging. A rapid recovery after stopping both drugs suggests the KRAS inhibitor is the cause and can be restarted at a lower dose; slower recovery points to the immunotherapy.

Erik van den Berg highlights a critical paradox in the current standard of care for BK virus infections post-transplant. The only available intervention is lowering immunosuppression to fight the virus, but this simultaneously increases the probability that the patient's immune system will reject the newly transplanted organ.

Data shows that patients who permanently stopped ipilimumab due to immune-related side effects still had exceptionally good outcomes. This gives clinicians confidence to manage toxicity by discontinuing the CTLA-4 inhibitor portion of the regimen while continuing nivolumab, without fearing a loss of efficacy.

The trial showed combining a CTLA-4 inhibitor (Tremelimumab) with a PD-L1 inhibitor (Durvalumab) significantly increased toxicity without improving efficacy over monotherapy. This result, consistent with other trials, questions the benefit-risk profile of dual checkpoint inhibition in the adjuvant setting for renal cell carcinoma.