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Nivolumab-Induced Hypothyoidism With Consequent Hypothyroid Related Myopathy
Purpose: Nivolumab is a fully human IgG4 programmed death 1 immune checkpoint inhibitor (ICI) antibody that has anti-tumor activity by selectively blocking the interaction of the programmed death 1 receptor with its two known programmed death ligands PD-L1 and PD-L2. In doing so, this immune checkpoint inhibitor removes the negative signal stifling T cell activation and proliferation within the tumor microenvironment and demonstrates favorable antitumor activity.
Case Report: We report an interesting case of immune checkpoint inhibitor-induced primary hypothyroidism with associated hypothyroid myopathy in a young patient with surgically resected stage IIIB melanoma receiving adjuvant nivolumab. He presented 12 weeks into therapy with severe myalgias, arthralgias, and intermittent disequilibrium of unclear etiology. Laboratory evaluation demonstrated a significant elevation in thyroid stimulating hormone and creatine kinase with an undetectable free T4 with standard laboratory measurement. With thyroid hormone replacement therapy alone, he had rapid improvement in his musculoskeletal symptoms and laboratory parameters over a threeweek period.
Discussion: This case emphasizes the serious nature of endocrine immune-related adverse events in patients receiving immune checkpoint inhibitors. Additionally, it highlights that unlike most other immunerelated adverse events, endocrine immune-related adverse events can generally be managed with adequate hormone replacement alone with swift improvements in symptoms. This allows patients to continue immune checkpoint inhibitors safely without immunosuppression which may dampen the anti-tumor activity of these agents.
Conclusion: This case highlights the importance of early recognition and the appropriate management of endocrine immune-related adverse events to maximize patient safety and good outcomes.
Purpose: Nivolumab is a fully human IgG4 programmed death 1 immune checkpoint inhibitor (ICI) antibody that has anti-tumor activity by selectively blocking the interaction of the programmed death 1 receptor with its two known programmed death ligands PD-L1 and PD-L2. In doing so, this immune checkpoint inhibitor removes the negative signal stifling T cell activation and proliferation within the tumor microenvironment and demonstrates favorable antitumor activity.
Case Report: We report an interesting case of immune checkpoint inhibitor-induced primary hypothyroidism with associated hypothyroid myopathy in a young patient with surgically resected stage IIIB melanoma receiving adjuvant nivolumab. He presented 12 weeks into therapy with severe myalgias, arthralgias, and intermittent disequilibrium of unclear etiology. Laboratory evaluation demonstrated a significant elevation in thyroid stimulating hormone and creatine kinase with an undetectable free T4 with standard laboratory measurement. With thyroid hormone replacement therapy alone, he had rapid improvement in his musculoskeletal symptoms and laboratory parameters over a threeweek period.
Discussion: This case emphasizes the serious nature of endocrine immune-related adverse events in patients receiving immune checkpoint inhibitors. Additionally, it highlights that unlike most other immunerelated adverse events, endocrine immune-related adverse events can generally be managed with adequate hormone replacement alone with swift improvements in symptoms. This allows patients to continue immune checkpoint inhibitors safely without immunosuppression which may dampen the anti-tumor activity of these agents.
Conclusion: This case highlights the importance of early recognition and the appropriate management of endocrine immune-related adverse events to maximize patient safety and good outcomes.
Purpose: Nivolumab is a fully human IgG4 programmed death 1 immune checkpoint inhibitor (ICI) antibody that has anti-tumor activity by selectively blocking the interaction of the programmed death 1 receptor with its two known programmed death ligands PD-L1 and PD-L2. In doing so, this immune checkpoint inhibitor removes the negative signal stifling T cell activation and proliferation within the tumor microenvironment and demonstrates favorable antitumor activity.
Case Report: We report an interesting case of immune checkpoint inhibitor-induced primary hypothyroidism with associated hypothyroid myopathy in a young patient with surgically resected stage IIIB melanoma receiving adjuvant nivolumab. He presented 12 weeks into therapy with severe myalgias, arthralgias, and intermittent disequilibrium of unclear etiology. Laboratory evaluation demonstrated a significant elevation in thyroid stimulating hormone and creatine kinase with an undetectable free T4 with standard laboratory measurement. With thyroid hormone replacement therapy alone, he had rapid improvement in his musculoskeletal symptoms and laboratory parameters over a threeweek period.
Discussion: This case emphasizes the serious nature of endocrine immune-related adverse events in patients receiving immune checkpoint inhibitors. Additionally, it highlights that unlike most other immunerelated adverse events, endocrine immune-related adverse events can generally be managed with adequate hormone replacement alone with swift improvements in symptoms. This allows patients to continue immune checkpoint inhibitors safely without immunosuppression which may dampen the anti-tumor activity of these agents.
Conclusion: This case highlights the importance of early recognition and the appropriate management of endocrine immune-related adverse events to maximize patient safety and good outcomes.
Vismodegib-Induced Rash: A Case Report
An 88-year-old male with locally advanced basal-cell carcinoma (BCC) of the scalp who had received multiple resections, stem cell graft, and amniotic allograft continued to progress with severe ulcerations that extended into the dura. Patient was initiated on vismodegib 150 mg daily and subsequently developed a diffuse maculopapular rash within 14 days of treatment. The rash resolved with topical triamcinolone 0.1% and discontinuation of vismodegib. Loratadine 10 mg daily was concurrently administered for rash prophylaxis upon vismodegib re-initiation. Within 7 days of therapy, the rash returned, and subsequently vismodegib was discontinued and oral prednisone taper was initiated. Given limited effective treatment options, vismodegib was continued at a modified schedule of 150 mg daily for 2 weeks then 1 week off with prednisone 5 mg daily. To date, patient has completed 2 years of treatment with no return of rash or disease progression.
BCC occurs in 2 million patients annually in the US. Fortunately, most of these cases are responsive to local therapy with rare metastatic progression. The emergence of novel Hedgehog pathway inhibitors (vismodegib, sonidegib) provide effective options for advanced BCC. Although vismodegib has been reported to cause Grade 3-4 adverse events in 25% of patients, there are no reports of vismodegib-induced rash nor recommendations regarding management.
For many novel targeted therapies, the appropriate management of toxicities has not been well described. This case study presents a patient that continues to respond to therapy with a novel modified dosing scheme in addition to low-dose prednisone. We present this case report to offer a potential treatment option in patients who experience a vismodegib-induced rash.
An 88-year-old male with locally advanced basal-cell carcinoma (BCC) of the scalp who had received multiple resections, stem cell graft, and amniotic allograft continued to progress with severe ulcerations that extended into the dura. Patient was initiated on vismodegib 150 mg daily and subsequently developed a diffuse maculopapular rash within 14 days of treatment. The rash resolved with topical triamcinolone 0.1% and discontinuation of vismodegib. Loratadine 10 mg daily was concurrently administered for rash prophylaxis upon vismodegib re-initiation. Within 7 days of therapy, the rash returned, and subsequently vismodegib was discontinued and oral prednisone taper was initiated. Given limited effective treatment options, vismodegib was continued at a modified schedule of 150 mg daily for 2 weeks then 1 week off with prednisone 5 mg daily. To date, patient has completed 2 years of treatment with no return of rash or disease progression.
BCC occurs in 2 million patients annually in the US. Fortunately, most of these cases are responsive to local therapy with rare metastatic progression. The emergence of novel Hedgehog pathway inhibitors (vismodegib, sonidegib) provide effective options for advanced BCC. Although vismodegib has been reported to cause Grade 3-4 adverse events in 25% of patients, there are no reports of vismodegib-induced rash nor recommendations regarding management.
For many novel targeted therapies, the appropriate management of toxicities has not been well described. This case study presents a patient that continues to respond to therapy with a novel modified dosing scheme in addition to low-dose prednisone. We present this case report to offer a potential treatment option in patients who experience a vismodegib-induced rash.
An 88-year-old male with locally advanced basal-cell carcinoma (BCC) of the scalp who had received multiple resections, stem cell graft, and amniotic allograft continued to progress with severe ulcerations that extended into the dura. Patient was initiated on vismodegib 150 mg daily and subsequently developed a diffuse maculopapular rash within 14 days of treatment. The rash resolved with topical triamcinolone 0.1% and discontinuation of vismodegib. Loratadine 10 mg daily was concurrently administered for rash prophylaxis upon vismodegib re-initiation. Within 7 days of therapy, the rash returned, and subsequently vismodegib was discontinued and oral prednisone taper was initiated. Given limited effective treatment options, vismodegib was continued at a modified schedule of 150 mg daily for 2 weeks then 1 week off with prednisone 5 mg daily. To date, patient has completed 2 years of treatment with no return of rash or disease progression.
BCC occurs in 2 million patients annually in the US. Fortunately, most of these cases are responsive to local therapy with rare metastatic progression. The emergence of novel Hedgehog pathway inhibitors (vismodegib, sonidegib) provide effective options for advanced BCC. Although vismodegib has been reported to cause Grade 3-4 adverse events in 25% of patients, there are no reports of vismodegib-induced rash nor recommendations regarding management.
For many novel targeted therapies, the appropriate management of toxicities has not been well described. This case study presents a patient that continues to respond to therapy with a novel modified dosing scheme in addition to low-dose prednisone. We present this case report to offer a potential treatment option in patients who experience a vismodegib-induced rash.