Fortunato D

Purpose: Review the clinical presentation and pathophysiology of hypercalcemia in diffuse large B-cell lymphoma.

Methods: Case study of a 59-year-old man with untreateddiffuse large B-cell lymphoma (DLBCL) who presented with anorexia, constipation, and weight loss in the setting of a fungating breast mass.

Results: The patient presented to an outside hospital 1.5 years prior for a left breast mass biopsy that was diagnosed as triple-hit DLBCL. However, he deferred treatment at that time. He subsequently experienced anorexia, nausea, vomiting, consti-pation, and a 20-pound unintentional weight loss. At hospital presentation, a physical examination revealed enlargement of the left breast mass measuring 8 x 14 cm with central ulceration and malodorous purulent discharge and a proximal 7 x 4 cm firm axillary mass. The patient reported no abdominal pain or fever. He was found to have acute kidney injury (creatinine 2.9 mg/dL); hyperuricemia (13.3 mg/dL); and corrected hypercalcemia (17.4 mg/dL). Empiric treatment for tumor lysis syndrome with rasburicase, allopurinol, and aggressive IV hydration was initiated. Further evaluation revealed normal lactate dehydrogenase and K+.The patient was found to have an elevated vitamin D 1,25-OH (244 pg/mL) but low parathyroid hormone (PTH) (6.4 pg/mL); normal PTH-rP; mild hyperphosphatemia (5.5 mg/dL); and negative serum protein electrophoresis/urine protein electrophoresis. Clinical presentation was suggestive of vitamin D-mediated hypercalcemia. The patient received pamidronate and aggressive IV hydration. Electrolyte abnormalities and renal function gradually improved. Computed tomography and positron emission tomography imaging revealed masses localized to the left chest wall with ipsilateral axillary lymphadenopathy. Surgical biopsy of the mass reconfirmed DLBCL ultimately staged as IIE. Following stabilization, the patient declined more aggressive chemotherapy and received R-CHOP with a complete response.

Conclusions: The patient presented with vitamin D-mediated hypercalcemia in the setting of aggressive triple-hit DLBCL. Vitamin D-mediated hypercalcemia occurs in < 1% of lymphomas, and < 0.5% of breast tumors are primary lymphomas. This case study presents a rare constellation of findings at diagnosis. The patient responded to IV hydration and pamidronate and subsequently received R-CHOP for stage IIE DLBCL. While hypercalcemia in the setting of malignancy is associated with poor prognosis, treatment of hypercalcemia does not improve survival.

Purpose: Review the clinical presentation and pathophysiology of hypercalcemia in diffuse large B-cell lymphoma.

Methods: Case study of a 59-year-old man with untreateddiffuse large B-cell lymphoma (DLBCL) who presented with anorexia, constipation, and weight loss in the setting of a fungating breast mass.

Results: The patient presented to an outside hospital 1.5 years prior for a left breast mass biopsy that was diagnosed as triple-hit DLBCL. However, he deferred treatment at that time. He subsequently experienced anorexia, nausea, vomiting, consti-pation, and a 20-pound unintentional weight loss. At hospital presentation, a physical examination revealed enlargement of the left breast mass measuring 8 x 14 cm with central ulceration and malodorous purulent discharge and a proximal 7 x 4 cm firm axillary mass. The patient reported no abdominal pain or fever. He was found to have acute kidney injury (creatinine 2.9 mg/dL); hyperuricemia (13.3 mg/dL); and corrected hypercalcemia (17.4 mg/dL). Empiric treatment for tumor lysis syndrome with rasburicase, allopurinol, and aggressive IV hydration was initiated. Further evaluation revealed normal lactate dehydrogenase and K+.The patient was found to have an elevated vitamin D 1,25-OH (244 pg/mL) but low parathyroid hormone (PTH) (6.4 pg/mL); normal PTH-rP; mild hyperphosphatemia (5.5 mg/dL); and negative serum protein electrophoresis/urine protein electrophoresis. Clinical presentation was suggestive of vitamin D-mediated hypercalcemia. The patient received pamidronate and aggressive IV hydration. Electrolyte abnormalities and renal function gradually improved. Computed tomography and positron emission tomography imaging revealed masses localized to the left chest wall with ipsilateral axillary lymphadenopathy. Surgical biopsy of the mass reconfirmed DLBCL ultimately staged as IIE. Following stabilization, the patient declined more aggressive chemotherapy and received R-CHOP with a complete response.

Conclusions: The patient presented with vitamin D-mediated hypercalcemia in the setting of aggressive triple-hit DLBCL. Vitamin D-mediated hypercalcemia occurs in < 1% of lymphomas, and < 0.5% of breast tumors are primary lymphomas. This case study presents a rare constellation of findings at diagnosis. The patient responded to IV hydration and pamidronate and subsequently received R-CHOP for stage IIE DLBCL. While hypercalcemia in the setting of malignancy is associated with poor prognosis, treatment of hypercalcemia does not improve survival.

Purpose: Review the clinical presentation and pathophysiology of hypercalcemia in diffuse large B-cell lymphoma.

Methods: Case study of a 59-year-old man with untreateddiffuse large B-cell lymphoma (DLBCL) who presented with anorexia, constipation, and weight loss in the setting of a fungating breast mass.

Results: The patient presented to an outside hospital 1.5 years prior for a left breast mass biopsy that was diagnosed as triple-hit DLBCL. However, he deferred treatment at that time. He subsequently experienced anorexia, nausea, vomiting, consti-pation, and a 20-pound unintentional weight loss. At hospital presentation, a physical examination revealed enlargement of the left breast mass measuring 8 x 14 cm with central ulceration and malodorous purulent discharge and a proximal 7 x 4 cm firm axillary mass. The patient reported no abdominal pain or fever. He was found to have acute kidney injury (creatinine 2.9 mg/dL); hyperuricemia (13.3 mg/dL); and corrected hypercalcemia (17.4 mg/dL). Empiric treatment for tumor lysis syndrome with rasburicase, allopurinol, and aggressive IV hydration was initiated. Further evaluation revealed normal lactate dehydrogenase and K+.The patient was found to have an elevated vitamin D 1,25-OH (244 pg/mL) but low parathyroid hormone (PTH) (6.4 pg/mL); normal PTH-rP; mild hyperphosphatemia (5.5 mg/dL); and negative serum protein electrophoresis/urine protein electrophoresis. Clinical presentation was suggestive of vitamin D-mediated hypercalcemia. The patient received pamidronate and aggressive IV hydration. Electrolyte abnormalities and renal function gradually improved. Computed tomography and positron emission tomography imaging revealed masses localized to the left chest wall with ipsilateral axillary lymphadenopathy. Surgical biopsy of the mass reconfirmed DLBCL ultimately staged as IIE. Following stabilization, the patient declined more aggressive chemotherapy and received R-CHOP with a complete response.

Conclusions: The patient presented with vitamin D-mediated hypercalcemia in the setting of aggressive triple-hit DLBCL. Vitamin D-mediated hypercalcemia occurs in < 1% of lymphomas, and < 0.5% of breast tumors are primary lymphomas. This case study presents a rare constellation of findings at diagnosis. The patient responded to IV hydration and pamidronate and subsequently received R-CHOP for stage IIE DLBCL. While hypercalcemia in the setting of malignancy is associated with poor prognosis, treatment of hypercalcemia does not improve survival.