Background Giant cell tumor of bone (GCTB) is a skeletal neoplasm that most commonly occurs in long bones and rarely in the skull. These tumors are considered benign but tend to be locally aggressive and carry a high rate of local recurrence. True malignant transformation is rare and even metastatic disease carries a rather benign course. Clinical manifestations depend on tumor location and are mostly due to mass effect into the surrounding tissues. We describe a patient with a GCTB, located at the sellar-suprasellar region which resulted in optic chiasm compression and panhypopituitarism. Clinical Case Case of a 28-years-old female who initially presented with recurrent headaches for which brain imaging was done and a suprasellar mass was noted. It initially measured2.3x 3.2x 2. 0 cm. The mass was invading the left cavernous sinus and displacing the pituitary gland and infundibulum to the right. At that time no optic chiasm compression was noted, and no pituitary hormonal excess or deficiency was identified. The mass was treated conservatively with gamma knife radiation, with reduction in size. About 10 months later, patient complained of visual problems for which brain imaging was repeated and noted with interval increase in tumor size. Patient was started on dexamethasone due to mass effect and referred to ER. Review of systems at that time was remarkable for oligomenorrhea and decreased peripheral vision. Patient denied general malaise, dizziness, galactorrhea, weight changes, palpitations, dry skin or striae, bowel changes, polyuria, increased thirst nor changes in shoe or ring size. Physical examination showed unremarkable vital signs. Upon confrontation there was evidence of bitemporal hemianopsia confirmed on formal visual field testing. Laboratory studies showed mildly elevated prolactin, low-normal TSH with mildly low FT4 suggesting overt central hypothyroidism and suppressed morning cortisol. Patient was scheduled for craniotomy, which resulted in an overall decrease of tumor bulk. After the surgery, patient developed DI requiring desmopressin administration. Currently, patient continues with panhypopituitarism treated with hormonal replacement. Pathology report was compatible with a GCTB. On follow up MRI about 6 months after surgery, there was mild interval increase in size, no distant metastases identified. Treatment with denosumab was started as recommended by oncology service in an attempt to control tumor growth. At this time, patient has tolerated denosumab well and has not developed further headaches or visual symptoms. Follow up imaging is pending to assess response to treatment. Conclusion GCTB of the sella-suprasellar region, albeit rare, have been described and always should be included in the differential diagnosis of sellar lesions. Imaging alone is insufficient to make a definitive diagnosis of these tumors and tissue sampling either by biopsy or surgical resection should be considered in order to determine treatment alternatives. Presentation: No date and time listed
Background Breakthroughs in oncology have led to the incorporation of immunotherapy to improve the prognosis in patients with advanced malignancies. Checkpoint inhibitors are immunomodulatory antibodies that enhance the immune system using PD-1/PD-L1 and CTLA-4 as primary targets. Pharmacologic disruption in checkpoints can trigger autoimmune-like manifestations in various organs systems, known as immune-related adverse effects. Endocrinopathies of the pituitary, thyroid, or adrenal glands have been described; with the most common being hypothyroidism, hyperthyroidism and hypophysitis. We report a case of hypophysitis induced by immunotherapy in a patient treated with ipilimumab and nivolumab for renal cell carcinoma with bone metastases. Clinical case Case of a 63-year-old male patient with left renal cell carcinoma treated with nivolumab and ipilimumab, who presented with general weakness, malaise, disorientation, slow mentation and severe hyponatremianine weeks after immunotherapy initiation. Denied headache, loss of consciousness, dizziness, involuntary movements, nausea, vomiting, abdominal pain, changes in bowel movements, swelling of skin or changes in skin color, decreased libido or erectile dysfunction, hair loss, polyuria, polydipsia, mood changes or hypoglycemia. Laboratory results showed serum sodium levels of 117mEq/L, inappropriately normal ACTH (18.8 pg/mL), low serum cortisol in early morning (1.97µg/dL), low TSH (0.17 mIU/mL) and low total T4 (4.39µg/dL). Serum sodium levels improved to 136 mEq/L after administration of 3% NaCl and glucocorticoids, that were given due to concerns for adrenal insufficiency. Patient was discharged home on oral hydrocortisone and immunotherapy was discontinued. Repeated hormonal workup revealed previously identified central hypothyroidism and secondary adrenal insufficiency. Additionally, had an inappropriate lynormal FSH (11.10 mIU/L) and LH (2.62 IU/L), in view of a low total testosterone (< 2.5 pg/mL), suggestive of hypogonadotropic hypogonadism. Since the patient was asymptomatic for sexual dysfunction, hormonal work up was repeated later on, and found with normal gonadotropins and normal total testosterone levels (444 ng/dL; 93-740 ng/dL), with no evidence of hypogonadism. There was no indication for growth hormone therapy in view of anormal IGF-1 for age (236 ng/mL). He is currently clinically stable on replacement therapy with hydrocortisone and levothyroxine. Conclusion Immunotherapy-induced endocrinopathies are important adverse effects that clinicians should be aware of and monitored routinely in patients treated with checkpoint inhibitors. Hypophysitis typically manifests with fatigue and headache in the presence of adrenal insufficiency, hypothyroidism and hypogonadism with preservation of growth hormone. It This condition has been described with different immune checkpoint inhibitors, although incidence is higher with ipilimumab, as reported in this case. Recovery of some pituitary function is common, but persistent deficiences can occur, particularly adrenal insufficiency that rarely resolves. Complications associated with hormonal deficiencies can be life-threatening and prompt recognition is warranted. Presentation: No date and time listed
Introduction Adrenocortical carcinoma (ACC) is a rare malignancy of the adrenal glands, but often presents an aggressive behavior with variable prognosis. Median age of diagnosis is in the fifth to sixth decade of life with a median survival rate of 3-4 years. Complete surgical resection is the first line and only curative therapy. In patients with high-risk ACC, adjuvant therapy with mitotane, alone or in combination with other cytotoxic agents, may be used. Case description Case of a 33-year-old female with history of thyroid nodules presenting with a one year history of amenorrhea and hirsutism. One year prior to evaluation, the patient developed an intense right flank pain requiring abdominal-pelvic CT. It showed a solid heterogeneous right flank mass measuring 16×16×12 cm, 44Hounsfield units without enhanced contrast washout. Hormonal workup at that time resulted with DHEA-S > 10,000ng/mL(nl 350-4300), androstenedione 10.7 ng/mL (nl 0.35–2.78), total testosterone 3.21 ng/mL (nl < 0.52), midnight salivary cortisol at 14 nmol/L (nl < 3.6) and normal FSH, ACTH and serum morning cortisol. Staging chest CT exhibited bilateral pulmonary embolisms. Patient underwent right open total adrenalectomy of a necrotic/hemorrhagic mass measuring 20×16×9 cm with complete resection. Histology consistent with a low-grade ACC with a mitotic rate 18/50 HPF, with capsular invasion but no lymphovascular invasion and clear margins. It was stratified as stage T2N0M0. Immunohistochemistry's were positive for Melan-A, calretinin, synaptophysin, and inhibin. Ki67 was 80%. She was started on hydrocortisone replacement. PET/CT scan showed hypermetabolic focus at the right thyroid lobe (previously biopsied with benign findings), but otherwise no pathologic 18 FDG uptake related to known oncologic disease. Due to her high risk of recurrence, the patient was started on mitotane 2 g daily as adjuvant therapy but had to discontinue therapy after 1 month due to lack of availability. One year after initial presentation, she was evaluated at our clinics and after discussion with Oncology Service restarting mitotane was recommended. However, marked transaminitis was noted along with right abdominal discomfort. Abdominal MRI revealed hepatic hypo-enhancing masses suggestive of liver metastases, with the largest measuring 6.7cm. Patient underwent right partial hepatectomy and was found with extensive metastatic carcinoma and lymph node involvement. Therapy with mitotane was restarted, pending chemotherapy initiation. Conclusion The goal of any therapy for ACC is to alleviate symptoms and prolong survival. Mitotane, an adrenolytic drug used as palliative treatment, is among therapeutic options. Due to the rarity of the disease, data regarding its use is mixed due to limited randomized controlled trials. Nevertheless, it supports improvement in recurrence-free and possibly overall-survival after complete radical resection in stage I, II or III ACC. Unfortunately, there is still marked individual variation in outcomes. Presentation: No date and time listed
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