scholarly journals Reversible Posterior Leukoencephalopathy Syndrome Developing After Restart of Sunitinib Therapy for Metastatic Renal Cell Carcinoma

2016 ◽  
Vol 2016 ◽  
pp. 1-5 ◽  
Author(s):  
Shinji Fukui ◽  
Yuta Toyoshima ◽  
Takeshi Inoue ◽  
Yoriaki Kagebayashi ◽  
Shoji Samma

A 64-year-old Japanese man had started molecular-targeted therapy with sunitinib for lymph node metastasis 5 years after nephrectomy for left renal cell carcinoma (clear cell carcinoma, G2, pT2N0M0). He was transported to our emergency department because of generalized tonic-clonic seizure, vision loss, and impaired consciousness with acute hypertension after 8 cycles of treatment (2 years after the initiation of sunitinib therapy, including a drug withdrawal period for one year). MRI of the brain (FLAIR images) showed multiple high-intensity lesions in the white matter of the occipital and cerebellar lobes, dorsal brain stem, and left thalamus. Reversible posterior leukoencephalopathy syndrome caused by sunitinib was suspected. In addition to the immediate discontinuation of sunitinib therapy, the administration of antihypertensive agents and anticonvulsants improved the clinical symptoms without neurological damage. Physicians should be aware that sunitinib causes reversible posterior leukoencephalopathy syndrome. The early recognition of reversible posterior leukoencephalopathy syndrome is critical to avoid irreversible neurological damage.

2011 ◽  
pp. 152-161
Author(s):  
Farheen M. Shah-Khan ◽  
Daryl Pinedo ◽  
Prabodh Shah

Reversible Posterior Leukoencephalopathy Syndrome (RPLS) is a well recognized entity with a variety of benign and malignant conditions. Recently it has been found to be associated with the use of anti-neoplastic agents including targeted therapies. RPLS occurs rapidly with the use of some drugs and more slowly with others. Combined therapies are associated with a more frequent and more rapid presentation. This review was based on a literature search for English Language articles concerning RPLS and chemotherapeutic agents published from June 1996 to March 2007. We used the PubMed database with keywords: “RPLS”, “Posterior reversible encephalopathy syndrome”, “(PRES)”, “Chemotherapy” and “MRI”. This syndrome has classical Clinical-Radiologic features that are easy to recognize. Early recognition and withdrawal of the offending agent is all that is needed in most cases. This review highlights the features of the syndrome. It draws our attention to an entity which is being more frequently recognized and whose exact pathologic mechanisms need to be further studied. This syndrome is associated with the use of neurotoxic as well as non-neurotoxic agents and usually runs a benign course if there is an early diagnosis and management.


2020 ◽  
Vol 2020 ◽  
pp. 1-4
Author(s):  
Filipe Bessa ◽  
Pedro Gaspar ◽  
Pedro Antunes Meireles ◽  
Maria Inês Parreira ◽  
Juliana Serrazina Pedro ◽  
...  

Renal cell carcinoma accounts for approximately 3% of adult malignancies. Designated in the literature as “the great masquerader,” the great diversity of clinical manifestations is associated with the several paraneoplastic syndromes that potentially accompany it. Paraneoplastic amyloidosis is described in about 3–8% of cases, only exceptionally as an initial manifestation, with uncommon gastrointestinal involvement. A rare case of malabsorption by intestinal amyloidosis is presented as initial manifestation of renal cell carcinoma, emphasizing the need for early recognition of these paraneoplastic conditions.


2021 ◽  
Vol 1 (1) ◽  
pp. 69-73
Author(s):  
Bogdan Silviu Ungureanu ◽  
Victor Mihai Sacerdoțianu ◽  
Dan Nicolae Florescu ◽  
Lucian Mihai Florescu ◽  
Ion Rogoveanu ◽  
...  

Cholestatic jaundice is usually linked to a malignant disease when it is secondary to a mechanical obstruction of the bile duct or due to hepatic metastasis. As a paraneoplastic syndrome, cholestasis has been described in lymphoproliferative disorders, in prostate cancer and as the Stauffer syndrome with non-metastatic dysfunction in patients with renal cell carcinoma (RCC). We present the case of a 61 year old patient with a paraneoplastic manifestation with cholestatic jaundice due to RCC with kindney and lung metastases. Clinical characteristics of patients with RCC vary and sometimes manifest in a peculiar way. Cholestatic jaundice is a rare paraneoplastic syndrome associated with RCC and with the exclusion of more frequent causes, it should be taken into account in the differential diagnosis. This rare but possible association requires prompt recognition, as prognosis correlates with disease stage and influences patient’s overall survival, and an early recognition of this syndrome may improve, sometimes, patients’ outcome.


2018 ◽  
Vol 42 (6) ◽  
pp. 391-398 ◽  
Author(s):  
Laura D. Selby ◽  
Hillary C. Stiefel ◽  
Alison H. Skalet ◽  
Molly S. Cardenal ◽  
Kavita V. Bhavsar ◽  
...  

2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A567-A568
Author(s):  
Anastasia Tambovtseva ◽  
Rima Gandhi ◽  
Randa Abdelmasih ◽  
Elio Paul Monsour ◽  
Alan Hamza

Abstract Introduction: Metastatic sellar masses are very contributing to 2% of all sellar masses, and up to 0.87% of all metastases to the brain. Breast and lung cancer contribute for up to 60% of all sellar metastases but it is important to recognize other cancers that can also metastasize to pituitary gland. Renal Cell carcinoma (RCC) is number nine on that list. Here we present a case of rare RCC metastasis to pituitary which was mistaken as pituitary adenoma to emphasize early recognition and management of pituitary metastases which may result in better patient’s outcomes and prognosis. Case Presentation: 7 2 year-old male with a remote history of left sided RCC presented with worsening diplopia, blurry vision and headaches for 2 months. Physical exam was remarkable for right sided ptosis with right oculomotor, trochlear and abducens palsy. Computed Tomography Imaging (CT) of the brain showed hyperdense sellar/suprasellar fullness. Magnetic Resonance Imaging (MRI) with and without contrast of the brain showed 2.2 x 1.7 cm enhancing mass in the right cerebellopontine angle with local mass effect concerning for a pituitary tumor. Laboratory work-up was remarkable for hyperprolactinemia 36.5 ng/mL, low TSH <0.015 mU/L, and normal ACTH, FSH and LH levels. Patient underwent endoscopic trans-nasal resection of pituitary tumor. Surgical pathology of the tumor was consistent with metastatic renal cell carcinoma. He was discharged with appropriate multidisciplinary outpatient follow up with endocrinology, oncology and radiology. Discussion: Pituitary metastasis is very rare and often mistaken for pituitary adenoma. Only 7% of Pitutary metastases are symptomatic. Symptom presentation depends on the location of metastases. They include diabetes insipidus (45.2%), visual field defects (27.9%), hypopituitarism (23.6%), ophthalmoplegia (21%), headache (15.8%) and hyperprolactinemia (6.3%). Although, there is no gold standard imaging for sellar masses, both thin-section CT and MRI are beneficial. CT is used for visualizing bony destruction and calcification, on the other hand MRI demarcates lesions in that area. Due to its rarity, there is no standardized guideline therapy for pituitary metastasis and it should be individualized based on patient’s presentation, but it should be multidisciplinary approach of surgical resection, postoperative stereotactic radiosurgery, chemotherapy, and hormone replacement therapy. Prognosis of metastases to pituitary is very poor, with reported six to twenty-two months post resection survival. Factors contributing to prolonged survival are younger age, single/small metastases, and locally guided radiation therapy. Conclusion: This case is to shed light on early recognition of sellar metastasis as a challenging diagnosis especially in patients with rapidly growing pituitary mass and neurological symptoms with history of malignancy for better outcomes.


2017 ◽  
Vol 35 (6_suppl) ◽  
pp. 457-457
Author(s):  
Yuji Miura ◽  
Chiyo K. Imamura ◽  
Keita Uchino ◽  
Takeshi Kishida ◽  
Nobuaki Matsubara ◽  
...  

457 Background: Axitinib is one of the standard second-line therapies after sunitinib in patients (pts) with metastatic renal cell carcinoma (mRCC). The previous study showed that higher exposure and diastolic blood pressure (dBP) were independently associated with better clinical outcomes. However, many factors, such as antihypertensive agents use, usually affect dBP. Therefore, axitinib dose adjustment based on its exposure could be more adequate than that based on dBP. Methods: We conducted a prospective phase II trial of axitinib dose adjustment for Japanese pts with mRCC previously treated with sunitinib. Starting dose of axitinib was 5 mg BID. We assayed blood axitinib levels on day 1 and calculated the area under concentration-time curve from 0 to 12 hours (AUC0-12). We determined the individual sufficient dose (SD) to reach AUC0-12 value at the steady state of 150 ng*hr/mL. After day 15, axitinib dose was adjusted to keep over SD according to adverse drug reaction for each patient. The primary endpoint is 6-month progression-free survival (6m-PFS) rate. Secondary endpoints include toxicity and objective response rate. With power of 80% and one-sided alpha of 10%, thirty-two pts were required to reject 48% of 6m-PFS rate under expected 69% 6m-PFS rate. Results: Between May 2013 to March 2015, 26 pts were enrolled when the trial closed for poor accrual. Pts’ characteristics were: median age 71 years, male 20 (77%), PS 0 19 (73%), and International Metastatic RCC Database Consortium intermediate risk 24 (92%). Median SD of axitinib was 3 mg BID (range 1-16). SD was given at a median of 78% (range 0-100) of total administration day until 6 months. Two pts did not receive the planned SD because their SD was over 10 mg BID. Therefore, the two pts were excluded from safety analysis; meanwhile all pts were included in efficacy analysis. The 6m-PFS rate was 85% (95% CI 66-94, p < 0.01). The median PFS was 10.6 months (95% CI 7.2-16.7). The most common grade 3 to 4 adverse events during the first 6 months were hypertension (79%), decrease appetite (29%), fatigue (13%), and hand-foot syndrome (13%). Conclusions: The individual dose adjustment of axitinib to keep over 150 ng*hr/mL of AUC0-12 on day 1 for sunitinib-pretreated mRCC is feasible. Clinical trial information: UMIN000009579.


2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A590-A591
Author(s):  
Hani Rjoob ◽  
Tayyab S Khan

Abstract Background: Immune checkpoint inhibitors are immunomodulatory antibodies directed against programmed cell death 1 (PD-1), Nivolumab, or cytotoxic T-lymphocyte antigen-4 (CTLA-4) Ipilimumab. They have improved outcomes in patients with advanced cancers including renal cell carcinoma, non-small cell lung cancer and melanoma. Several immune related adverse events (irAEs) have been recognized with use of immune checkpoint inhibitors, including those involving the endocrine system. We present a case of a patient presenting with isolated central adrenal insufficiency in the context of Nivolumab use. Clinical Case: Our patient is a 54-year old man with pre-existing primary hypothyroidism and metastatic renal cell carcinoma treated with Nivolumab. After receiving a total of 14 cycles of Nivolumab, he presented to the Emergency room with his sister, who found him confused and lethargic. On presentation, he was found to be hypoglycemic (random glucose was 2.2 mmol/L). On physical examination, his vital signs were stable and he appeared euvolemic. He was disoriented without focal neurological deficits. Initial blood work revealed sodium 134 mmol/L, (Normal 135-145mmol/L), potassium 4.5 mmol/L (Normal 3.5-5 mmol/L), and TSH being 12.6 mIU/L (Normal 0.4-4 mIU/L). He was resuscitated with IV Dextrose 50% bolus then admitted to hospital and kept on an IV dextrose infusion. While his glucose improved, he was found to have hyponatremia, and confusion persisted. His nadir sodium was 116 mmol/L without seizures or loss of consciousness and required treatment with hypertonic saline. Giving hypoglycemia and hyponatremia, morning cortisol and ACTH were checked and came back 4 nmol/L (Normal 133-537 nmol/L) and undetectable (&lt; 0.7 pmol/L, Normal 1.6-13.9 pmol/L) respectively. The diagnosis of central adrenal insufficiency was made likely secondary to Nivolumab. He was started on Dexamethasone 8 mg daily. Sodium level normalized and glucose level improved with steroids. He was discharged home on prednisone 50 mg and then switched to hydrocortisone. Further work up confirmed preserved other anterior pituitary hormones. MRI of Sella did not show pituitary enlargement or inflammation. Conclusion: Our patient presented with hypoglycemia and hyponatremia; both could be the presenting manifestations of central adrenal insufficiency. Nivolumab has been commonly associated with thyroid dysfunction and thyroiditis. Given lack of expression of PD-1 in the pituitary, PD-1 inhibitors are less likely to be associated with hypopituitarism in general, or central adrenal insufficiency in particular. However, our report adds to the growing body of literature associating it with central adrenal insufficiency, which can be isolated. In so doing, it underscores the need for early recognition this association with Nivolumab, so as to avoid the potentially life threatening consequences of this condition.


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