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      Relapse of Lung Adenocarcinoma Manifested by Spontaneous Tumor Lysis Syndrome

      case-report

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          Abstract

          Introduction

          Tumor lysis syndrome (TLS) is an oncologic emergency characterized by several metabolic derangements, such as hyperuricemia, hyperkalemia, hyperphosphatemia, and hypocalcemia. TLS is typically observed in hematologic malignancies, especially after starting the first administration of antineoplastic therapies. TLS in a solid malignancy is very unusual, and exceedingly rare when occurring spontaneously, in the absence of chemotherapy.

          Case Presentation

          We report a case of a 76-year-old man with lung adenocarcinoma, which started as a cancer with indolent behavior and small tumor burden but relapsed in 5 months with rapidly proliferating metastatic disease. Spontaneous TLS was the presenting clinical manifestation of the tumor relapse, and it led to the patient’s death.

          Conclusion

          To our knowledge, this is the first case of spontaneous TLS in a relapsed adenocarcinoma of the lung reported in the medical literature. The development of the metabolic derangements of TLS should prompt the consideration of tumor relapse during the follow-up of patients with solid malignancies.

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          Most cited references7

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          Hyperuricemia as a trigger of immune response in hypertension and chronic kidney disease

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            Pathophysiology, clinical consequences, and treatment of tumor lysis syndrome.

            Tumor lysis syndrome is an oncologic emergency that is characterized by severe electrolyte abnormalities and, frequently, by acute renal failure. The syndrome typically occurs in patients with lymphoproliferative malignancies, most often after initiation of treatment. The pathophysiology involves massive tumor cell lysis resulting in the release of large amounts of potassium, phosphate, and uric acid. Deposition of uric acid and calcium phosphate crystals in the renal tubules may lead to acute renal failure, which is often exacerbated by concomitant intravascular volume depletion. The kidney normally excretes these products, and consequently preexisting renal failure exacerbates the metabolic derangements of tumor lysis syndrome. Standard treatment aims to clear high plasma levels of potassium, uric acid, and phosphorus; correct acidosis; and prevent acute renal failure by way of aggressive intravenous hydration; lowering serum potassium levels; use of allopurinol; urinary alkalinization; or renal replacement therapy (if necessary). Allopurinol is the standard of care for treating hyperuricemia of malignancy, but is associated with drawbacks. Recombinant urate oxidase (rasburicase), which recently became available in the United States, provides a safe and effective alternative to allopurinol for lowering uric acid levels and preventing uric acid nephropathy.
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              Intrarenal dynamics in the pathogenesis and prevention of acute urate nephropathy.

              Tubular fluid flow, urine osmolality, and pH were selectively altered to determine the relative protective roles of these factors in a rat model of acute urate nephrophathy. Various prehyper uricemic conditions were established in five groups of animals: (a) normopenic Wistar rats given no pretreatment (Group I); (b) Wistar rats given acetazolamide, 20 mg/kg, and isotonic NaHCO3 to produce urine alkalinization (Group II); (c) Wistar rats in which a moderate diuresis, similar to that observed in Group II but without urine alkalinization, was induced with furosemide, 2 mg/kg (Group III); (d) Wistar rats in which a high-flow solute diuresis was induced with furosemide, 15 mg/kg (Group IV); (e) Brattleboro rats, homozygous for pituitary diabetes insipidus, that had a spontaneous high-flow water diuresis (Group V). A comparable level of hyperuricemia (19.4+/-2.2 mg/100 ml) was achieved in all animals with intravenous urate infusion. Clearance and micropuncture studies were performed before and 1 h after induction of hyperuicemia. Group I rats had mean falls in renal plasma flow and glomerular filtration rate of 83 and 86%, respectively; nephron filtration rate decreased 66%, and tubular and microvascular pressures increased twofold. In Group II there were 45 and 47% declines in renal plasma flow and glomerular filtration rate, respectively, a 66% fall in nephron filtration rate, and a 30% increase in tubular and vascular pressures. Moderate amounts of urate were seen in the kidneys. Group III had changes in renal function identical to Group II suggesting that the moderate prehyperuricemic diuresis in the latter group and not urine alkalinization produced the partial protection observed. Groups IV and V were completely and comparably protected with renal function studies unchanged from controls. It is concluded that high tubular fluid flow, whether induced by a solute or water diuresis, is the primary mechanism of protection in acute urate nephropathy. At most, urine alkalinization plays a minor preventive role.
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                Author and article information

                Journal
                Case Rep Oncol
                Case Rep Oncol
                CRO
                CRO
                Case Reports in Oncology
                S. Karger AG (Basel, Switzerland )
                1662-6575
                6 November 2023
                Jan-Dec 2023
                6 November 2023
                : 16
                : 1
                : 1306-1310
                Affiliations
                [a ]Internal Medicine, Guthrie Robert Packer Hospital, Sayre, PA, USA
                [b ]Pulmonary and Critical Care, Guthrie Robert Packer Hospital, Sayre, PA, USA
                [c ]Hematology-Oncology, Guthrie Robert Packer Hospital, Sayre, PA, USA
                Author notes
                Correspondence to: Giampaolo Talamo, Giampaolo.Talamo@ 123456Guthrie.org
                Article
                534398
                10.1159/000534398
                10629853
                37942403
                7036b9f7-dc40-443d-acb7-2d1a26fd58db
                © 2023 The Author(s). Published by S. Karger AG, Basel

                This article is licensed under the Creative Commons Attribution-NonCommercial 4.0 International License (CC BY-NC) ( http://www.karger.com/Services/OpenAccessLicense). Usage and distribution for commercial purposes requires written permission.

                History
                : 4 September 2023
                : 28 September 2023
                : 2023
                Page count
                Figures: 2, References: 7, Pages: 5
                Funding
                No financial support was obtained for this publication.
                Categories
                Case Report

                Oncology & Radiotherapy
                tumor lysis syndrome,non-small cell lung cancer,pulmonary adenocarcinoma,spontaneous lysis,case report

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