Santoso, D.; Thaha, M.; Empitu, M.A.; Kadariswantiningsih, I.N.; Suryantoro, S.D.; Haryati, M.R.; Hertanto, D.M.; Pramudya, D.; Bintoro, S.U.Y.; Nasronudin, N.; Alsagaff, M.Y.; Susilo, H.; Wungu, C.D.K.; Budhiparama, N.C.; Hogendoorn, P.C.W. Brown Tumour in Chronic Kidney Disease: Revisiting an Old Disease with a New Perspective. Cancers2023, 15, 4107.
Santoso, D.; Thaha, M.; Empitu, M.A.; Kadariswantiningsih, I.N.; Suryantoro, S.D.; Haryati, M.R.; Hertanto, D.M.; Pramudya, D.; Bintoro, S.U.Y.; Nasronudin, N.; Alsagaff, M.Y.; Susilo, H.; Wungu, C.D.K.; Budhiparama, N.C.; Hogendoorn, P.C.W. Brown Tumour in Chronic Kidney Disease: Revisiting an Old Disease with a New Perspective. Cancers 2023, 15, 4107.
Santoso, D.; Thaha, M.; Empitu, M.A.; Kadariswantiningsih, I.N.; Suryantoro, S.D.; Haryati, M.R.; Hertanto, D.M.; Pramudya, D.; Bintoro, S.U.Y.; Nasronudin, N.; Alsagaff, M.Y.; Susilo, H.; Wungu, C.D.K.; Budhiparama, N.C.; Hogendoorn, P.C.W. Brown Tumour in Chronic Kidney Disease: Revisiting an Old Disease with a New Perspective. Cancers2023, 15, 4107.
Santoso, D.; Thaha, M.; Empitu, M.A.; Kadariswantiningsih, I.N.; Suryantoro, S.D.; Haryati, M.R.; Hertanto, D.M.; Pramudya, D.; Bintoro, S.U.Y.; Nasronudin, N.; Alsagaff, M.Y.; Susilo, H.; Wungu, C.D.K.; Budhiparama, N.C.; Hogendoorn, P.C.W. Brown Tumour in Chronic Kidney Disease: Revisiting an Old Disease with a New Perspective. Cancers 2023, 15, 4107.
Abstract
Osteitis fibrosa cystica (OFC) and Brown Tumour are two related but distinct types of bone lesions that result from overactivity of osteoclasts most often associated with chronic kidney disease (CKD). Despite their potential consequences, these conditions are poorly understood because of their rare prevalence and variability in their clinical manifestation. Canonically, OFC and Brown Tumours are caused by secondary hyperparathyroidism in CKD. Recent literature showed that multiple factors such as hyperactivation of the renin-angiotensin-aldosterone system and chronic inflammation may also contribute to the occurrence of these diseases through osteoclast activation. Moreover, hotspot KRAS mutations were identified in these lesions placing them in the spectrum of RAS-MAPK-driven neoplasms, while until recently thought to be reactive lesions. Some risk factors contributed to the occurrence of OFC and Brown Tumour such as age, gender, comorbidities, and certain medications. The diagnosis of OFC and Brown Tumour includes clinical symptoms involving chronic bone pain and laboratory finding of hyperparathyroidism. In radiological imaging, the X-ray and Computed tomography (CT) scan could show lytic or multi-lobular cystic alterations. Histologically both lesions are characterized by clustered osteoclast in a fibrotic hemorrhagic background. Based on the latest understanding of the mechanism of OFC, this review elaborates on the manifestation, diagnosis, and available therapies that can be leveraged to prevent the occurrence of OFC and Brown Tumour.
Keywords
Bone Tumour; hyperparathyroidism; giant cell; osteoclast
Subject
Medicine and Pharmacology, Pathology and Pathobiology
Copyright:
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.