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- W3028274328 abstract "A 47-year-old woman with morbid obesity (body mass index: 41 kg/m2) and a history ofhypertension, pulmonary embolism and successfully treated gout (one year ago) presented withnephrotic syndrome (15 g/24 h) and loss of kidney function (endogenous creatinine clearance 27ml/min/1.73 m2). A kidney biopsy revealed AA amyloid. An extensive investigation was performedto detect an underlying inflammatory disease process by testing blood and urine, imaging andgenetic testing for autoinflammatory diseases. Serum levels of C-reactive protein (CRP) andserum amyloid A protein (SAA) were continuously elevated. Serum amyloid P component (SAP)-scintigraphy showed intense uptake in a massively enlarged liver and in the spleen. This extensiveinvestigation did not reveal an underlying inflammatory process. Her gout became asymptomaticalmost immediately after start of treatment. Therefore, we concluded that morbid obesity was themost probable cause of her AA amyloidosis. Treatment with colchicine and prednisolone did notsubstantially reduce the SAA and CRP levels. Also, treatment with anakinra (interleukin-1 receptorantagonist) and tocilizumab (interleukin-6 receptor antagonist) failed. The downhill course of thedisease progressed to complete renal failure within three years and dialysis was started. This caseindicates that the long-standing low-grade inflammation seen in morbid obesity may be a potentialcause of systemic AA amyloidosis and may be difficult to treat. However, it is essentially a diagnosisof exclusion, since known underlying inflammatory conditions should be excluded first." @default.
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- W3028274328 date "2020-01-01" @default.
- W3028274328 modified "2023-10-17" @default.
- W3028274328 title "Obesity-induced AA amyloidosis: A diagnosis of exclusion" @default.
- W3028274328 doi "https://doi.org/10.37532/1758-4272.2019.15(2).26-32" @default.
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