Background: To investigate obesity as susceptibility factor in patients with idiopathic AA amyloidosis.
Methods: Clinical, biochemical and genetic data were obtained from 146 patients with AA amyloidosis. Control groups comprised 40 patients with long-standing inflammatory diseases without AA amyloidosis and 56 controls without any inflammatory disease.
Findings: Patients with AA amyloidosis had either familial Mediterranean fever (FMF) or long-standing rheumatic diseases as underlying inflammatory disease (n = 111, median age 46 years). However, in a significant proportion of patients with AA amyloidosis no primary disease was identified (idiopathic AA; n = 37, median age 60 years). Patients with idiopathic AA amyloidosis were more obese and older than patients with AA amyloidosis secondary to FMF or rheumatic diseases. Serum leptin levels correlated with the body mass index (BMI) in all types of AA amyloidosis. Elevated leptin levels of more than 30 µg/l were detected in 18% of FMF/rheumatic + AA amyloidosis and in 40% of patients with idiopathic AA amyloidosis (p = .018). Finally, the SAA1 polymorphism was confirmed as a susceptibility factor for AA amyloidosis irrespective of the type of the disease.
Conclusions: Obesity, age and the SAA1 polymorphism are susceptibility factors for idiopathic AA amyloidosis. Recent advances in treatment of FMF and rheumatic disorders will decrease the incidence of AA amyloidosis due to these diseases. Idiopathic AA, however, might be an emerging problem in the ageing and increasingly obese population.
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http://dx.doi.org/10.1080/13506129.2018.1429391 | DOI Listing |
Amyloid
January 2025
Division of Hematology, Department of Medicine, Mayo Clinic, Rochester, MN, USA.
Background: Cardiac AL and ATTR are potentially fatal cardiomyopathies. Current therapies do not address mechanisms of tissue dysfunction because these remain unknown. Our prior work focused on the amyloid plaque proteome, which may not capture tissue-wide proteomic alterations.
View Article and Find Full Text PDFJ Hand Surg Asian Pac Vol
January 2025
Department of Orthopaedic Surgery, Kochi Medical School, Kochi University, Nankoku, Japan.
Carpal tunnel syndrome (CTS) due to amyloid deposition was reported to precede fatal cardiac amyloidosis by several years. Although nerve conduction study (NCS) supports CTS diagnosis, the incidence of positive amyloid deposition in electrophysiologically proven CTS is unclear. We retrospectively analysed the demographic data including age, gender, bilateral hand involvement, amyloid deposition and NCS results, of 111 consecutive CTS patients with postoperative symptom improvement (mean 71.
View Article and Find Full Text PDFMedicina (Kaunas)
December 2024
Fundeni Clinical Institute, 022328 Bucharest, Romania.
: Amyloidosis is a disorder characterized by the abnormal folding of proteins, forming insoluble fibrils that accumulate in tissues and organs. This accumulation disrupts normal tissue architecture and organ function, often with serious consequences, including death if left untreated. Light-chain amyloidosis (AL) and hereditary transthyretin-type amyloidosis (hATTR) are two of the most common types.
View Article and Find Full Text PDFDiagnostics (Basel)
December 2024
Unit of Clinical Pathology, Department of Medical and Surgical Sciences, University of Foggia, University Hospital "Policlinico Riuniti", Viale Luigi Pinto, 71122 Foggia, Italy.
Monoclonal gammopathy of renal significance (MGRS) refers to a group of renal disorders caused by a monoclonal immunoglobulin (MIg), secreted by a non-malignant B-cell clone. Unlike overt multiple myeloma or B-cell proliferation, MGRS does not meet those diagnostic criteria. However, it is associated with significant morbidity, due to severe renal, and sometimes systemic, lesions induced by the MIg.
View Article and Find Full Text PDFFront Cardiovasc Med
December 2024
National Key Laboratory for Innovation and Transformation of Luobing Theory, Jinan, China.
Background: Cardiac amyloidosis (CA) is a challenging diagnosis, particularly when the classic signs, such as increased wall thickness in a non-dilated left ventricle (LV), are absent. This makes the diagnosis more difficult in patients with normal LV wall thickness. We present a case of CA without increased wall thickness and without the characteristic granular sparkling echotexture in a non-dilated LV.
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