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Crystal arthritides - gout and calcium pyrophosphate arthritis : Part 1: Epidemiology and pathophysiology.
Z Gerontol Geriatr. 2018 Jun; 51(4):453-460.ZG

Abstract

Gout and calcium pyrophosphate deposition disease (CPPD, pseudogout) are still the most frequent inflammatory arthritides in multimorbid elderly patients. Gout and CPPD are different diseases and based on different pathophysiological principles. Gout is closely associated with the metabolic syndrome and is an independent risk factor for cardiovascular mortality. The prevalence of asymptomatic hyperuricemia is estimated to be 10-20% of adults in industrial nations and prevalence is strongly associated with age. More than 7% of persons aged over 65 years suffer from clinically manifest gout. The underlying pathophysiological principle is an imbalance between the formation and elimination of uric acid. The degradation of the purine bases adenine and guanosine to uric acid is catalysed by xanthine oxidase and genetic polymorphisms and mutations play an important role in absorption and excretion processes. Furthermore, carrier proteins, such as URAT-1 or OAT-4 also have an influence on these processes. An imbalance of the physiological processes results in the solubility product being exceeded, which in consequence leads to crystallization of urate. This induces a cascade of massive inflammatory reactions at the molecular and cellular level with the activation of cytokines. The inflammatory process can be stopped by neutrophil extracellular traps (NETs) that modulate aggregation and degradation of chemokines and cytokines and partitioning of crystallized urate against immune cells. Calcium pyrophosphate dehydrate (CPP) crystals are formed in the cartilage and CPP deposition can be found in 30% of people aged over 80 years. Inorganic pyrophosphate (PPi) is synthesized in chondrocytes and plays an important part in the formation of calcium pyrophosphate crystals. The degradation is catalyzed by inorganic pyrophosphatases. If there is dysregulation of this homeostasis more PPi is produced, which ultimately contributes to the formation of the CPP crystals.

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Authors+Show Affiliations

Schlee S
Klinik für Allgemeine Innere Medizin und Geriatrie, Barmherzige Brüder Regensburg, Prüfeninger Str. 86, 93049, Regensburg, Germany. steffen.schlee@barmherzige-regensburg.de.
Bollheimer LC
Lehrstuhl für Altersmedizin, RWTH Aachen University, Pauwelsstraβe 30, 52074, Aachen, Germany.
Bertsch T
Institut für Klinische Chemie, Laboratoriumsmedizin und Transfusionsmedizin, Klinikum Nürnberg, Paracelsus Medizinische Privatuniversität, Prof.-Ernst-Nathan-Str. 1, 90419, Nürnberg, Germany.
Sieber CC
Klinik für Allgemeine Innere Medizin und Geriatrie, Barmherzige Brüder Regensburg, Prüfeninger Str. 86, 93049, Regensburg, Germany. Institut für Biomedizin des Alterns, Friedrich-Alexander-Universität Erlangen-Nürnberg, Nürnberg, Germany.
Härle P
Klinik für Rheumatologie, Klinische Immunologie und Physikalische Therapie, Zentrum für Rheumatologische Akutdiagnostik, Katholisches Klinikum Mainz, Standort St. Vincenz und Elisabeth Hospital, An der Goldgrube 11, 55131, Mainz, Germany.

MeSH

AgedAged, 80 and overCalciumCalcium PhosphatesCalcium PyrophosphateChondrocalcinosisCrystallizationGoutHumansUric Acid

Pub Type(s)

Journal Article
Review

Language

eng

PubMed ID

28233117

Citation

Schlee, S, et al. "Crystal Arthritides - Gout and Calcium Pyrophosphate Arthritis : Part 1: Epidemiology and Pathophysiology." Zeitschrift Fur Gerontologie Und Geriatrie, vol. 51, no. 4, 2018, pp. 453-460.
Schlee S, Bollheimer LC, Bertsch T, et al. Crystal arthritides - gout and calcium pyrophosphate arthritis : Part 1: Epidemiology and pathophysiology. Z Gerontol Geriatr. 2018;51(4):453-460.
Schlee, S., Bollheimer, L. C., Bertsch, T., Sieber, C. C., & Härle, P. (2018). Crystal arthritides - gout and calcium pyrophosphate arthritis : Part 1: Epidemiology and pathophysiology. Zeitschrift Fur Gerontologie Und Geriatrie, 51(4), 453-460. https://doi.org/10.1007/s00391-017-1197-3
Schlee S, et al. Crystal Arthritides - Gout and Calcium Pyrophosphate Arthritis : Part 1: Epidemiology and Pathophysiology. Z Gerontol Geriatr. 2018;51(4):453-460. PubMed PMID: 28233117.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Crystal arthritides - gout and calcium pyrophosphate arthritis : Part 1: Epidemiology and pathophysiology. AU - Schlee,S, AU - Bollheimer,L C, AU - Bertsch,T, AU - Sieber,C C, AU - Härle,P, Y1 - 2017/02/23/ PY - 2015/08/06/received PY - 2017/01/17/accepted PY - 2017/2/25/pubmed PY - 2019/8/29/medline PY - 2017/2/25/entrez KW - Calcium pyrophosphate deposition disease KW - Elderly patients KW - Gout KW - Hyperuricemia KW - Uric acid crystals SP - 453 EP - 460 JF - Zeitschrift fur Gerontologie und Geriatrie JO - Z Gerontol Geriatr VL - 51 IS - 4 N2 - Gout and calcium pyrophosphate deposition disease (CPPD, pseudogout) are still the most frequent inflammatory arthritides in multimorbid elderly patients. Gout and CPPD are different diseases and based on different pathophysiological principles. Gout is closely associated with the metabolic syndrome and is an independent risk factor for cardiovascular mortality. The prevalence of asymptomatic hyperuricemia is estimated to be 10-20% of adults in industrial nations and prevalence is strongly associated with age. More than 7% of persons aged over 65 years suffer from clinically manifest gout. The underlying pathophysiological principle is an imbalance between the formation and elimination of uric acid. The degradation of the purine bases adenine and guanosine to uric acid is catalysed by xanthine oxidase and genetic polymorphisms and mutations play an important role in absorption and excretion processes. Furthermore, carrier proteins, such as URAT-1 or OAT-4 also have an influence on these processes. An imbalance of the physiological processes results in the solubility product being exceeded, which in consequence leads to crystallization of urate. This induces a cascade of massive inflammatory reactions at the molecular and cellular level with the activation of cytokines. The inflammatory process can be stopped by neutrophil extracellular traps (NETs) that modulate aggregation and degradation of chemokines and cytokines and partitioning of crystallized urate against immune cells. Calcium pyrophosphate dehydrate (CPP) crystals are formed in the cartilage and CPP deposition can be found in 30% of people aged over 80 years. Inorganic pyrophosphate (PPi) is synthesized in chondrocytes and plays an important part in the formation of calcium pyrophosphate crystals. The degradation is catalyzed by inorganic pyrophosphatases. If there is dysregulation of this homeostasis more PPi is produced, which ultimately contributes to the formation of the CPP crystals. SN - 1435-1269 UR - https://www.unboundmedicine.com/medline/citation/28233117/Crystal_arthritides___gout_and_calcium_pyrophosphate_arthritis_:_Part_1:_Epidemiology_and_pathophysiology_ L2 - https://dx.doi.org/10.1007/s00391-017-1197-3 DB - PRIME DP - Unbound Medicine ER -