Schlee S, Bollheimer L C, Bertsch T, Sieber C C, Härle P
Klinik für Allgemeine Innere Medizin und Geriatrie, Barmherzige Brüder Regensburg, Prüfeninger Str. 86, 93049, Regensburg, Germany.
Lehrstuhl für Altersmedizin, RWTH Aachen University, Pauwelsstraße 30, 52074, Aachen, Germany.
Z Gerontol Geriatr. 2018 Jun;51(4):453-460. doi: 10.1007/s00391-017-1197-3. Epub 2017 Feb 23.
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.
痛风和焦磷酸钙沉积病（CPPD，假痛风）仍是多病共存老年患者中最常见的炎性关节炎。痛风和CPPD是不同的疾病，基于不同的病理生理原理。痛风与代谢综合征密切相关，是心血管疾病死亡的独立危险因素。在工业化国家，无症状高尿酸血症的患病率估计为成年人的10% - 20%，且患病率与年龄密切相关。65岁以上人群中超过7%患有临床显性痛风。其潜在的病理生理原理是尿酸生成与排泄之间的失衡。嘌呤碱基腺嘌呤和鸟嘌呤降解为尿酸由黄嘌呤氧化酶催化，基因多态性和突变在吸收和排泄过程中起重要作用。此外，载体蛋白，如URAT - 1或OAT - 4也对这些过程有影响。生理过程的失衡导致超过溶解度积，进而导致尿酸盐结晶。这在分子和细胞水平引发一系列大规模炎症反应并激活细胞因子。炎症过程可被中性粒细胞胞外陷阱（NETs）阻止，NETs可调节趋化因子和细胞因子的聚集与降解以及结晶尿酸盐与免疫细胞的分隔。焦磷酸钙脱水（CPP）晶体在软骨中形成，80岁以上人群中30%可发现CPP沉积。无机焦磷酸（PPi）在软骨细胞中合成，在焦磷酸钙晶体形成中起重要作用。其降解由无机焦磷酸酶催化。如果这种内环境稳定失调，会产生更多PPi，最终导致CPP晶体形成。
