Iannello S, Cavaliere G, Ferro G, Giuffrì M V, Impellizzieri D, Incognito C, Lizzio G, Neri S, Rapisarda A, Belfiore F
Cattedra di Medicina Interna, Università degli Studi, Catania.
Minerva Med. 1998 Nov-Dec;89(11-12):419-37.
Aim of this paper is to describe and discuss, on the basis of the available current literature, the case of a female patient affected by a tophaceous gout associated with plurimetabolic syndrome. Hyperuricemia and gout may be seen today in all the populations of developed countries, with increasing frequency on the last fifty years. Increased production or reduced urinary excretion of uric acid (and hypoxanthine and xanthine) are the most important pathogenetic mechanisms of primary or secondary hyperuricemia. Gout is an acute rheumatic disorder (characterized by a limited range of manifestations) which occurs in humans in connection with deposition of crystals of monosodium urate (the final product of purine metabolism) in the articular and soft periarticular tissues. Hyperuricemia and/or gout are often associated with hyperinsulinemia, obesity, diabetes mellitus, hyperlipemia, hypertension and atherosclerosis to form the syndrome called "Plurimetabolic syndrome" or "Syndrome X". Here we report the clinical case of a 64-year-old female patient who had android obesity, type 2 diabetes mellitus, hypertension, dyslipidemia and hyperuricemia and had been suffering (over many years) from intermittent episodes of severe pain and inflammatory joint swelling (first metacarpo- and metatarso-phalangeal joints) with development of pronounced multiple tophi in bone articular and soft periarticular tissues. Hyperuricemia and acute episodes had never been treated with anti-hyperuricemic drugs because gouty arthritis had never been diagnosed. This severe tophaceous gout associated to multiple metabolic disorders prompted us to present knowledge on gout and to focus on the interrelationships between hyperuricemia and/or gout and plurimetabolic syndrome, important risk factors for coronary heart disease.
本文旨在基于现有文献,描述并讨论一位患有痛风石性痛风合并多代谢综合征的女性患者的病例。如今,在发达国家的所有人群中都可见高尿酸血症和痛风,且在过去五十年中发病率不断上升。尿酸(以及次黄嘌呤和黄嘌呤)生成增加或尿排泄减少是原发性或继发性高尿酸血症最重要的发病机制。痛风是一种急性风湿性疾病(表现形式有限),在人类中,它与尿酸钠晶体(嘌呤代谢的终产物)在关节及关节周围软组织中的沉积有关。高尿酸血症和/或痛风常与高胰岛素血症、肥胖、糖尿病、高脂血症、高血压和动脉粥样硬化相关,形成所谓的“多代谢综合征”或“X综合征”。在此,我们报告一例64岁女性患者的临床病例,该患者有男性型肥胖、2型糖尿病、高血压、血脂异常和高尿酸血症,多年来一直遭受严重疼痛和炎症性关节肿胀(第一掌指关节和跖趾关节)的间歇性发作,并在骨关节和关节周围软组织中出现明显的多个痛风石。由于痛风性关节炎从未被诊断出来,高尿酸血症和急性发作从未用抗高尿酸血症药物治疗过。这种与多种代谢紊乱相关的严重痛风石性痛风促使我们介绍痛风的相关知识,并关注高尿酸血症和/或痛风与多代谢综合征之间的相互关系,这两者是冠心病的重要危险因素。