Alfred Baring Garrod (1819-1907).
Alfred Baring Garrod (1819-1907).
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阿尔弗雷德·巴林·加罗德 (1819-1907)。
DOI：
10.1093/rheumatology/40.10.1189
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发表时间：
2001
期刊：
影响因子：
5.5
通讯作者：
G. Storey
中科院分区：
文献类型：
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作者：
G. Storey
加罗德出生于伊普斯威奇。他的父亲罗伯特·加罗德（Robert Garrod）是一个佃农，他创办了一家成功的拍卖商和房地产经纪公司。阿尔弗雷德决定从医。他最初在伊普斯威奇医院（Ipswich Hospital）师从查尔斯·钱伯斯·哈蒙德（Charles Chambers Hammond），后来转到大学学院医院（University College Hospital），1842年取得医学博士资格，1843年取得医学博士资格。然后，他被任命为化学部门的临床助理，在那里，他“主要负责分析医院病例中出现的并由医务人员送到他那里的病态液体和其他物质”。当时他是助理医师西伦敦医院，也是医生在Aldersgate药房和讲师在Aldersgate学校1846年至1847年。1848年，他对我们了解痛风的病因做出了重大贡献。在1848年2月8日的一次公开演讲中，他证明了痛风患者血液中尿酸的增加，而急性风湿病或布赖特病则没有这种增加。当时他是大学附属医院的助理医师。后来，在1854年，他开发了“螺纹测试”，并于1859年，证明了正常血清中的尿酸含量较低。他还证明了痛风关节软骨中尿酸盐的沉积。他的研究结果的重要性最初并没有得到普遍的接受，直到1960年，霍兰德才在痛风的滑液中发现尿酸晶体。加罗德于1849年被任命为大学学院医院的全职医生，并继续在医院讲课，有时在夏天早上8点开始。他在医院事务中发挥了充分的作用，并组织建立了一个中药博物馆。在1859年，他作出了他的其他重大贡献，流变学。很可能，类风湿性关节炎作为一种疾病已经存在了很长一段时间，当然是从西德纳姆的时候开始，但是命名法与风湿性痛风，慢性风湿病，风湿痛，坏血病风湿病等术语混淆了，直到1800年，当隆德雷博韦描述了典型的病例与病理学，人们才清楚地知道这种疾病是一个单独的实体。Garrod在1859年的论文中讨论了这些不同情况的鉴别诊断。他拒绝了慢性风湿病的赫伯登和风湿性痛风的富勒和选择的名称'类风湿性关节炎'的疾病，并提供了插图。他将其分为急性型、慢性型和不规则型的全身型和局限型。这个名字一直保留至今。
Garrod was born in Ipswich. He was the son of Robert Garrod, himself the son of a tenant farmer who had founded a successful firm of auctioneers and estate agents. Alfred decided to follow a medical career. He was initially apprenticed to Charles Chambers Hammond at Ipswich Hospital but moved to University College Hospital, where he qualified MB in 1842 and MD in 1843. He was then appointed clinical assistant to the chemical department, where he ‘shall be occupied chiefly in the analysis of morbid fluids and other substances occurring in cases in the hospital and sent to him by the medical officer’. He was then assistant physician to the West London Hospital and also physician at the Aldersgate Dispensary and lecturer at the Aldersgate School 1846–7. In 1848 he made his major contribution to our knowledge of the causation of gout. At a public lecture on 8 February 1848, reported in the Medical Chirurgical Transactions, he demonstrated the increase in uric acid in the blood of patients with gout, whereas there was no such increase in acute rheumatism or Bright’s disease. At this time he was assistant physician to University College Hospital. Later, in 1854, he developed the ‘thread test’and, in 1859, demonstrated smaller quantities of uric acid in the normal serum. He also demonstrated deposits of urate in the articular cartilage of gout.The importance of his results did not at first receive universal acceptance and it was not until 1960 that Hollander identified uric acid crystals in the synovial fluid in gout. Garrod was appointed full physician to University College Hospital in 1849 and continued lecturing at the hospital, sometimes starting at 8 am in the summer. He played a full part in hospital affairs and organized the establishment of a museum of materia medica. In 1859 he made his other major contribution to rheumatology. It is likely that rheumatoid arthritis had been present as a disease for a long time, certainly since the time of Sydenham, but the nomenclature had been confused with terms like rheumatic gout, chronic rheumatism, rheumalgia, scorbutic rheumatism, etc. And it was not until 1800, when Londré Beauvais described typical cases with pathology, that it became clear that the disease was a separate entity. Garrod, in his treatise of 1859, discussed the differential diagnosis of these various conditions. He rejected the chronic rheumatism of Heberden and the rheumatic gout of Fuller and chose the name ‘rheumatoid arthritis’ for the disease, and provided illustrations. He divided it into acute, chronic and irregular forms of generalized and localized type. The name has remained ever since.