Thomas Addison is best remembered for two conditions that bear his name—progressive adrenal disease with deficiency of adrenal cortical hormones; and pernicious anaemia. He was born in April 1793,1 at Long Benton, Newcastle-upon-Tyne and died on June 29 1860, at 15 Wellington Villas, Brighton. The son of Sarah and Joseph Addison, a grocer and flour dealer in Long Benton,2 Addison was first sent to school in a roadside cottage where his teacher was John Rutter, the parish clerk, who years later also taught Robert Stephenson. He proceeded to the Royal Free Grammar School, Newcastle-upon-Tyne, and learned Latin so well that he made notes in that language. This explains his lifelong precision in language. His father endeavoured to provide an education and a social status much higher than his own. In 1812 Thomas became a medical student at the University of Edinburgh and in August 1815 gained an MD with a thesis ‘Concerning Syphilis and Mercury’ (now in the Wellcome Library, London). In that year he moved to Skinner Street, Snow Hill, London, to become house surgeon at the Lock Hospital, and entered as pupil to the Public Dispensary. Thomas Bateman (1778-1821), an acclaimed dermatologist, instilled in him a lasting interest in skin diseases. He progressed rapidly: the 1817 Guy's Hospital records show: ‘Dec. 13, 1817, from Edinburgh, T. Addison, M.D., paid pounds 22-1s to be a perpetual Physician's pupil.’ He obtained his LRCP in December 1819, was promoted to assistant physician and in 1827 became lecturer in materia medica. His lectures were so popular that his lecture-fees were assessed at £700 or £800 a year. In 1835 Addison with Richard Bright gave lectures on practical medicine, and in 1837 Addison became full physician to Guy's Hospital. Unlike the charming and cheerful Bright with wealthy parentage and broad education, Addison concealed nervousness and timidity beneath a proud and haughty exterior. In the words of Samuel Wilks: As a library, NLM provides access to scientific literature. Inclusion in an NLM database does not imply endorsement of, or agreement with, the contents by NLM or the National Institutes of Health. Learn more: PMC Disclaimer | PMC Copyright Notice Logo of jrsocmed J R Soc Med. 2004 Jun; 97(6): 297–300. doi: 10.1258/jrsm.97.6.297 PMCID: PMC1079500PMID: 15173338 Thomas Addison (1793-1860) J M S Pearce, MD FRCP Author information Copyright and License information PMC Disclaimer Thomas Addison is best remembered for two conditions that bear his name—progressive adrenal disease with deficiency of adrenal cortical hormones; and pernicious anaemia. He was born in April 1793,1 at Long Benton, Newcastle-upon-Tyne and died on June 29 1860, at 15 Wellington Villas, Brighton. The son of Sarah and Joseph Addison, a grocer and flour dealer in Long Benton,2 Addison was first sent to school in a roadside cottage where his teacher was John Rutter, the parish clerk, who years later also taught Robert Stephenson. He proceeded to the Royal Free Grammar School, Newcastle-upon-Tyne, and learned Latin so well that he made notes in that language. This explains his lifelong precision in language. His father endeavoured to provide an education and a social status much higher than his own. In 1812 Thomas became a medical student at the University of Edinburgh and in August 1815 gained an MD with a thesis ‘Concerning Syphilis and Mercury’ (now in the Wellcome Library, London). In that year he moved to Skinner Street, Snow Hill, London, to become house surgeon at the Lock Hospital, and entered as pupil to the Public Dispensary. Thomas Bateman (1778-1821), an acclaimed dermatologist, instilled in him a lasting interest in skin diseases. He progressed rapidly: the 1817 Guy's Hospital records show: ‘Dec. 13, 1817, from Edinburgh, T. Addison, M.D., paid pounds 22-1s to be a perpetual Physician's pupil.’ He obtained his LRCP in December 1819, was promoted to assistant physician and in 1827 became lecturer in materia medica. His lectures were so popular that his lecture-fees were assessed at £700 or £800 a year. In 1835 Addison with Richard Bright gave lectures on practical medicine, and in 1837 Addison became full physician to Guy's Hospital. Unlike the charming and cheerful Bright with wealthy parentage and broad education, Addison concealed nervousness and timidity beneath a proud and haughty exterior. In the words of Samuel Wilks:​Wilks: An external file that holds a picture, illustration, etc. Object name is 297f1g.jpg An external file that holds a picture, illustration, etc. Object name is 297f1ag.jpg Figure 1 Thomas Addison [Courtesy of Guys' Hospital] ‘a quick hasty and impassioned manner of expression is not unfrequently the result of a deficient controlling power. We know... that, although wearing the outward garb of resolution, he was beyond most other men, most liable to sink under trial.’1 Probably for these reasons his professional preferment came late in life. For example, not until 1838 was he elected a Fellow of the Royal College of Physicians. His shyness and occasional severity stood in the way of a large private practice; nevertheless, his diagnostic brilliance and his lucid and forceful teaching were appreciated at Guy's, where he showed devotion to patients and students alike. His enquiring mind and scientific curiosity were apparent, for in a biographical prefix to his published writings he was described as ‘Possessing unusually vigorous perceptive powers, being shrewd and sagacious beyond the average of men, the patient before him was scanned with a penetrating glance from which few diseases could escape detection... [he] would remain at the bedside with a dogged determination to track out the disease to its very source for a period which often wearied his class and his attendant friends.’3 The story of ‘Addison’s disease’ begins with the adrenal glands, first described by Eustachius in 1714. Addison first wrote a short article in the London Medical Gazette (1849): ‘Anaemia—disease of the suprarenal capsules in which the disease is not distinctly separated from a new form of anaemia’. Then, in 1855, came his monograph, one of the unsurpassed medical works of the nineteenth century. Addison describes here for the first time two chronic diseases which he could not clearly separate—‘On the Constitutional and Local Effects of Disease of the Suprarenal Capsule’.3 The entity he related was doubted by Hughes Bennett (1812-1875) in Edinburgh but confirmed by Trousseau (1801-1867) in Paris, who recognized suprarenal failure and named it Addison's disease. The monograph describes how, when investigating a peculiar form of anaemia, he found pathological changes in both suprarenal glands that appeared to be independent of the anaemia. He had with Samuel Wilks collected 11 patients. He described the symptoms of 11 cases: ‘The discoloration pervades the whole surface of the body, but is commonly most strongly manifested on the face, neck, superior extremities, penis, scrotom, and in the flexures of the axillae and around the navel... The leading and characteristic features of the morbid state to which I would direct your attention are, anaemia, general languor and debility, remarkable feebleness of the heart's action, irritability of the stomach, and a peculiar change of the colour in the skin, occurring in connection with a diseased condition of the suprarenal capsules.’ One patient had been treated by Bright, who had noted typical clinical features but failed to incriminate the adrenals. Indeed Addison critically commented: ‘It did not appear that Dr. Bright either entertained a suspicion of the disease of the capsules before death, or was led at any period to associate the colour of the skin with the diseased condition of the organs, although his well-known sagacity induced him to suggest the probable existence of some internal malignant disease. In this as in most other cases, we have the same remarkable prostration, the usual gastric symptoms, the same absence of any very obvious and adequate cause of the patient's actual condition together with a discoloration of the skin, sufficiently striking to have arrested Dr. Bright's attention even during the life of the patient.’ Interestingly, to his pupils his essay on suprarenal failure ranked far below his elucidation of phthisis and his impressive teaching. In most cases of Addison's disease today the pathogenesis is autoimmune, as exemplified by the polyglandular autoimmune syndromes where it is evident in two-thirds of type 1 and almost all cases of type 2. Tuberculosis now accounts for about 20% of primary adrenal insufficiency in developed countries, whereas in Addison's day it was found at autopsy in 70-90% of cases. The description of ‘Addison's anaemia’ came in 1849, in a lecture to the South London Medical Society.4 But in 1822 James Scarth Combe, in the Transactions of the Medico-Surgical Society of Edinburgh, had described ‘idiopathic anaemia’ and never sought priority for this new disease—pernicious anaemia. In the Medical Times and Gazette of London in 1874, Biermer of Zurich wrote of a new ‘idiopathic anaemia’ not yet described in England. Within a week, Samuel Wilks refuted this claim in the British Medical Journal, stating that the disease was well known in England since Addison had lectured on it in 1843. Addison observed its insidious onset in either sex, usually in middle life. He related: ‘the countenance gets pale, the whites of the eyes become pearly, the general frame flabby rather than wasted... the whole surface of the body presents a blanched, smooth and waxy appearance; the lips, gums, and tongue seem bloodless... extreme languor and faintness supervene, breathlessness and palpitations being produced by the most trifling exertion or emotion; some slight oedema is probably perceived in the ankles; the debility becomes extreme... the disease... resisted all remedial efforts and sooner or later terminated fatally... On examining the bodies I have failed to discover any organic lesion that could properly or reasonably be assigned as an adequate cause...’ The condition became known as pernicious anaemia—usually caused by loss of the ‘intrinsic factor’ required for absorption of cyanocobalamin. Addison made other signal contributions (Box 1). He wrote volume 1 of Elements of the Practice of Medicine (1839), but the planned two further volumes with Bright never emerged. It contained an early and comprehensive account of ‘Inflammation of the caecum and appendix vermiformis’. He also gave an identifiable account of biliary cirrhosis,5 previously described by Pierre-François-Olive Rayer in Traité théorique et pratique des maladies de la peau (1826-1827), Paris, 1835. In 1824 Addison founded the Department of Dermatology at Guy's, which still possesses a collection of wax models of skin disorders prepared under his supervision. ‘On a certain affection of the skin, vitilogoidea plana tuberosa’, presents a seminal account of xanthoma planum et tuberosum, a common sequel to hypercholesterolaemia. Addison with Sir William Gull (1816-1890) described xanthoma diabeticorum, and he also depicted circumscribed scleroderma (morphoea). In 1843 he correctly described the pathology of pneumonia, which until that time was thought to be an interstitial pneumonitis. He had traced the bronchial branches to their alveolar termination where he discovered ‘pneumonic deposits in the air cells’.