The early history of antirheumatic drugs

Rodnan, Gerald P.; Benedek, Thomas G.

doi:10.1002/art.1780130207

Cited by 82 publications

(23 citation statements)

References 33 publications

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“…Tetracyclines were, of course, first used to treat RA in the late 1960s because it was believed that RA was caused by an infection (9)(10)(11). This was the same reason that gold was used to treat RA in the 1920s (23) and sulfasalazine in the 1940s (24). Whether RA is caused, triggered, or perpetuated by an infectious agent or agents is still not delineated.…”

Section: Discussionmentioning

confidence: 99%

Treatment of early seropositive rheumatoid arthritis: A two-year, double-blind comparison of minocycline and hydroxychloroquine

O'Dell

Blakely

Mallek³

et al. 2001

Arthritis & Rheumatism

133

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Section: Discussionmentioning

confidence: 99%

Treatment of early seropositive rheumatoid arthritis: A two-year, double-blind comparison of minocycline and hydroxychloroquine

O'Dell

Blakely

Mallek³

et al. 2001

Arthritis & Rheumatism

133

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“…The metabolic and excretory pathways of gold compounds have been of interest to investigators since their benefit in the treatment of rheumatoid arthritis was first reported more than 40 years ago (1). Abundant data are available regarding gold concentrations in blood and its components and in the urine and feces of human and experimental animal models (2-6).…”

mentioning

confidence: 99%

Tissue gold concentration in a rheumatoid arthritic receiving chrysotherapy

Gottlieb

Smith

1972

Arthritis & Rheumatism

133

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Postmortem specimens from a patient with rheumatoid arthritis who had received 5 g of aurothioglucose were examined histologically, and their gold content was determined by activation analysis. The highest concentration of gold was found in the lymph nodes followed by the adrenal gland, renal cortex and other organs of the reticuloendothelial system. Comparatively low concentrations were found in tissues comprising the joint structure. Organs in which the greatest quantities of gold were stored include the bone marrow, liver, skin and bone. These findings demonstrate the body's capacity to store relatively large quantities of gold without adverse reaction, support the concept of a systemic rather than local mechanism of action (at the joint level) and demonstrate in vivo gold concentrations in the range expected to produce local cellular biologic effects.The metabolic and excretory pathways of gold compounds have been of interest to investigators since their benefit in the treatment of rheumatoid arthritis was first reported more than 40 years ago (1). Abundant data are available regarding gold concentrations in blood and its components and in the urine and feces of human and experimental animal models (2-6). T' issue distribution of gold, on the other hand, has been adequately studied only in animals (7,8) Submitted for publication Apr 6, 1971; accepted June 21, 1971. tissues has never been systematically measured. There are scanty reports of gold levels in human skin, synovium, synovial fluid, etc, but methods of gold analysis were relatively insensitive and some of the patients studied had received only one injection of a radioactive gold-labeled compound rather than a course of gold therapy (2,3,9,10). No information is available regarding gold concentrations in internal organs or in the musculoskeletal system of a patient with rheumatoid arthritis on longterm chrysotherapy. The sudden death of such a patient afforded us the opportunity to analyze tissues for their gold content. CASE REPORTMV was a 68-year-old white female with classic rheumatoid arthritis, by the ARA criteria. of 16 years duration who died in November 1969, of an overdose of barbiturate. When first seen in the Arthritis Clinic at Jackson Memorial Hospital in June 1958, she related a 5-year history of progressive polyarthritis with morning stiffness. Physical examination showed active synovitis of metacarpal phalangeal and proximal interphalangeal joints, 16Arthritis and Rheumatism, Vol. 15, No. 1 (Januafy-FebrurIy 1 9 n )

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“…The active compound was initially extracted from the plant autumn crocus [2] but the active chemical compound was isolated only in 1820 [3] . In 1889, a large dose of tincture of Colchicum was injected in two dogs leading to the observation that anatelophases was blocked during mitosis and providing the first cellular explanation of the activity of the "poison-drug" [4] : this is functioning as a mitotic spindle poison.…”

Section: Colchicine Is a Venerable Drugmentioning

confidence: 99%

Colchicine: A Promising Drug in Clinical Translation, A Minireview Focused on Cardiovascular Diseases

Lattuca¹,

Leclercq²,

Macia³

et al. 2015

Journal of Cardiology and Therapy

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Colchicine is a venerable drug used for centuries for rheumatic diseases with potential pleiotropic anti-inflammatory effects. One of the main concerns remains the tolerability especially digestive side effects, but this aspect has been improved by many pharmacological improvements. Nowadays, colchine is a promising drug for cancer therapy and cardiovascular diseases with several studies currently going on, an improved therapeutic window and a wider range of translations in cardioprotection but also in atrial fibrillation, ischemic cardiopathy or pericarditis. COLCHICINE IS A VENERABLE DRUGColchicine has been used for centuries for the treatment and prevention of gouty attacks and rheumatic complaints and is one of the oldest drugs still currently available as recently reviewed [1] .The active compound was initially extracted from the plant autumn crocus [2] but the active chemical compound was isolated only in 1820 [3] . In 1889, a large dose of tincture of Colchicum was injected in two dogs leading to the observation that anatelophases was blocked during mitosis and providing the first cellular explanation of the activity of the "poison-drug" [4] : this is functioning as a mitotic spindle poison. The structure of the active compound was elucidated only in 1955. Colchicine exerts its well-known effects including anti-cancer ones, first by blocking the tubules in the cell (spindle poison) [1] . Secondly, it could exert pleiotropic anti-inflammatory effects. Colchicine could have also direct anti-inflammatory effects (reviewed in [5] ) by inhibiting key inflammatory signaling networks known as the inflammasome and proinflammatory cytokines. The crystals involved in the pathogeny of gout and chondrocalcinosis have been shown to engage the caspase-1-activating NALP3 inflammasome [6] , resulting in the production of active interleukin-1β (IL-1β) and IL-18. Moreover, impaired neutrophil influx is observed in an in vivo model of crystal-induced peritonitis in inflammasome-deficient mice or IL-1β-receptor-deficient mice [6] . Although the most important effect of colchicine in gouty inflammation is inhibition of neutrophil migration [7] , these data suggest an alternative mechanism for the effectiveness of colchicine through anti-inflammatory functions,

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The early history of antirheumatic drugs

Cited by 82 publications

References 33 publications

Treatment of early seropositive rheumatoid arthritis: A two-year, double-blind comparison of minocycline and hydroxychloroquine

Treatment of early seropositive rheumatoid arthritis: A two-year, double-blind comparison of minocycline and hydroxychloroquine

Tissue gold concentration in a rheumatoid arthritic receiving chrysotherapy

Colchicine: A Promising Drug in Clinical Translation, A Minireview Focused on Cardiovascular Diseases

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