Category:Anti-inflammatories - Revision history

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	The older anti-inflammatory medicines retain specific clinical niches. [[wikipedia:Colchicine\|Colchicine]], extracted from the autumn crocus ''[[wikipedia:Colchicum autumnale\|Colchicum autumnale]]'' by the French chemists [[wikipedia:Pierre Joseph Pelletier\|Pelletier]] and [[wikipedia:Joseph Bienaimé Caventou\|Caventou]] in 1820, has been used for [[wikipedia:Gout\|gout]] for more than two centuries and is now used additionally for [[wikipedia:Familial Mediterranean fever\|familial Mediterranean fever]] (since the 1972 discovery by Goldfinger that low-dose colchicine prevents both the febrile attacks and the secondary amyloidosis), for [[wikipedia:Pericarditis\|recurrent pericarditis]] (CORP and CORE trials), and for [[wikipedia:Atherosclerosis\|atherosclerotic cardiovascular disease]] (LoDoCo and LoDoCo2 trials in stable coronary disease).<ref name="lodoco2">Nidorf SM, Fiolet ATL, Mosterd A, Eikelboom JW, Schut A, Opstal TSJ, The SHK, Xu XF, Ireland MA, Lenderink T, et al. Colchicine in patients with chronic coronary disease. ''New England Journal of Medicine''. 2020 Nov 5;383(19):1838-1847. PMID 32865380.</ref> Dapsone, originally an antimycobacterial introduced for leprosy in 1908 by Fromm and Wittmann, is now used in dermatology for the bullous and neutrophilic dermatoses (dermatitis herpetiformis, pyoderma gangrenosum). The [[:Category:5-aminosalicylates\|5-aminosalicylates]] (sulfasalazine, mesalamine in various delivery formulations, balsalazide) are the foundational anti-inflammatory medicines for ulcerative colitis and milder Crohn's disease.		The older anti-inflammatory medicines retain specific clinical niches. [[wikipedia:Colchicine\|Colchicine]], extracted from the autumn crocus ''[[wikipedia:Colchicum autumnale\|Colchicum autumnale]]'' by the French chemists [[wikipedia:Pierre Joseph Pelletier\|Pelletier]] and [[wikipedia:Joseph Bienaimé Caventou\|Caventou]] in 1820, has been used for [[wikipedia:Gout\|gout]] for more than two centuries and is now used additionally for [[wikipedia:Familial Mediterranean fever\|familial Mediterranean fever]] (since the 1972 discovery by Goldfinger that low-dose colchicine prevents both the febrile attacks and the secondary amyloidosis), for [[wikipedia:Pericarditis\|recurrent pericarditis]] (CORP and CORE trials), and for [[wikipedia:Atherosclerosis\|atherosclerotic cardiovascular disease]] (LoDoCo and LoDoCo2 trials in stable coronary disease).<ref name="lodoco2">Nidorf SM, Fiolet ATL, Mosterd A, Eikelboom JW, Schut A, Opstal TSJ, The SHK, Xu XF, Ireland MA, Lenderink T, et al. Colchicine in patients with chronic coronary disease. ''New England Journal of Medicine''. 2020 Nov 5;383(19):1838-1847. PMID 32865380.</ref> Dapsone, originally an antimycobacterial introduced for leprosy in 1908 by Fromm and Wittmann, is now used in dermatology for the bullous and neutrophilic dermatoses (dermatitis herpetiformis, pyoderma gangrenosum). The [[:Category:5-aminosalicylates\|5-aminosalicylates]] (sulfasalazine, mesalamine in various delivery formulations, balsalazide) are the foundational anti-inflammatory medicines for ulcerative colitis and milder Crohn's disease.

	The clinical use of anti-inflammatory medicines has been progressively refined toward "treat-to-target" frameworks similar to those developed in [[:Category:Antihypertensives\|hypertension]] and [[:Category:Antihyperglycemic_agents\|diabetes]] management. The composite disease-activity indices (DAS28 in rheumatoid arthritis, BASDAI in ankylosing spondylitis, PASI in psoriasis, the Mayo score in ulcerative colitis) define a measurable target that justifies escalation of therapy until the target is reached. The pharmacological cost of long-term anti-inflammatory therapy includes immunosuppression with associated infection risk (including the reactivation of latent tuberculosis and hepatitis B that has shaped contemporary biologic prescribing), demyelinating disease (TNF inhibitors), heart-failure exacerbation (TNF inhibitors), ~~drug~~-induced lupus, paradoxical psoriasis and uveitis (TNF inhibitors), thrombotic events (Janus kinase inhibitors), and the specific class effects of the corticosteroids (described under [[:Category:Corticosteroids\|corticosteroids]]) when those are used as adjunctive anti-inflammatory therapy.		The clinical use of anti-inflammatory medicines has been progressively refined toward "treat-to-target" frameworks similar to those developed in [[:Category:Antihypertensives\|hypertension]] and [[:Category:Antihyperglycemic_agents\|diabetes]] management. The composite disease-activity indices (DAS28 in rheumatoid arthritis, BASDAI in ankylosing spondylitis, PASI in psoriasis, the Mayo score in ulcerative colitis) define a measurable target that justifies escalation of therapy until the target is reached. The pharmacological cost of long-term anti-inflammatory therapy includes immunosuppression with associated infection risk (including the reactivation of latent tuberculosis and hepatitis B that has shaped contemporary biologic prescribing), demyelinating disease (TNF inhibitors), heart-failure exacerbation (TNF inhibitors), medicine-induced lupus, paradoxical psoriasis and uveitis (TNF inhibitors), thrombotic events (Janus kinase inhibitors), and the specific class effects of the corticosteroids (described under [[:Category:Corticosteroids\|corticosteroids]]) when those are used as adjunctive anti-inflammatory therapy.

	== Classes indexed ==		== Classes indexed ==

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An '''anti-inflammatory''' is a medicine that suppresses one or more components of the inflammatory response. The category is intentionally broad: it includes the [[:Category:NSAIDs|non-steroidal anti-inflammatory medicines]] that block cyclo-oxygenase and so the production of inflammatory prostaglandins, the [[:Category:Corticosteroids|systemic and topical glucocorticoids]] that broadly suppress lymphocyte and macrophage function, the [[:Category:DMARDs|disease-modifying antirheumatic medicines]] (including the conventional synthetic and biologic agents) when their indication is inflammatory rheumatic disease, the targeted biologics that block specific cytokines, the older anti-inflammatory medicines colchicine and dapsone, and a small set of specialised agents (5-aminosalicylates for inflammatory bowel disease, hydroxychloroquine for connective-tissue disease, the IL-6 and Janus kinase inhibitors for cytokine release syndromes).

Inflammation as a clinical concept goes back to the [[wikipedia:Aulus Cornelius Celsus|Celsus]] formulation in the first century, ''rubor et tumor cum calore et dolore'' (redness and swelling with heat and pain), to which Virchow in the nineteenth century added ''functio laesa'' (loss of function). The pharmacology of inflammation was, until the mid-twentieth century, dominated by salicylate compounds derived from willow bark (described under [[:Category:Non-opioid_analgesics|non-opioid analgesics]] and [[:Category:NSAIDs|NSAIDs]]). The breakthrough that defined the modern category was the introduction of [[Cortisone|cortisone]] by [[wikipedia:Philip S. Hench|Philip Hench]] at the [[wikipedia:Mayo Clinic|Mayo Clinic]] on 21 September 1948 in a young woman with rheumatoid arthritis; the dramatic clinical response established the corticosteroid as the prototype anti-inflammatory medicine and is the founding event of clinical immunopharmacology (described in detail under [[:Category:Corticosteroids|corticosteroids]]). The 1971 demonstration by [[wikipedia:John Vane|John Vane]] that aspirin and related NSAIDs inhibited the synthesis of prostaglandins, and the 1990s identification of the inducible COX-2 isoform, provided the mechanistic framework that has organised the NSAID side of the category since (described under [[:Category:Non-opioid_analgesics|non-opioid analgesics]]).

The transformative event of contemporary anti-inflammatory pharmacology was the introduction of the targeted biologics in the 1990s and 2000s. The recognition that specific cytokines drove specific inflammatory diseases ([[wikipedia:Marc Feldmann|Marc Feldmann]] and [[wikipedia:Ravinder Maini|Ravinder Maini]]'s work on tumour necrosis factor alpha in rheumatoid arthritis; the parallel work on interleukin-6, interleukin-17, interleukin-23, the type I and type II interferons, and the JAK-STAT signalling network) created a clinical opportunity to block one cytokine at a time. The [[:Category:TNF_inhibitors|TNF inhibitors]] (etanercept 1998, infliximab 1998, [[Adalimumab|adalimumab]] 2002), the IL-6 receptor antagonist tocilizumab (2010), the IL-1 receptor antagonist anakinra (2001) and the IL-1β-specific canakinumab (2009), the IL-17 inhibitors secukinumab and ixekizumab (2015-2016), the IL-23 inhibitors guselkumab and risankizumab (2017-2019), the IL-12/23 inhibitor ustekinumab (2009), and the type I interferon receptor antagonist anifrolumab (2021) are the principal classes; collectively they have transformed the treatment of rheumatoid arthritis, ankylosing spondylitis, psoriatic arthritis, psoriasis, inflammatory bowel disease, systemic lupus erythematosus, the autoinflammatory syndromes, and atopic dermatitis. A parallel small-molecule class, the [[wikipedia:Janus kinase inhibitor|Janus kinase inhibitors]] (tofacitinib, baricitinib, upadacitinib, filgotinib), produces broadly similar clinical effect with the convenience of oral administration.

The older anti-inflammatory medicines retain specific clinical niches. [[wikipedia:Colchicine|Colchicine]], extracted from the autumn crocus ''[[wikipedia:Colchicum autumnale|Colchicum autumnale]]'' by the French chemists [[wikipedia:Pierre Joseph Pelletier|Pelletier]] and [[wikipedia:Joseph Bienaimé Caventou|Caventou]] in 1820, has been used for [[wikipedia:Gout|gout]] for more than two centuries and is now used additionally for [[wikipedia:Familial Mediterranean fever|familial Mediterranean fever]] (since the 1972 discovery by Goldfinger that low-dose colchicine prevents both the febrile attacks and the secondary amyloidosis), for [[wikipedia:Pericarditis|recurrent pericarditis]] (CORP and CORE trials), and for [[wikipedia:Atherosclerosis|atherosclerotic cardiovascular disease]] (LoDoCo and LoDoCo2 trials in stable coronary disease).<ref name="lodoco2">Nidorf SM, Fiolet ATL, Mosterd A, Eikelboom JW, Schut A, Opstal TSJ, The SHK, Xu XF, Ireland MA, Lenderink T, et al. Colchicine in patients with chronic coronary disease. ''New England Journal of Medicine''. 2020 Nov 5;383(19):1838-1847. PMID 32865380.</ref> Dapsone, originally an antimycobacterial introduced for leprosy in 1908 by Fromm and Wittmann, is now used in dermatology for the bullous and neutrophilic dermatoses (dermatitis herpetiformis, pyoderma gangrenosum). The [[:Category:5-aminosalicylates|5-aminosalicylates]] (sulfasalazine, mesalamine in various delivery formulations, balsalazide) are the foundational anti-inflammatory medicines for ulcerative colitis and milder Crohn's disease.

The clinical use of anti-inflammatory medicines has been progressively refined toward "treat-to-target" frameworks similar to those developed in [[:Category:Antihypertensives|hypertension]] and [[:Category:Antihyperglycemic_agents|diabetes]] management. The composite disease-activity indices (DAS28 in rheumatoid arthritis, BASDAI in ankylosing spondylitis, PASI in psoriasis, the Mayo score in ulcerative colitis) define a measurable target that justifies escalation of therapy until the target is reached. The pharmacological cost of long-term anti-inflammatory therapy includes immunosuppression with associated infection risk (including the reactivation of latent tuberculosis and hepatitis B that has shaped contemporary biologic prescribing), demyelinating disease (TNF inhibitors), heart-failure exacerbation (TNF inhibitors), drug-induced lupus, paradoxical psoriasis and uveitis (TNF inhibitors), thrombotic events (Janus kinase inhibitors), and the specific class effects of the corticosteroids (described under [[:Category:Corticosteroids|corticosteroids]]) when those are used as adjunctive anti-inflammatory therapy.

== Classes indexed ==

By mechanism and clinical category:

* '''[[:Category:Corticosteroids|Corticosteroids]]''' (cross-indexed; the foundational anti-inflammatory):
** Systemic, inhaled, topical, intranasal, intra-articular, ophthalmic preparations
* '''[[:Category:NSAIDs|NSAIDs]]''' (non-steroidal anti-inflammatory medicines, cross-indexed under [[:Category:Non-opioid_analgesics|non-opioid analgesics]]):
** Non-selective COX inhibitors: aspirin, ibuprofen, naproxen, diclofenac, indomethacin, ketorolac
** Preferential COX-2: meloxicam, etodolac, nabumetone
** Selective COX-2: celecoxib (rofecoxib withdrawn 2004)
* '''[[:Category:DMARDs|Disease-modifying antirheumatic medicines]]''' (cross-indexed; for inflammatory arthritis):
** Conventional synthetic: [[Methotrexate|methotrexate]], [[Hydroxychloroquine|hydroxychloroquine]], sulfasalazine, leflunomide
** Biologic: [[Adalimumab|adalimumab]] and the other TNF inhibitors; tocilizumab; abatacept; rituximab; the IL-1, IL-17, IL-23, and IL-12/23 antagonists
** Targeted synthetic (Janus kinase inhibitors): tofacitinib, baricitinib, upadacitinib, filgotinib
* '''5-aminosalicylates''' ([[:Category:5-aminosalicylates|inflammatory-bowel-disease specific]]): sulfasalazine, [[wikipedia:Mesalamine|mesalamine]] (various delivery preparations), balsalazide, olsalazine
* '''Colchicine and the IL-1 axis''' (gout, FMF, pericarditis, atherosclerotic CV disease): colchicine, anakinra, canakinumab, rilonacept
* '''Antimalarial-derived''' (lupus, RA): [[Hydroxychloroquine|hydroxychloroquine]], [[wikipedia:Chloroquine|chloroquine]]
* '''Dermatologic and neutrophilic-skin-disease specific''': [[wikipedia:Dapsone|dapsone]], topical calcineurin inhibitors (tacrolimus, pimecrolimus), topical PDE4 inhibitor crisaborole, topical JAK inhibitor ruxolitinib
* '''Mast cell stabilisers''' (allergic, mast-cell-mediated): cromolyn, nedocromil, ketotifen
* '''Leukotriene-pathway modulators''' (asthma, allergic rhinitis): montelukast, zafirlukast, zileuton

== Notes on scope ==

The boundary of this category is "medicine prescribed primarily to suppress inflammation." The [[:Category:Immunosuppressants|immunosuppressants]] used in transplantation are not principally anti-inflammatory in clinical use and are listed separately, although the categories overlap substantially in the autoimmune-disease setting where the same medicines are used for both indications. The [[:Category:Antineoplastics|antineoplastics]] that have anti-inflammatory effect as part of their action (the alkylating agents in low dose; methotrexate at rheumatoid-arthritis doses) are cross-indexed where appropriate. The [[:Category:Antibacterials|antibacterials]] used for their anti-inflammatory rather than antibacterial effect (low-dose doxycycline for rosacea and periodontal disease; macrolides for diffuse panbronchiolitis and severe asthma) are listed under their primary class. Analgesics that lack meaningful anti-inflammatory effect (paracetamol, the opioids) are not anti-inflammatories and belong to their own category. Topical anti-inflammatory preparations are cross-indexed under the topical-route categories ([[:Category:Topical_corticosteroids|topical corticosteroids]], topical NSAID gels and patches, topical immunomodulators).

== About these pages ==

This category page is an encyclopedia article about its subject. The actual index of medicines belonging to the category is generated automatically by the wiki engine, from category-membership declarations on the individual medicine pages, and appears at the foot of the page below the references.

== References ==

<references/>

[[Category:Medicines]]
[[Category:CuratedCategoryPage]]