Psoriasis medical therapy: Difference between revisions
Jump to navigation
Jump to search
No edit summary |
No edit summary |
||
Line 6: | Line 6: | ||
==Medical Therapy== | ==Medical Therapy== | ||
Therapies are administered according to disease severity and assessed by the Psoriasis Area and Severity Index (PASI, ranging from 0 to 72), which takes into account appearance and extension of the lesions. Interventions in medical therapy for psoriasis comprise of: | |||
* Topical therapy | |||
* Phototherapy | |||
* Systemic therapy (Immunosuppressive agents) | |||
* Biological therapy | |||
=== Topical therapy<ref name="pmid16916825">{{cite journal |vauthors=Smith CH, Barker JN |title=Psoriasis and its management |journal=BMJ |volume=333 |issue=7564 |pages=380–4 |year=2006 |pmid=16916825 |pmc=1550454 |doi=10.1136/bmj.333.7564.380 |url=}}</ref> === | |||
* Medicated creams and ointments applied directly to psoriatic lesions can help decrease inflammation, remove built-up scale, reduce skin turn over, and clear affected skin of plaques. | |||
* Approved drugs that can be used as topical therapy for acute management of psoriasis include: | |||
# Corticosteroids | |||
# Vitamin D analogues (calcipotriol)<ref name="pmid10753146">{{cite journal |vauthors=Ashcroft DM, Po AL, Williams HC, Griffiths CE |title=Systematic review of comparative efficacy and tolerability of calcipotriol in treating chronic plaque psoriasis |journal=BMJ |volume=320 |issue=7240 |pages=963–7 |year=2000 |pmid=10753146 |pmc=27334 |doi= |url=}}</ref> | |||
# Tar | |||
# Dithranol (anthralin) | |||
# Tazarotene (a retinoid) | |||
# Calcineurin inhibitors (Tacrolimus and primecrolimus- used specially foe flexural or facial psoriasis) | |||
# Aloe vera extract 0.5 % hydrophilic cream<ref name="pmid8765459">{{cite journal |vauthors=Syed TA, Ahmad SA, Holt AH, Ahmad SA, Ahmad SH, Afzal M |title=Management of psoriasis with Aloe vera extract in a hydrophilic cream: a placebo-controlled, double-blind study |journal=Trop. Med. Int. Health |volume=1 |issue=4 |pages=505–9 |year=1996 |pmid=8765459 |doi= |url=}}</ref> | |||
# Anti-IL-8 monoclonal antibody cream | |||
# Betamethasone 17-valerate 21-acetate plus tretinoin plus salicylic acid<ref name="pmid19445765">{{cite journal |vauthors=Naldi L, Rzany B |title=Psoriasis (chronic plaque) |journal=BMJ Clin Evid |volume=2009 |issue= |pages= |year=2009 |pmid=19445765 |pmc=2907770 |doi= |url=}}</ref> | |||
# Fish oil plus occlussion<ref name="pmid1451289">{{cite journal |vauthors=Escobar SO, Achenbach R, Iannantuono R, Torem V |title=Topical fish oil in psoriasis--a controlled and blind study |journal=Clin. Exp. Dermatol. |volume=17 |issue=3 |pages=159–62 |year=1992 |pmid=1451289 |doi= |url=}}</ref> | |||
# Combination of nicotinamide and calcipotriene<ref name="pmid20599292">{{cite journal |vauthors=Levine D, Even-Chen Z, Lipets I, Pritulo OA, Svyatenko TV, Andrashko Y, Lebwohl M, Gottlieb A |title=Pilot, multicenter, double-blind, randomized placebo-controlled bilateral comparative study of a combination of calcipotriene and nicotinamide for the treatment of psoriasis |journal=J. Am. Acad. Dermatol. |volume=63 |issue=5 |pages=775–81 |year=2010 |pmid=20599292 |doi=10.1016/j.jaad.2009.10.016 |url=}}</ref> | |||
* Combined treatment with vitamin D/corticosteroid on either the body or the scalp has significantly better outcomes than vitamin D alone.<ref name="urlTopical treatments for chronic plaque psoriasis - Mason - 2013 - The Cochrane Library - Wiley Online Library">{{cite web |url=http://onlinelibrary.wiley.com/doi/10.1002/14651858.CD005028.pub3/full |title=Topical treatments for chronic plaque psoriasis - Mason - 2013 - The Cochrane Library - Wiley Online Library |format= |work= |accessdate=}}</ref> | |||
* The disadvantages of topical agents are variably that they can often irritate normal skin, can be time consuming and awkward to apply, cannot be used for long periods, can stain clothing or have a strong odour. As a result, it is sometimes difficult for people to maintain the regular application of these medications. | |||
* Abrupt withdrawal of some topical agents, particularly corticosteroids, can cause an aggressive recurrence of the condition. | |||
* Some topical agents are used in conjunction with other therapies, especially phototherapy. | |||
===Phototherapy<ref name="pmid194457652">{{cite journal |vauthors=Naldi L, Rzany B |title=Psoriasis (chronic plaque) |journal=BMJ Clin Evid |volume=2009 |issue= |pages= |year=2009 |pmid=19445765 |pmc=2907770 |doi= |url=}}</ref>=== | |||
* It has long been recognized that daily, short, non-burning exposure to sunlight helped to clear or improve psoriasis. | |||
* [[Niels Ryberg Finsen|Niels Finsen]] was the first [[physician]] to investigate the therapeutic effects of sunlight scientifically and to use sunlight in clinical practice. This became known as phototherapy. | |||
* Narrow band part of the UVB spectrum (311 to 312 nm) is most helpful for psoriasis. Exposure to UVB several times per week, over several weeks can help people attain a remission from psoriasis. | |||
* Ultraviolet light treatment is frequently combined with topical (coal tar, calcipotriol) or systemic treatment (retinoids) as there is a synergy in their combination. | |||
* The Ingram regime, involves UVB and the application of anthralin paste. | |||
* The Goeckerman regime combines coal tar ointment with UVB. | |||
=== Systemic therapy === | |||
{| class="wikitable" | |||
! colspan="1" rowspan="1" |Type of agent | |||
! colspan="1" rowspan="1" |Mechanism of action | |||
! colspan="1" rowspan="1" |Name | |||
! colspan="1" rowspan="1" |Molecular target | |||
! colspan="1" rowspan="1" |Formulation | |||
! colspan="1" rowspan="1" |Administration route | |||
|- | |||
| colspan="1" rowspan="13" |Biologic | |||
| colspan="1" rowspan="3" |Anti-T cells | |||
| colspan="1" rowspan="1" |Alefacept | |||
| colspan="1" rowspan="1" |CD2 | |||
| colspan="1" rowspan="1" |Human LFA-3/IgG1 fusion protein | |||
| colspan="1" rowspan="1" |IM or IV | |||
|- | |||
| colspan="1" rowspan="1" |Efalizumab | |||
| colspan="1" rowspan="1" |CD11a | |||
| colspan="1" rowspan="1" |Humanized IgG1 monoclonal antibody | |||
| colspan="1" rowspan="1" |SC | |||
|- | |||
| colspan="1" rowspan="1" |Abatacept | |||
| colspan="1" rowspan="1" |CTLA-4 | |||
| colspan="1" rowspan="1" |Human CTLA4–Ig-IgG1 fusion protein | |||
| colspan="1" rowspan="1" |SC or IV | |||
|- | |||
| colspan="1" rowspan="10" |Anticytokine | |||
| colspan="1" rowspan="1" |Etanercept | |||
| colspan="1" rowspan="1" |TNF | |||
| colspan="1" rowspan="1" |Human TNF-R (p75)-lgG1 fusion protein | |||
| colspan="1" rowspan="1" |SC | |||
|- | |||
| colspan="1" rowspan="1" |Infliximab | |||
| colspan="1" rowspan="1" |TNF | |||
| colspan="1" rowspan="1" |Mouse-human IgG1 chimeric monoclonal antibody | |||
| colspan="1" rowspan="1" |IV | |||
|- | |||
| colspan="1" rowspan="1" |Adalimumab | |||
| colspan="1" rowspan="1" |TNF | |||
| colspan="1" rowspan="1" |Human IgG1 monoclonal antibody | |||
| colspan="1" rowspan="1" |SC | |||
|- | |||
| colspan="1" rowspan="1" |Ustekinumab | |||
| colspan="1" rowspan="1" |IL-12p40 (IL-2, IL-23) | |||
| colspan="1" rowspan="1" |Human IgG1 monoclonal antibody | |||
| colspan="1" rowspan="1" |SC | |||
|- | |||
| colspan="1" rowspan="1" |Briakinumab (discontinued in USA in 2011) | |||
| colspan="1" rowspan="1" |IL-12p40 (IL-12, IL-23) | |||
| colspan="1" rowspan="1" |Human IgG1 monoclonal antibody | |||
| colspan="1" rowspan="1" |SC | |||
|- | |||
| colspan="1" rowspan="1" |Guselkumab | |||
| colspan="1" rowspan="1" |IL-23p19 | |||
| colspan="1" rowspan="1" |Human IgG1 monoclonal antibody | |||
| colspan="1" rowspan="1" |SC | |||
|- | |||
| colspan="1" rowspan="1" |Brodalumab | |||
| colspan="1" rowspan="1" |IL-17R | |||
| colspan="1" rowspan="1" |Human IgG2 monoclonal antibody | |||
| colspan="1" rowspan="1" |SC | |||
|- | |||
| colspan="1" rowspan="1" |Ixekizumab | |||
| colspan="1" rowspan="1" |IL-17 | |||
| colspan="1" rowspan="1" |Humanized IgG4 monoclonal antibody | |||
| colspan="1" rowspan="1" |SC | |||
|- | |||
| colspan="1" rowspan="1" |Secukinumab | |||
| colspan="1" rowspan="1" |IL-17 | |||
| colspan="1" rowspan="1" |Human IgG1 monoclonal antibody | |||
| colspan="1" rowspan="1" |SC or IV | |||
|- | |||
| colspan="1" rowspan="1" |Fezakinumab | |||
| colspan="1" rowspan="1" |IL-22 | |||
| colspan="1" rowspan="1" |Human IgG1 monoclonal antibody | |||
| colspan="1" rowspan="1" |SC or IV | |||
|- | |||
| colspan="1" rowspan="5" |Small molecule | |||
| colspan="1" |PDE4 inhibitor | |||
| colspan="1" rowspan="1" |Apremilast | |||
| colspan="1" rowspan="1" |PDE4 | |||
| colspan="1" rowspan="1" |NA | |||
| colspan="1" rowspan="1" |Oral | |||
|- | |||
| colspan="1" rowspan="2" |JAK inhibitor | |||
| colspan="1" rowspan="1" |Tofacitinib | |||
| colspan="1" rowspan="1" |JAK1 and JAK3 | |||
| colspan="1" rowspan="1" |NA | |||
| colspan="1" rowspan="1" |Oral | |||
|- | |||
| colspan="1" rowspan="1" |Baricitinib | |||
| colspan="1" rowspan="1" |JAK1 and JAK2 | |||
| colspan="1" rowspan="1" |NA | |||
| colspan="1" rowspan="1" |Oral | |||
|- | |||
| colspan="1" rowspan="1" |PKC inhibitor | |||
| colspan="1" rowspan="1" |AEB071 | |||
| colspan="1" rowspan="1" |PKC | |||
| colspan="1" rowspan="1" |NA | |||
| colspan="1" rowspan="1" |Oral | |||
|- | |||
| colspan="1" rowspan="1" |A3AR agonist | |||
| colspan="1" rowspan="1" |CF101 | |||
| colspan="1" rowspan="1" |A3AR | |||
| colspan="1" rowspan="1" |NA | |||
| colspan="1" rowspan="1" |Oral | |||
|} | |||
SC: Sub-cutaneous | |||
IV: Intra-venous | |||
IM: Intra-muscular | |||
NA: Not Applicable | |||
PDE4: Phosphodiesterase 4 | |||
JAK: Janus Kinase | |||
PKC: Protein Kinase C | |||
==References== | ==References== |
Revision as of 18:12, 16 June 2017
Psoriasis Microchapters |
Diagnosis |
---|
Treatment |
Case Studies |
Psoriasis medical therapy On the Web |
American Roentgen Ray Society Images of Psoriasis medical therapy |
Risk calculators and risk factors for Psoriasis medical therapy |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
Medical Therapy
Therapies are administered according to disease severity and assessed by the Psoriasis Area and Severity Index (PASI, ranging from 0 to 72), which takes into account appearance and extension of the lesions. Interventions in medical therapy for psoriasis comprise of:
- Topical therapy
- Phototherapy
- Systemic therapy (Immunosuppressive agents)
- Biological therapy
Topical therapy[1]
- Medicated creams and ointments applied directly to psoriatic lesions can help decrease inflammation, remove built-up scale, reduce skin turn over, and clear affected skin of plaques.
- Approved drugs that can be used as topical therapy for acute management of psoriasis include:
- Corticosteroids
- Vitamin D analogues (calcipotriol)[2]
- Tar
- Dithranol (anthralin)
- Tazarotene (a retinoid)
- Calcineurin inhibitors (Tacrolimus and primecrolimus- used specially foe flexural or facial psoriasis)
- Aloe vera extract 0.5 % hydrophilic cream[3]
- Anti-IL-8 monoclonal antibody cream
- Betamethasone 17-valerate 21-acetate plus tretinoin plus salicylic acid[4]
- Fish oil plus occlussion[5]
- Combination of nicotinamide and calcipotriene[6]
- Combined treatment with vitamin D/corticosteroid on either the body or the scalp has significantly better outcomes than vitamin D alone.[7]
- The disadvantages of topical agents are variably that they can often irritate normal skin, can be time consuming and awkward to apply, cannot be used for long periods, can stain clothing or have a strong odour. As a result, it is sometimes difficult for people to maintain the regular application of these medications.
- Abrupt withdrawal of some topical agents, particularly corticosteroids, can cause an aggressive recurrence of the condition.
- Some topical agents are used in conjunction with other therapies, especially phototherapy.
Phototherapy[8]
- It has long been recognized that daily, short, non-burning exposure to sunlight helped to clear or improve psoriasis.
- Niels Finsen was the first physician to investigate the therapeutic effects of sunlight scientifically and to use sunlight in clinical practice. This became known as phototherapy.
- Narrow band part of the UVB spectrum (311 to 312 nm) is most helpful for psoriasis. Exposure to UVB several times per week, over several weeks can help people attain a remission from psoriasis.
- Ultraviolet light treatment is frequently combined with topical (coal tar, calcipotriol) or systemic treatment (retinoids) as there is a synergy in their combination.
- The Ingram regime, involves UVB and the application of anthralin paste.
- The Goeckerman regime combines coal tar ointment with UVB.
Systemic therapy
Type of agent | Mechanism of action | Name | Molecular target | Formulation | Administration route |
---|---|---|---|---|---|
Biologic | Anti-T cells | Alefacept | CD2 | Human LFA-3/IgG1 fusion protein | IM or IV |
Efalizumab | CD11a | Humanized IgG1 monoclonal antibody | SC | ||
Abatacept | CTLA-4 | Human CTLA4–Ig-IgG1 fusion protein | SC or IV | ||
Anticytokine | Etanercept | TNF | Human TNF-R (p75)-lgG1 fusion protein | SC | |
Infliximab | TNF | Mouse-human IgG1 chimeric monoclonal antibody | IV | ||
Adalimumab | TNF | Human IgG1 monoclonal antibody | SC | ||
Ustekinumab | IL-12p40 (IL-2, IL-23) | Human IgG1 monoclonal antibody | SC | ||
Briakinumab (discontinued in USA in 2011) | IL-12p40 (IL-12, IL-23) | Human IgG1 monoclonal antibody | SC | ||
Guselkumab | IL-23p19 | Human IgG1 monoclonal antibody | SC | ||
Brodalumab | IL-17R | Human IgG2 monoclonal antibody | SC | ||
Ixekizumab | IL-17 | Humanized IgG4 monoclonal antibody | SC | ||
Secukinumab | IL-17 | Human IgG1 monoclonal antibody | SC or IV | ||
Fezakinumab | IL-22 | Human IgG1 monoclonal antibody | SC or IV | ||
Small molecule | PDE4 inhibitor | Apremilast | PDE4 | NA | Oral |
JAK inhibitor | Tofacitinib | JAK1 and JAK3 | NA | Oral | |
Baricitinib | JAK1 and JAK2 | NA | Oral | ||
PKC inhibitor | AEB071 | PKC | NA | Oral | |
A3AR agonist | CF101 | A3AR | NA | Oral |
SC: Sub-cutaneous
IV: Intra-venous
IM: Intra-muscular
NA: Not Applicable
PDE4: Phosphodiesterase 4
JAK: Janus Kinase
PKC: Protein Kinase C
References
- ↑ Smith CH, Barker JN (2006). "Psoriasis and its management". BMJ. 333 (7564): 380–4. doi:10.1136/bmj.333.7564.380. PMC 1550454. PMID 16916825.
- ↑ Ashcroft DM, Po AL, Williams HC, Griffiths CE (2000). "Systematic review of comparative efficacy and tolerability of calcipotriol in treating chronic plaque psoriasis". BMJ. 320 (7240): 963–7. PMC 27334. PMID 10753146.
- ↑ Syed TA, Ahmad SA, Holt AH, Ahmad SA, Ahmad SH, Afzal M (1996). "Management of psoriasis with Aloe vera extract in a hydrophilic cream: a placebo-controlled, double-blind study". Trop. Med. Int. Health. 1 (4): 505–9. PMID 8765459.
- ↑ Naldi L, Rzany B (2009). "Psoriasis (chronic plaque)". BMJ Clin Evid. 2009. PMC 2907770. PMID 19445765.
- ↑ Escobar SO, Achenbach R, Iannantuono R, Torem V (1992). "Topical fish oil in psoriasis--a controlled and blind study". Clin. Exp. Dermatol. 17 (3): 159–62. PMID 1451289.
- ↑ Levine D, Even-Chen Z, Lipets I, Pritulo OA, Svyatenko TV, Andrashko Y, Lebwohl M, Gottlieb A (2010). "Pilot, multicenter, double-blind, randomized placebo-controlled bilateral comparative study of a combination of calcipotriene and nicotinamide for the treatment of psoriasis". J. Am. Acad. Dermatol. 63 (5): 775–81. doi:10.1016/j.jaad.2009.10.016. PMID 20599292.
- ↑ "Topical treatments for chronic plaque psoriasis - Mason - 2013 - The Cochrane Library - Wiley Online Library".
- ↑ Naldi L, Rzany B (2009). "Psoriasis (chronic plaque)". BMJ Clin Evid. 2009. PMC 2907770. PMID 19445765.