• Users Online: 6557
  • Home
  • Print this page
  • Email this page
Home About us Editorial board Ahead of print Current issue Search Archives Submit article Instructions Subscribe Contacts Login 


 
 Table of Contents  
EDITORIAL
Year : 2019  |  Volume : 5  |  Issue : 1  |  Page : 1-5

Biologics in psoriasis: Indian experience


Department of Dermo-Cosmetology, Lilavati Hospital and Research Centre, Mumbai, Maharashtra, India

Date of Web Publication22-Jul-2019

Correspondence Address:
Dr. Shrichand G Parasramani
Anisha Clinic - Mangal Sudha, SV Road, Khar, Mumbai - 400 052, Maharashtra
India
Login to access the Email id

Source of Support: None, Conflict of Interest: None


DOI: 10.4103/ijdd.ijdd_33_19

Rights and Permissions

How to cite this article:
Parasramani SG, Pillai J. Biologics in psoriasis: Indian experience. Indian J Drugs Dermatol 2019;5:1-5

How to cite this URL:
Parasramani SG, Pillai J. Biologics in psoriasis: Indian experience. Indian J Drugs Dermatol [serial online] 2019 [cited 2024 Mar 29];5:1-5. Available from: https://www.ijdd.in/text.asp?2019/5/1/1/263096



Biological therapy became available for psoriasis for the last two decades. Increased understanding of the underlying immunopathogenesis and genetics of psoriasis has led to the development of highly targeted and effective therapies which have not only improved but also helped to clear psoriasis and its comorbidities including psoriatic arthritis (PsA) (prevalence of 10%–30%),[1] inflammatory bowel disease (IBD),[2] and cancers (especially cancers associated with alcohol drinking and smoking).[3] Recent studies have established psoriasis as being associated with a palate of lifestyle comorbidities, metabolic syndrome, obesity, hyperlipidemia, nonalcoholic steatohepatitis, diabetes, and cardiovascular disease. Biologics help to target these comorbidities.

Alefacept was the first biological agent approved by the US Food and Drug Administration for the treatment of moderate-to-severe chronic plaque psoriasis in 2003.[4] It blocked the co-stimulation between CD2 and LFA3, and since 2011, it has been discontinued. Efalizumab approved in 2003 blocked the stimulation between LFA1 and ICAM1. It was discontinued in 2009 as patients showed signs of progressive multifocal encephalopathy;[5] among tumor necrosis factor (TNF)-alpha blockers, etanercept was the first biologic to be introduced in the year 2000[6] and its approval for psoriasis was obtained in 2004, infliximab in 2006,[7] adalimumab in 2008,[8] golimumab for PsA in 2009,[9] and certolizumab pegol was approved in 2018 for the treatment of psoriasis.

Itolizumab, an Indian biologic which acted upstream by blocking the co-stimulation between CD6 and activated leukocyte-cell adhesion molecule (ALCAM), was approved in 2013 for psoriasis.[10] Ustekinumab, an interleukin (IL) IL-12 and IL-23 p40 subunit blocker, was approved for psoriasis in 2009.[11]

IL-17 blockers, for example, secukinumab, were approved in 2015 for psoriasis in adult patients,[12] while brodalumab was approved in the year 2017 and ixekizumab in 2016.

IL-23 P19 subunit blockers are newer biologics, with tildrakizumab being approved in 2018,[13] guselkumab in 2017, and risankizumab in 2019.


  Biologics Available in India Top


Biologics available in India include TNF-alpha blockers, etanercept and infliximab, which are innovator drugs, while adalimumab is a biosimiliar. Itolizumab, an Indian innovator biologic, is administered intravenously. Secukinumab, an innovator drug, is also available and administered subcutaneously.


  Indications of Biological Therapy Top


Biologics are indicated in patients who are intolerant, are unresponsive, or have contraindications to standard systemic therapy.[14] They are also used in patients who have significant, coexistent comorbidity, which precludes the use of standard systemic agents.[14] These can be used as first-line therapy in patients having severe, unstable, life-threatening diseases, for example, pustular psoriasis and erythrodermic psoriasis and also where the disease affects high-impact sites irrespective of the Psoriasis Area and Severity Index (PASI)-hands, feet, head, neck, and genitalia.[14] In patients where there is significant functional or psychological morbidity, they can be a first-line indication. They can also be used in patients with moderate-to-severe psoriasis having a PASI score of 10 or more, body surface area of 10% or greater, and a Dermatology Life Quality Index >10 (range: 0–30).[14] Biologics are indicated in those where phototherapy has failed or is contraindicated or the safe exposure limits of ultraviolet A (UVA) and ultraviolet B have been exceeded and where patients cannot visit a phototherapy center for logistic reasons.[14] It can be offered to those who are unwilling to use systemic therapy due to the fear of end-organ toxicities and are willing to start biologics as the first-line therapy in spite of the cost involved.


  Patient Workup Before Starting Biologics Top


All patients who are candidates for biologics need to carry out the following investigations before starting these drugs: complete blood count; erythrocyte sedimentation rate; C-reactive protein; liver function test (LFT); serum creatinine; blood sugars (fasting and postprandial); tests for HIV, hepatitis B virus (HBV) surface antigen (HBsAg)/HBV core antigen (HBcAg), and hepatitis C virus; antinuclear antibody test; Mantoux test; QuantiFERON® gold test (interferon [IFN] gamma release assay [IGRA]) if Mantoux test is positive; X-ray chest; electrocardiogram; routine urine examination; routine stool examination; urinary pregnancy test (females) and abdominal sonography if indicated or in elderly patients.


  Adverse Events Top


Dermatological

Although rare, dermatitis, erythema nodosum, urticaria, leukocytoclastic vasculitis, lichenoid reactions,[15] erythema multiforme, and toxic epidermal necrolysis have been reported.


  Reaction to Biologics Top


Urticarial reaction to etanercept has been reported.[16] Infusion-related reaction, and rarely serum sickness, has been reported with infliximab.[15] Injection-site reaction with subcutaneous injections may occur, and this could be due to local irritation following a high concentration of drug or vehicle and faulty injection technique.[17] Immune-mediated reactions due to the presence of antibodies can occur, and these may be type 1 or type 3 hypersensitivity reaction. Infliximab should be given in a hospital with premedication comprising of injection chlorpheniramine maleate and injection hydrocortisone. Sites where biologics are administered should be equipped for resuscitation measures in case of reactions.


  Paradoxical Worsening of the Existing Psoriasis Top


It has been reported with anti-TNF-α therapies after days to years. The inhibition of TNF-α stimulates dendritic cells to produce increased levels of IFN-α, thereby activating Th-1 cells. In one study, 52% of patients developed pustular psoriasis; 49%, plaque psoriasis; 16%, guttate psoriasis; and 53% were due to infliximab, etanercept (29%), and adalimumab (18%).[18]


  Malignancy Top


Most of the studies have been conducted on patients with rheumatoid arthritis (RA) and IBD. RA patients are on multiple immunosuppressive drugs. The baseline risk of lymphoma (Hodgkin's and cutaneous T-cell lymphoma) irrespective of treatment is high in patients with psoriasis and RA.[19] The risk is increased in patients who have taken psoralen and UVA therapy and cyclosporine. All patients and those with a history of multiple immunosuppressive therapies should be screened for malignancy before and during biologic therapy. Skin and lymph node examination should be carried out at baseline, 6 monthly for the 1st year, and yearly thereafter.[19] Avoid biologics for 3 years in those with a history of squamous cell carcinoma, basal cell carcinoma, and nonmelanoma skin cancers in the past and for 5 years in patients with a history of melanoma and lymphoma.


  Some Special Situations to Consider With Biologic Usage Top


Pregnancy category B

The British Association of Dermatologists and European S3 guidelines recommend discontinuing biologics prior to conception.[20] Etanercept should be discontinued 3 weeks prior to conception, whereas infliximab and adalimumab should be discontinued 6 months and 5 months before conception, respectively. Secukinumab and itolizumab should not be used in pregnancy due to lack of safety data.

Nursing mothers

Many drugs and immunoglobulins are excreted in human milk and because of the potential for adverse reactions of biologics in nursing infants, women on biologics should not breastfeed their infants.[21]

Etanercept can pass into breastmilk, infliximab is not detected in breastmilk, adalimumab and secukinumab transfer in small amount, and there is no data as regards itolizumab.

Pediatric patients

Etanercept can be used above 6 years of age at a dose of 0.8 mg/kg given once a week not exceeding 50-mg dose.[22],[23] Adalimumab can be used above 4 years of age at a dose of 0.8 mg/kg given on day 0 and day 7, and thereafter once every 2 weeks not exceeding 40-mg dose.[22],[23] Data for infliximab are lacking. Secukinumab and itolizumab are not indicated for pediatric use.

Vaccinations

Live or live attenuated vaccines are contraindicated 2 weeks before, during, and for 6 months after the discontinuation of biologic therapy. These are bacillus Calmette–Guérin, yellow fever, nasal influenza, cholera, oral typhoid, oral polio, and measles, mumps, and rubella.[14]

Inactivated vaccines are recommended and should be administered 2 weeks before starting a biologic to ensure an optimum immune response. These include influenza, meningococcal, diphtheria, pertussis and tetanus, human papillomavirus, pneumovax, and inactivated polio vaccines.[14]

HIV patients

Etanercept can be given to HIV patients, and adalimumab has also been used. Infliximab, secukinumab, and itolizumab should be avoided in HIV patients. These patients should be managed in collaboration with an infectious disease specialist for close monitoring of CD4 count and viral load along with antiretroviral therapy.[24]

Biologics in hepatitis B virus patients

In patients who are HbsAg positive, TNF-α inhibitors can lead to viral reactivation; thus, these should be given along with antiviral prophylaxis (tenofovir is preferred over lamivudine) and with close monitoring of LFTs and viral titers. Patients who are anti-HbcAg positive have lesser risk of HBV reactivation than HbsAg-positive patients, and hence, they can be administered TNF-α inhibitors with close monitoring of LFTs and viral titers.[24] Secukinumab appears safe if used after antiviral prophylaxis. Itolizumab is best avoided as there is a lack of data.

Biologics in hepatitis C virus patients

TNF-α inhibitors can be used with a close monitoring of LFTs and viral titers and in conjunction with antiviral therapy (directly-acting antiviral agents). IL-17 inhibitors, secukinumab, appear to have a favorable safety profile, but data are limited.[24]


  Surgery and Biologicals Top


It takes five half-lives for a product to be completely eliminated from the body. Biologics should be stopped before major surgery and can be restarted postoperatively if there is no evidence of infection and wound healing is satisfactory. For clean surgical procedures (i.e., arthroscopy), washout = 3 × half-life.[25] For high-infection-risk procedures (i.e., gastrointestinal tract surgery), washout = 5 × half-life.[25]

The half-life of etanercept is 3–5 days and thus, discontinuation time is 2–3 weeks. For adalimumab, the half-life is 14–19 days and discontinuation time is 8–11 weeks.[26] For infliximab, the half-life is 8–9 days and thus discontinuation time is 4–5 weeks.[26] The half-life of secukinumab and itolizumab is 22–31 days and 12–18 days, respectively.


  Tuberculosis Top


All patients must be evaluated for the risk of tuberculosis, be it active, latent, and reactivation. Personal history of tuberculosis or possible previous contact with tuberculosis should be evaluated in all patients. Appropriate screening tests, i.e., tuberculin skin test, chest X-ray, and IGRA, should be performed in all patients. When biologics are given, there may be reactivation of latent infection, and this can be determined by carrying out an IGRA test. IGRA is more pertinent for patients already on immunosuppressives. Two types of IGRA tests are available namely QuantiFERON®-TB and T-SPOT®-TB test. If latent tuberculosis infection (LTBI) is diagnosed, a combination regimen of isoniazid and rifampicin is given for at least 1 month before starting biologic and should be continued for at least 4 months. In case of active infection, treat Kochs and do not use biologicals. Patients must be monitored closely for infections, including miliary, extrapulmonary, atypical, and disseminated forms of tuberculosis infection, while on and for 1 year after treatment with biologicals. Treatment must be discontinued if the patient develops a serious infection or sepsis. It is safe to use IL-17 inhibitor secukinumab in patients with LTBI.[24]


  Cardiac Events Top


TNF-α inhibitors are contraindicated in patients with moderate or severe heart failure (New York Heart Association 3 and 4).[14] Secukinumab and itolizumab can be used safely.


  Hepatobiliary Events Top


Features of autoimmune hepatitis have been reported in patients receiving infliximab. Mild-to-moderate elevations of serum glutamic-oxaloacetic transaminase and serum glutamic-pyruvic transaminase have been observed in patients receiving infliximab without progression to severe hepatic injury. If elevations of aminotransferases are observed to be more than five times the upper limit of normal, infliximab should be discontinued.[27]


  Neurological Events Top


TNF-α inhibitors have been associated with rare cases of optic neuritis, seizures, and evidence of demyelinating disorders including multiple sclerosis and Guillain–Barré syndrome. Patients with a personal or family history of these should not be administered TNF-α inhibitors. Secukinumab and itolizumab do not cause demyelinating disorders.[14]


  Indian Experience Top


Etanercept is a dimeric fusion protein that consists of soluble TNF-alpha receptor p75 fused to the Fc portion of human immunoglobulin G (IgG). It binds and neutralizes both TNF-alpha and TNF-beta, binding to both soluble- and receptor-bound TNF-alpha. The molecular weight of etanercept is 150 kDa, with a half-life of 3–5 days, and its absolute bioavailability after subcutaneous injection is 58%.[28] It is approved for chronic plaque psoriasis and PsA. In our experience on Indian patients, PASI 50 was seen within 8 weeks and PASI 75 by 16 weeks, with 50-mg dose per week. In two patients, PASI 100 was seen by 8 weeks (one patient of pustular psoriasis and one of erythrodermic psoriasis). PASI 75 was maintained for 6 months in one study of ours.

Infliximab is an IgG-1 monoclonal chimeric antibody which neutralizes both soluble- and receptor-bound TNF-alpha, but it does not neutralize TNF-beta. Being a protein, it is not metabolized by cytochrome P450 enzymes. Its molecular weight is 150 kDa, with a half-life of 8–9 days,[29] and given at a dose of 5 mg/kg on day 0, week 2, and week 6, and thereafter, it is administered once every 2 months intravenously slowly over 3–4 h. It is distributed in the vascular compartment and metabolized by proteolysis. It is approved in treating chronic plaque psoriasis and PsA. In our study, PASI 50 was obtained by week 6 and PASI 75 by week 14 and maintained till week 30. In an Indian study of three patients by Sridhar et al. who received three doses, all the patients attained PASI 50 by 3.8 weeks and PASI 75 at 9.6 weeks. Relapse was reported at 18.6 weeks after the first infusion.[30]

Adalimumab is a fully recombinant, human monoclonal IgG1 antibody against TNF-alpha having a molecular weight of 148 kDa.[31] It functions by specifically binding to TNF-alpha and obstructs its interaction with p55 and p75 cell surface TNF receptors. Intracellular signaling mediated by TNF occurs through interactions with cell-bound TNF receptors. These receptors are present on almost all the cells.

After subcutaneous administration, serum concentration reaches its peak after 5 days. Its bioavailability is 64%. Its mean terminal phase half-life is approximately 14–19 days. It is given at 80 mg on day 0, followed by 40 mg on week 1 and 40 mg for every 2 weeks.

It is approved for RA, juvenile idiopathic arthritis, Crohn's disease and ulcerative colitis, ankylosing spondylitis, PsA, chronic plaque psoriasis, hidradenitis suppurativa, and uveitis. In our study, PASI 50 was seen by week 1, PASI 75 by week 3, and PASI 90 by week 7. PASI 90 was maintained up to 36 weeks.

Itolizumab is a humanized recombinant anti-CD6 monoclonal antibody exerting an immunomodulatory action upstream on T cells by preventing co-stimulation between CD6 on T cell and ALCAM on antigen-presenting cells, thereby leading to reduction of downstream cytokines and chemokines. Its molecular weight is 148 kDa with a half-life of 12–18 days.[32] It is available as a preservative-free, single-use 25-mg/5-ml vial and is administered intravenously at a dose of 1.6 mg/kg once every 2 weeks for the first 3 months and then once a month for the next 3 months (total infusion is 250 ml). The infusion solution is administered over a period of not less than 3 h.

Adverse events reported with itolizumab include infusion reactions, upper respiratory tract infections (URTIs), pyrexia, pruritus, and diarrhea. These are generally mild and did not cause most patients to stop taking itolizumab.

In our study on 13 patients, PASI 50 was achieved by week 6, PASI 75 by week 10, and PASI 90 by week 12. At week 52, almost all patients except one relapsed as PASI fell by 50%. One patient maintained PASI 90 for 4.5 years, receiving one infusion every 3 months.

Secukinumab is a fully recombinant human IgG1 that selectively binds to and neutralizes the pro-inflammatory cytokine IL-17A. It works by targeting IL-17A and inhibits its interaction with IL-17 receptor, which is expressed on various cell types including keratinocytes. Its molecular weight is 150 kDa.[33] Its average absolute bioavailability is 73%. The mean elimination half-life has been estimated to be 27 days (22–31 days) in plaque psoriasis patients. It is approved for moderate-to-severe plaque psoriasis in adults who are candidates for systemic therapy, PsA, ankylosing spondylitis, RA, nail psoriasis, and palmoplantar psoriasis. It is given as an induction dose of 300 mg every week for 5 weeks and thereafter as a maintenance regimen of 300 mg once a month administered subcutaneously.

Adverse events reported with secukinumab are nasopharyngitis, headache, URTI, arthralgia, diarrhea, back pain, cough, candidiasis, neutropenia, and IBD.[34]

In our study on 22 patients, PASI 50 was achieved by week 2, PASI 75 by week 8, and PASI 90 by week 12 (nine patients achieved PASI 100 by week 12). PASI 90 was maintained for 52 weeks in 19 patients. In three patients, PASI 90 was maintained for 130 weeks.


  Conclusion Top


Although the availability of biologics is limited in our country, the available biologics are quite effective. The cost of these drugs is an impediment to use them for patients who really need them. Its long-term use again adds to the economic burden as psoriasis is a disease which can be controlled but cannot be cured. The safety profile of secukinumab, etanercept, and adalimumab is fairly good. Patients who have used biologics for long term have done well. The loss of efficacy with biologics due to immunogenicity has to be borne in mind in case of these patients. Biologics have revolutionized the therapy of psoriasis as patients who are no longer satisfied with PASI 50/PASI 75 response are now able to achieve PASI 90 and even PASI 100 response.



 
  References Top

1.
Madland TM, Apalset EM, Johannessen AE, Rossebö B, Brun JG. Prevalence, disease manifestations, and treatment of psoriatic arthritis in Western Norway. J Rheumatol 2005;32:1918-22.  Back to cited text no. 1
    
2.
Persson PG, Leijonmarck CE, Bernell O, Hellers G, Ahlbom A. Risk indicators for inflammatory bowel disease. Int J Epidemiol 1993;22:268-72.  Back to cited text no. 2
    
3.
Boffetta P, Gridley G, Lindelöf B. Cancer risk in a population-based cohort of patients hospitalized for psoriasis in Sweden. J Invest Dermatol 2001;117:1531-7.  Back to cited text no. 3
    
4.
Menter A, Cather JC. Alefacept. Therapy 2005;2:23-35.  Back to cited text no. 4
    
5.
Schwab N, Ulzheimer JC, Fox RJ, Schneider-Hohendorf T, Kieseier BC, Monoranu CM, et al. Fatal PML associated with efalizumab therapy: Insights into integrin αLβ2 in JC virus control. Neurology 2012;78:458-67.  Back to cited text no. 5
    
6.
Hassett B, Singh E, Mahgoub E, O'Brien J, Vicik SM, Fitzpatrick B, et al. Manufacturing history of etanercept (Enbrel®): Consistency of product quality through major process revisions. MAbs 2018;10:159-65.  Back to cited text no. 6
    
7.
Gall JS, Kalb RE. Infliximab for the treatment of plaque psoriasis. Biologics 2008;2:115-24.  Back to cited text no. 7
    
8.
Scheinfeld N. Adalimumab (HUMIRA): A review. J Drugs Dermatol 2003;2:375-7.  Back to cited text no. 8
    
9.
Mazumdar S, Greenwald D. Golimumab. MAbs 2009;1:422-31.  Back to cited text no. 9
    
10.
Jayaraman K. Biocon's first-in-class anti-CD6 mAb reaches the market. Nat Biotechnol 2013;31:1062-3.  Back to cited text no. 10
    
11.
Cingoz O. Ustekinumab. MAbs 2009;1:216-21.  Back to cited text no. 11
    
12.
Fala L. Cosentyx (Secukinumab):First IL-17A antagonist receives FDA approval for moderate-to-severe plaque psoriasis. Am Health Drug Benefits 2016;9:60-3.  Back to cited text no. 12
    
13.
Markham A. Tildrakizumab:First global approval. Drugs 2018;78:845-9.  Back to cited text no. 13
    
14.
Smith CH, Anstey AV, Barker JN, Burden AD, Chalmers RJ, Chandler DA, et al. British Association of Dermatologists' guidelines for biologic interventions for psoriasis 2009. Br J Dermatol 2009;161:987-1019.  Back to cited text no. 14
    
15.
Cheifetz A, Smedley M, Martin S, Reiter M, Leone G, Mayer L, et al. The incidence and management of infusion reactions to infliximab: A large center experience. Am J Gastroenterol 2003;98:1315-24.  Back to cited text no. 15
    
16.
Batycka-Baran A, Flaig M, Molin S, Ruzicka T, Prinz JC. Etanercept-induced injection site reactions: Potential pathomechanisms and clinical assessment. Expert Opin Drug Saf 2012;11:911-21.  Back to cited text no. 16
    
17.
Bavbek S, Ataman Ş, Bankova L, Castells M. Injection site reaction to adalimumab: Positive skin test and successful rapid desensitisation. Allergol Immunopathol (Madr) 2013;41:204-6.  Back to cited text no. 17
    
18.
Collamer AN, Guerrero KT, Henning JS, Battafarano DF. Psoriatic skin lesions induced by tumor necrosis factor antagonist therapy: A literature review and potential mechanisms of action. Arthritis Rheum 2008;59:996-1001.  Back to cited text no. 18
    
19.
Bongartz T, Sutton AJ, Sweeting MJ, Buchan I, Matteson EL, Montori V. Anti-TNF antibody therapy in rheumatoid arthritis and the risk of serious infections and malignancies: Systematic review and meta-analysis of rare harmful effects in randomized controlled trials. JAMA 2006;295:2275-85.  Back to cited text no. 19
    
20.
Lynch M, Kirby B, Warren RB. Treating moderate to severe psoriasis-best use of biologics. Expert Rev Clin Immunol 2014;10:269-79.  Back to cited text no. 20
    
21.
Witzel SJ. Lactation and the use of biologic immunosuppressive medications. Breastfeed Med 2014;9:543-6.  Back to cited text no. 21
    
22.
Napolitano M, Megna M, Balato A, Ayala F, Lembo S, Villani A, et al. Systemic treatment of pediatric psoriasis: A review. Dermatol Ther (Heidelb) 2016;6:125-42.  Back to cited text no. 22
    
23.
Smith CH, Jabbar-Lopez ZK, Yiu ZZ, Bale T, Burden AD, Coates LC, et al. British Association of Dermatologists guidelines for biologic therapy for psoriasis 2017. Br J Dermatol 2017;177:628-36.  Back to cited text no. 23
    
24.
Kaushik SB, Lebwohl MG. Psoriasis: Which therapy for which patient: Focus on special populations and chronic infections. J Am Acad Dermatol 2019;80:43-53.  Back to cited text no. 24
    
25.
Kerrigan N. Clinical Guideline for: Interruption of Biologic Therapies for Elective Surgery in Adults and Children RA, JI, AS. Specialist Nurse in Rheumatology. CGAP; 2017.  Back to cited text no. 25
    
26.
Choi YM, Debbaneh M, Weinberg JM, Yamauchi PS, Van Voorhees AS, Armstrong AW, et al. From the medical board of the national psoriasis foundation: Perioperative management of systemic immunomodulatory agents in patients with psoriasis and psoriatic arthritis. J Am Acad Dermatol 2016;75:798-805.  Back to cited text no. 26
    
27.
Ozorio G, McGarity B, Bak H, Jordan AS, Lau H, Marshall C, et al. Autoimmune hepatitis following infliximab therapy for ankylosing spondylitis. Med J Aust 2007;187:524-6.  Back to cited text no. 27
    
28.
Nguyen TU, Koo J. Etanercept in the treatment of plaque psoriasis. Clin Cosmet Investig Dermatol 2009;2:77-84.  Back to cited text no. 28
    
29.
Leman J, Burden A. Treatment of severe psoriasis with infliximab. Ther Clin Risk Manag 2008;4:1165-76.  Back to cited text no. 29
    
30.
Sridhar J, Desylva P, Singh YD. Chimeric monoclonal antibody to tumor necrosis factor alpha (infliximab) in psoriasis. Indian J Dermatol Venereol Leprol 2006;72:133-5.  Back to cited text no. 30
[PUBMED]  [Full text]  
31.
Alwawi EA, Mehlis SL, Gordon KB. Treating psoriasis with adalimumab. Ther Clin Risk Manag 2008;4:345-51.  Back to cited text no. 31
    
32.
Menon R, David BG. Itolizumab – A humanized anti-CD6 monoclonal antibody with a better side effects profile for the treatment of psoriasis. Clin Cosmet Investig Dermatol 2015;8:215-22.  Back to cited text no. 32
    
33.
Roman M, Madkan VK, Chiu MW. Profile of secukinumab in the treatment of psoriasis: Current perspectives. Ther Clin Risk Manag 2015;11:1767-77.  Back to cited text no. 33
    
34.
Frieder J, Kivelevitch D, Menter A. Secukinumab: A review of the anti-IL-17A biologic for the treatment of psoriasis. Ther Adv Chronic Dis 2018;9:5-21.  Back to cited text no. 34
    



This article has been cited by
1 An Open-Label, Randomized, Prospective, Comparative, Three-Arm Clinical Trial to Evaluate the Safety and Effectiveness of Apremilast with Three Different Titration Methods in Patients with Chronic Plaque Psoriasis in India
Vishalakshi Viswanath, Pradnya Joshi, Prakash Lawate, Dakshata Tare, Dhiraj Dhoot, Namrata Mahadkar, Hanmant Barkate
Psoriasis: Targets and Therapy. 2022; Volume 12: 53
[Pubmed] | [DOI]
2 Portraying molecular modulation and therapeutic aspects of psoriasis: Retrospection and current status
Kajal Sharma,Shalki Choudhary,Om Silakari
Journal of Molecular Structure. 2021; : 130770
[Pubmed] | [DOI]
3 The Use of Apremilast in Psoriasis: An Indian Perspective on Real-World Scenarios
Murlidhar Rajagopalan,Sunil Dogra,Abir Saraswat,Sachin Varma,Pravin Banodkar
Psoriasis: Targets and Therapy. 2021; Volume 11: 109
[Pubmed] | [DOI]



 

Top
 
 
  Search
 
Similar in PUBMED
   Search Pubmed for
   Search in Google Scholar for
Access Statistics
Email Alert *
Add to My List *
* Registration required (free)

 
  In this article
Biologics Availa...
Indications of B...
Patient Workup B...
Adverse Events
Reaction to Biol...
Paradoxical Wors...
Malignancy
Some Special Sit...
Surgery and Biol...
Tuberculosis
Cardiac Events
Hepatobiliary Events
Neurological Events
Indian Experience
Conclusion
References

 Article Access Statistics
    Viewed17840    
    Printed494    
    Emailed0    
    PDF Downloaded791    
    Comments [Add]    
    Cited by others 3    

Recommend this journal


[TAG2]
[TAG3]
[TAG4]