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 Table of Contents  
Year : 2020  |  Volume : 6  |  Issue : 1  |  Page : 53-57

Viva voce: Adalimumab

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

Date of Submission10-Feb-2020
Date of Decision18-Apr-2020
Date of Acceptance30-Apr-2020
Date of Web Publication23-Jun-2020

Correspondence Address:
Dr. Manasi Shirolikar
C-1, DAE (BARC) Building, 15th Road, Bandra West, Mumbai - 400 050, Maharashtra
Login to access the Email id

Source of Support: None, Conflict of Interest: None

DOI: 10.4103/ijdd.ijdd_5_20

Rights and Permissions

How to cite this article:
Parasramani SG, Pillai J, Shirolikar M. Viva voce: Adalimumab. Indian J Drugs Dermatol 2020;6:53-7

How to cite this URL:
Parasramani SG, Pillai J, Shirolikar M. Viva voce: Adalimumab. Indian J Drugs Dermatol [serial online] 2020 [cited 2021 Jun 13];6:53-7. Available from: https://www.ijdd.in/text.asp?2020/6/1/53/287434

  Introduction Top

Psoriasis is a chronic inflammatory disease affecting 1%–3% of population worldwide.[1] Chronic plaque psoriasis is the most common type of psoriasis accounting for 90% of cases apart from guttate, erythrodermic, pustular, and inverse forms of psoriasis. Along with cutaneous disease and psoriatic arthritis, these patients are at an increased risk of heart disease, depression, metabolic syndrome, diabetes, and some malignancies (i.e. lymphoma).[2] Psoriasis affects health-related quality of life and poses substantial medical, social, and economic burden.

  What is Adalimumab? Top

Adalimumab, the first fully human, tumor necrosis factor (TNF)-alpha, IgG1 monoclonal antibody, which blocks its interaction with the p55 and p75 cell surface receptors, was introduced in the year 2003 for various dermatological and nondermatological conditions. It was originally known as D2E7 and was obtained using phage display technology and successfully produced in a mammalian expression system. Among the dermatologic conditions, it is approved by the US Food and Drug Administration (FDA) for the treatment of moderate-to-severe chronic plaque psoriasis.

It also lyses the cells that express surface TNF-α in the presence of complement.[3],[4] Adalimumab rapidly reverses the decrease in epidermal Langerhans cell density in psoriatic plaques and helps in the restoration of their density.

  Pharmacokinetics Top

Adalimumab, initially named as D2E7, is a protein comprising 1330 amino acids with a molecular weight of 148 kDa. It is an IgG antibody composed of two kappa light chains each with a molecular weight of approximately 24 kDa and two IgG1z, heavy chains each with a molecular weight of approximately 49 kDa. Each light chain consists of 214 amino acid residues and each heavy chain consists of 451 amino acid residues.[5] It is a purely human IgG1 monoclonal anti-tumor necrosis factor-alpha antibody which is administered subcutaneously as a 40 mg dose once every 2 weeks.[6] It has high affinity and selectivity for TNF-α and acts on the soluble as well as the membrane-bound TNF-α.[7] Bioavailability following a single subcutaneous injection is 64%. It is slowly absorbed mainly through the lymphatics with peak concentrations at 1–2 weeks. The half-life of the drug is 14–19 days.[4] The therapeutic effect is seen within 24 h to 1 week with maximum effect being observed at 2 weeks. The mean steady state trough level was 5–6 μg/ml when adalimumab was given every other week.[8] There appears to be no effect of gender or body weight on the serum concentrations of adalimumab. It is believed to be metabolized by proteolysis.

  Mechanism of Action Top

TNF-α, a pro-inflammatory cytokine, is a key motive cytokine driving the activity of macrophages. It binds the membrane receptors p55 and p75, which are expressed on fibroblasts, neutrophils, and vascular endothelial cells. Macrophages are key etiologic force behind inflammatory arthritis. TNF-α exerts various local and systemic effects in the development of inflammatory and autoimmune diseases by regulating numerous cellular and molecular signals which are implicated in the causation of inflammatory cascades of the autoimmune diseases. Adalimumab binds specifically to TNF-α, not to TNF-β, and blocks its interaction with p55 and p75 soluble and membrane-bound receptors. It is structurally and functionally indistinguishable from naturally occurring human immunoglobulin G1 antibody. The active substance is adalimumab, a recombinant monoclonal antibody directed to human TNF-α.[5]

Its bioavailability is 64% after a single 40 mg dose. The half-life is 14 days, which leads to every other week dosing. It is indicated for use in rheumatoid arthritis, ankylosing spondylitis, inflammatory bowel disease, psoriatic arthritis, and juvenile idiopathic arthritis and was approved for the treatment of plaque psoriasis in 2008.[5]

  Indications Top

Adalimumab is approved by the US FDA for the use in:

  • Rheumatoid arthritis
  • Psoriatic arthritis[9]
  • Juvenile idiopathic arthritis
  • Ankylosing spondylitis
  • Crohn's disease
  • Ulcerative colitis
  • Moderate-to-severe chronic plaque psoriasis.[10]

Apart from psoriasis, other dermatologic indications where adalimumab has been used include:

  • Hidradenitis suppurativa[11]
  • Neutrophilic dermatosis – pyoderma gangrenosum,[12] Behcet's disease
  • Wegener's granulomatosis
  • Sarcoidosis[13]
  • Pemphigus
  • Multicentric reticulohistiocytosis
  • Alopecia areata.[14]


Adalimumab is given as an initial dose of 80 mg subcutaneous injection, second dose of 40 mg after 1 week, and thereafter 40 mg every other week.

This dose is given for plaque psoriasis, psoriatic arthritis, ankylosing arthritis, and rheumatoid arthritis.

If no response is seen in 12–16 weeks, treatment may be reconsidered. In patients who respond, treatment may be continued as per the clinical response. In hidradenitis suppurativa and inflammatory bowel disease, dose varies.


  • Infections
  • Hypersensitivity to the drug
  • Neurological disorders
  • Congestive cardiac failure
  • Malignancies.

Adverse effects

Various clinical studies have shown adalimumab to be a safe drug. The adverse events noted were mild and did not require discontinuation of the therapy.

Development of serious adverse reactions was rare.

  1. Local injection-site reactions: Patients may complain of pain or pruritus. Reaction may present as erythema or urticarial plaques. These reactions are usually mild and do not require treatment.
  2. Hypersensitivity reactions: Anaphylaxis and angioedema have been reported following treatment with adalimumab.
  3. Cutaneous adverse events: Skin infections, allergic rash, urticaria, eczematous and psoriasiform eruptions, ulceration, and vasculitis[15] have all been described.
  4. Infections: The most frequent infections observed in clinical studies were rhinitis, upper respiratory tract infections, bronchitis, and urinary tract infections. It also increases the predisposition to rare infections such as fungal pneumonia, septic arthritis, and pyelonephritis.[16] Re-activation of hepatitis B may also occur while on adalimumab treatment.

  Tuberculosis Top

It may cause progression of latent tuberculosis (TB) to overt TB, new-onset TB, or dissemination of TB.[17] Re-activation of latent TB usually occurs within the first 8 months of treatment. Hence, it is recommended to do a complete blood count, erythrocyte sedimentation rate (ESR), tuberculin skin test, and chest radiograph prior to the treatment with adalimumab. Interferon gamma release assay (IGRAs) such as QuantiFERON-TB test, the QuantiFERON-TB Gold test, and the T-SPOT TB approved by the US FDA can also be used to aid in the diagnosis of latent and active tubercular infection.[18] In the presence of any of these tests being positive, initiating patients on adalimumab is not recommended.

Other opportunistic infections reported with adalimumab include:

  • Bacterial: Listeriosis,[19] legionella pneumonias,[20] and mycobacterial infections
  • Fungal: Aspergillosis, blastomycosis, coccidioidomycosis, candidiasis, histoplasmosis, pneumocystosis, and paracoccidioidomycosis.


Lymphoma (Hodgkins and non-Hodgkins lymphoma) and nonmelanoma cancers (basal cell carcinoma and squamous cell carcinoma)

Patients with psoriasis and rheumatoid arthritis, especially those with chronic or severe disease, who have been on immunosuppressants, have an additional risk of developing lymphomas than the general population even in the absence of treatment with adalimumab.[21]

Neurological reactions

New-onset or exacerbation of previous demyelinating disorder including multiple sclerosis, optic neuritis, and Guillain–Barre syndrome has been reported with adalimumab. Hence, adalimumab therapy should be avoided in patients with a personal history of or a first-degree relative with a demyelinating disorder.[22] If neurological symptoms suggestive of demyelination develop during therapy, treatment should be withdrawn.

Hematological abnormalities

Thrombocytopenia, leukopenia, and aplastic anemia have been reported with the use of adalimumab.

Congestive heart failure

It is known to cause worsening of symptoms in congestive heart failure, and cases of new-onset congestive heart failure have also been observed in clinical studies. Hence, caution must be exercised in treating heart failure patients with adalimumab and they should be monitored carefully. Avoid in NYHA 3 and 4 cardiac failure patients.[23]


Increase in hepatic enzymes may be observed during treatment with anti-TNF agents. It is more often related to concomitant drugs (i.e., NSAIDS, methotrexate) or to reactivation of chronic hepatitis B virus (HBV) or hepatitis C virus infections. Liver damage directly induced by the drug has been described in patients treated with infliximab or adalimumab.[24]

  Drug -Induced Lupus Erythematosus Top

Lupus erythematosus (LE) may be seen with use of infliximab,[25] however one should be aware of this condition even in patients on adalimumab.[26] If clinical signs and symptoms of LE develop and ANA titer increases, then add methotrexate and continue biologic in use. If ANA increases but no clinical signs and symptoms, occur continue the biologic. If signs and symptoms of LE occur and in spite of adding methotrexate, patient does not improve clinically, then stop the biologic being used (adalimumab or Infliximab) and switch over to secukinumab or ustekinumab.


Before initiating adalimumab therapy, the following investigations should be advised:

  • Complete blood count
  • ESR and C-reactive protein
  • Liver function tests
  • Renal function tests
  • Urine routine and microscopy
  • Mantoux test, IGRA test
  • Chest radiograph
  • Hepatitis B surface antigen, anti-Hepatitis B core IgM antibody, anti-Hepatitis C antibody, and ELISA for human immunodeficiency virus.

On treatment initiation, the patient should be monitored for the development of signs and symptoms of infections. If infections develop, consider appropriate diagnostic tests and institute appropriate treatment.

Special situations


Adalimumab is classified by the US FDA as Category B drug. However, there is no consensus regarding the use of biologics during pregnancy.

According to British association of dermatology and European S3 guidelines, adalimumab should be discontinued 5 months prior to conception.[27]

Anti-TNF agents approved for use in psoriasis contain an IgG Fc portion. This crosses the placenta in the second and third trimesters.

There is a case report of maintenance adalimumab use during pregnancy. The pregnancy was uncomplicated and surveillance sonograms revealed normal growth without visible congenital anomalies.[28]


Many drugs and immunoglobulins are excreted in human milk, and because of the potential for adverse reactions in nursing infants, women should not breastfeed their infants. Adalimumab transfers in small amounts in breastmilk.[29]

The half-life of immunoglobulins is up to several months in children, increasing the potential risk of infections, and may require delaying scheduled live-attenuated vaccinations.[30]

Pediatric patients

Adalimumab is given to children above 4 years for treating pustular psoriasis and chronic plaque psoriasis. It is used as 0.8 mg/kg up to a maximum of 40 mg at week 0 and 1 and then every 2 weeks.[31]

Surgery and biologicals

It takes five half-lives for a product to be completely eliminated from the body. The half-life of adalimumab is 14–19 days. It should be stopped 8–11 weeks before surgery.[32]

Biologicals 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.[33]

For high infection risk procedures (i.e., gastrointestinal tract surgery) washout = 5 × half-life.[33]


Live or live attenuated vaccines such as bacillus Calmette Guérin, yellow fever, nasal influenza, cholera, oral typhoid, oral polio, and measles, mumps and rubella are contraindicated <2 weeks before, during, and for 6 months after discontinuation of biologic therapy.[34] Inactivated vaccines are recommended, however these should be administered 2 weeks before starting biologic to ensure an optimum immune response. These are Influenza, meningococcal, diphtheria, pertussis, tetanus, human papillomavirus, pneumovax, and inactivated polio.[34]

  Hiv Patients Top

Etanercept is recommended but adalimumab has been used.[35]

  Biologics in Hepatitis B Virus Patients Top

In patients who are HbsAg positive, TNF-α inhibitors and ustekinumab can lead to viral reactivation, but IL-17 inhibitors appear safe if used after antiviral prophylaxis (tenofovir is preferred over lamivudine) and with close monitoring of liver function tests (LFTs) and viral titers.[35]

Patients who are Anti-Hbc positive have lesser risk of HBV reactivation than HbsAg-positive patients; TNF-α inhibitors, ustekinumab, and IL-17 inhibitors can be used with close monitoring of LFTs and viral titers.[35]

  Biologics in Hepatitis C Virus Patients Top

TNF-α inhibitors can be used with close monitoring of liver function and viral titers, and in conjunction with antiviral therapy.[35]

  Herpes Zoster Top

Varicella zoster vaccination should be given to those above 60 years before starting biologics. There is less risk with etanercept than infliximab and adalimumab.

Adalimumab efficacy in Phase 3 clinical trials

PASI 75 at week 16 was seen in 71% of patients in Phase 3 trials,[36] while in the champion trial,[37] it was 80%. PASI 90 response at week 16 was 45% in the Phase 3 trials[36] and 52% in the champion trial.[37] Physician Global Assessment (PGA) 0/1 was 62% in Phase 3 trial[36] and 73% in the champion trial.[37]

In the REVEAL trial, PASI 75 at 1 year was 79%. For patients with sustained PASI 75 responses during REVEAL trial, efficacy was well maintained over 3 years. At week 100, PASI response rates of 75%/90%/100% were seen in 83%/59%/33% of patients, respectively. In patients who took continuous therapy for 160 days, PASI response rates of 75%/90%/100% were seen in 76%/50%/31% of patients, respectively.[38]

Adalimumab was vastly superior to methotrexate; PASI 75 at week 16 with adalimumab was 79.6% in comparison to methotrexate which showed 35.5% PASI 75 response at week 16. PASI 90 response at week 16 with adalimumab was 51.9%, while with methotrexate it was 13.6%.[37]

Adalimumab efficacy in real world

Salsa study from Japan showed 56% of patients achieving PASI 75 at week 16 which improved to 65.6% at week 24. PASI 90 response was achieved by 28.4% and 43.3% of patients at weeks 16 and 24, respectively. The mean DLQI scores improved from 9.1 ± 6.2 at baseline to 3.0 ± 4.4 at week 16 and 2.4 ± 3.8 at week 24.[39]

Five-year analysis from Espirit study showed that PGA clear or minimal (PGA 0/1) was achieved by 57.0% patients at 12 months and 64.7% patients at 60 months of treatment.[40]

A 10-year study from Singapore revealed that 77.8% of the patients achieved PASI 75 at week 16. They showed significant improvement in PASI score from a mean PASI of 19.3–5.1 at 16 weeks. Their one patient had been receiving adalimumab for 7.9 years and was doing well. They also showed that two of their patients with generalized pustular psoriasis who had failed conventional therapy improved successfully with adalimumab. They did not report any worsening of psoriasis, erythrodermic flare, or development of palmoplantar pustulosis with TNF-α, adalimumab.[41]

Safety of adalimumab in real world

Adverse drug reactions (ADR) were reported by 26.1% of patients, while serious ADR (SADR) were reported by 3.3% of patients. ADR reported included pyrexia, abnormal hepatic function, nasopharyngitis, injection-site reaction, folliculitis, malaise, peripheral edema, worsening of psoriasis, and upper respiratory tract infection. SADR reported were facial cellulitis, herpes zoster, bacterial meningitis, pneumococcal pneumonia, and pulmonary TB. Frequency of ADR was significantly higher in patients with higher body mass index, a history of allergy, circulatory disorders, and hypertension. Patients who had taken corticosteroids and phototherapy also showed higher incidence of ADR. The frequency of SADR was significantly higher in patients previously treated by phototherapy and with MTX.[39]

A total of 6059 patients (58% male, mean age 47 years) were enrolled. The rate of treatment emergent (TE) melanoma was 0.8, TE Non-melanoma skin cancer (NMSC) was 0.8, 0.4, 0.6, and 0.7 E/100 Per year (PY), and the event rate of TE lymphoma was 0, 0, <0.1, and 0 E/100 PY, respectively; there were no cases of hepatosplenic T-cell lymphoma. The event rate of other TE malignancies was 1.4, 0.4, 0.2, and 0.2 E/100 PY, respectively, for patients with = 1, >1–3, >3–5, and >5 years of total exposure. The only TE malignancies reported in > 0.1% of patients overall were basal cell carcinoma (0.3 E/100 PY) and squamous cell carcinoma of the skin (0.2 E/100 PY). TE malignancies were the primary cause of seven deaths (<0.1 E/100 PY). As seen in the last 5 years, 97.9% of patients remained free of TE malignancies.[42]

Five-year analysis from ESPIRIT 10-year postmarketing surveillance registry of adalimumab did not show any new safety signals. The observed number of deaths was below expected. As-observed effectiveness remained stable through 60 months. The rate of serious TE AEs was 4.3 events/100 PY of total adalimumab exposure (E/100PY); the most common was infection (1.0 E/100PY). The rate of events leading to death regardless of causality was 0.1 E/100PY. The most common event leading to death was myocardial infarction (MI) (\0.1 E/100PY). Cardiovascular-related TE AEs of special interest included cerebrovascular accident (0.1 E/100PY), MI (0.1 E/100PY), and congestive heart failure (\0.1 E/100PY). The overall incidence rate for malignancy was 0.9 E/100PY (\0.1 E/100PY for each of melanoma and lymphoma and 0.6 E/100PY for nonmelanoma skin cancer) and 0.3 E/100PY for other malignancies. The overall incidence rate of infections was 7.7 E/100PY (\0.1 E/100PY for each of oral candidiasis, active TB, latent TB, and opportunistic infection other than oral candidiasis or TB).[40]

Upper respiratory tract infections, headache, injection-site reaction, pneumonia, transaminitis, urosepsis, pulmonary TB, latent TB, abnormal blood sugars, LFTs, and raised serum creatinine were reported by a tertiary dermatology center in Singapore over 10 years.[41]

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.

  References Top

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What is Adalimumab?
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