Guideline for

Management of
Rheumatoid Arthritis
in Adult Patient
Guideline for management of Rheumatoid Arthritis
in Adult patient
Introduction:
Rheumatoid arthritis (RA) is a chronic inflammatory disease that may result in
significant disability. It is the most common autoimmune inflammatory arthritis in
adults 1. RA has a significant negative impact on the ability to perform daily activities,
including work and household tasks, and health related quality of life, and it
increases mortality 2.3.The management of RA has seen significant advances during
the past 2 decades. Although some patients with RA experience mild illness with
minimal joint destruction, disease progression can lead to significant deformity of the
affected joints.
RA is characterized by inflammation and swelling of the synovium of the joint, with
subsequent destruction of articular structures.4 Patients with active RA also
experience systemic inflammation that is associated with a variety of comorbidities,
most importantly cardiovascular disease, which contribute to the increased morbidity
and mortality noted in this group compared with the general population.5.6

The pain, fatigue, and disability associated with RA result in a significant reduction in
health-related quality of life.7 Additionally, RA imposes a substantial economic
burden upon patients, due to both increased cost of medical care and loss or
reduction of employment, frequently during peak working years.8.9
Reason to develop this guideline:
The reason to develop this guideline due to:
• Some of the RA medications are known or suspected to cause adverse drug reactions or
have black box warning.
• High budget impact of Biologic Disease-modifying anti-rheumatic drugs and Small molecule
DMARDS Janus kinase inhibitors.
• Availability in Saudi Arabia of some RA medications, especially for biologics.
• Presence of bio-similar medications.

Methodology:
It was adopted from international guideline like: ( 2016 European League Against
Rheumatism (EULAR) , 2015 American College of Rheumatology (ACR) and BSR
and BHPR guideline on prescribing drugs in pregnancy and breastfeeding—Part I:
standard and biologic disease modifying anti-rheumatic drugs and corticosteroids),
Studies in the literature review included systematic reviews, randomized controlled
trials (RCTs) and meta-analysis ,review the available drugs in the Ministry Of Health
(MOH), expert opinion of consultant rheumatologist and consultant rheumatologist
clinical pharmacist.
Table 1: Implications of strong and conditional GRADE (Grading of
Recommendations Assessment, Development, and Evaluation) methodology
recommendations.
*=majority means >50% of the people.

Table 2: Grading of Recommendations Assessment, Development and

Evaluation (GRADE)
Code Quality of Definition
Evidence
A High
Further research is very unlikely to change our
confidence in the estimate of effect.
• Several high-quality studies with consistent
results
• In special cases: one large, high-quality multi-
center trial
B Moderate
Further research is likely to have an important impact
on our confidence in the estimate of effect and may
change the estimate.
• One high-quality study
• Several studies with some limitations
C Low
Further research is very likely to have an important
impact on our confidence in the estimate of effect
and is likely to change the estimate.
• One or more studies with severe limitations
D Very Low
Any estimate of effect is very uncertain.
• Expert opinion
• No direct research evidence
• One or more studies with very severe limitations
 Population:
Adult 18 years and elderly male and female with RA.

Epidemiology:

Incidence:
Rheumatoid arthritis is a relatively common disorder that affects men and women at
the prime of their lives. Only 30% of the causes of rheumatoid arthritis can be
attributed to genetic factors; the rest remain unexplained. Descriptive and analytic
epidemiologic methods may lead to a better understanding of the causative,
precipitating, and modulatory factors in rheumatoid arthritis.10

Prognosis:
Depending on how bad the progression of the disease is, there are some possible
complications patients may experience outside of the regular joint-related symptoms.
These complications and side effects include:

• Heart disease, Hypertension

• Eye inflammation
• Osteoporosis
• Anemia
• Depression and anxiety
• Increased risk of illness and infection
• Cancer – especially lymphoma
• Respiratory conditions caused by nodules.

Factors that Determine Rheumatoid Arthritis Prognosis:

Some of the factors that can affect the rheumatoid arthritis prognosis in
patients include:

• Seropositive (positive for rheumatoid factor or anti-CCP)

• Patient’s age at diagnosis
• How soon treatment began after symptoms appeared
• Patient’s overall health including diet, exercise, and smoking habits
• Whether or not complications have developed through the course of the disease
• Patient’s personalized treatment plan
• Response to treatment
• How active the condition has been including the frequency of flare-ups and
remission periods.11
Mortality:
Rheumatoid arthritis life expectancy is difficult to determine. As a chronic disease,
rheumatoid arthritis tends to be progressive. This means that it’s a long-term disease
in which symptoms tend to get worse over time. As of now, doctors do not know
what triggers the disease although it is likely brought on by a combination of factors
including genetics and environmental influences.
Because there isn’t one specific cause of the disease, there is also no known cure
for rheumatoid arthritis. Today’s medical technology and research, however,
provides a variety of treatment options, which can improve the prognosis.
All of these factors make it difficult to predict an exact rheumatoid arthritis life
expectancy for patients. What research has found is that it isn’t the disease itself that
reduces the life expectancy of patients. Life expectancy is shortened by the varying
complications that develop as a result of the disease.
Rheumatoid arthritis complications like respiratory and cardiovascular conditions,
can compound over time and lead to a shortened lifespan and possibly eventual
fatality.12

Disease impact and Comorbidities:

Comorbidities and extra-articular manifestations of RA

Blood vessels:
Major cutaneous vasculitis, atherogenesis, vasculitis, Raynaud’s syndrome
Bone
Osteoporosis, low bone mineral density, fractures.
Brain and nerves
Reduced cognitive function, depression, neuropathy, myelopathy, low stress tolerance
Cardiovascular system
Pericarditis, ischemic heart disease, congestive heart failure.
Nervous system
Stroke
Liver
Acute phase response, iron redistribution, altered lipid metabolism
Mouth
Secondary Sjögren’s syndrome, periodontitis
Muscle
Insulin resistance, sarcopenia
Joints
Septic arthritis
Eyes
Scleritis, retinal vasculitis, secondary Sjögren’s syndrome, kerato-conjunctivitis sicca
Lungs
Pleuritis, pulmonary fibrosis, bronchiolitis, pneumonia
Spleen
Felty’s syndrome.13
Assessment:
1- A definitive diagnosis in a patient with early rheumatoid arthritis should only be made after a
careful history taking and clinical examination, which should also guide laboratory testing and
additional procedures.
2- Early RA is defined as disease duration within 6 months.
3- Treatment target should ideally be remission. In patients with established RA or those in whom
remission can’t be achieved, an alternative target of therapy would be low disease activity.
4- Management of early Rheumatoid arthritis should aim at the best care and must be based on a
shared decision between the patient and the rheumatologist.
5- Rheumatologists are the specialists who should primarily care for patients with
Rheumatoid arthritis.
6- The main goal of DMARD treatment is to achieve clinical remission, and regular monitoring of
disease activity, adverse events and comorbidities should guide decisions on choice and
changes in treatment strategies to reach this target.
7- Treatment decisions should be based on the severity of disease activity, as measured by
quantitative method such as the DAS28 or CDAI and the prognostic factors associated with poor
outcomes.
8- Functional status assessment using a standardized, validated measure should be performed
routinely for RA patients, at least once per year, but more frequently if disease is active.
Examples of commonly used functional status measures include Health, Assessment
Questionnaire, Health Assessment Questionnaire II, Multidimensional Health Assessment
Questionnaire, PROMIS)
9- Monitoring of disease activity should include tender and swollen joint counts, patient and
physician global assessments, ESR and CRP, usually by applying a composite measure.
10- Arthritis activity should be assessed at 1-month to 3-month intervals until the treatment target
(Remission or low disease activity) has been reached.
11- Radiographic and patient-reported outcome measures, such as functional assessments, can be
used to complement disease activity monitoring.
12- A treatment recommendation favoring one medication over another means that the preferred
medication would be the recommended first option. However, favoring one medication over the
other does not imply that the no favored medication is contraindicated for use in that situation; it
may still be a potential option under certain conditions.
13- Among the DMARDs, methotrexate is considered to be the anchor drug and, unless
contraindicated, should be part of the first treatment strategy. (LOE low)
14- NSAIDs are effective symptomatic therapies but should be used at the minimum effective dose
for the shortest time possible, after evaluation of gastrointestinal, renal and cardiovascular risks.
15- Systemic glucocorticoids reduce pain, swelling and structural progression, but in view of their
cumulative side effects, they should be used at the lowest dose necessary as temporary (<6
months) adjunctive treatment. Intra-articular glucocorticoid injections should be considered for
the relief of local symptoms of inflammation. (LOE very low)
16- Consider adding low-dose glucocorticoids (10 mg/day of prednisone or equivalent) in patients
with moderate or high RA disease activity when starting disease-modifying antirheumatic drugs
(DMARDs) and in patients with DMARD failure or biologic failure.

Approach to management of RA:

Medications for RA typically fall into five categories:
• Conventional Synthetic Disease-modifying anti-rheumatic drugs (csDMARDS).
• Biologic Disease-modifying anti-rheumatic drugs.
• Small molecule DMARDS (sDMARDs) Janus kinase (JAK) inhibitors.
• Glucocorticoids.
• Non-steroidal anti-inflammatory drugs (NSAIDs).
Mechanism of Action and adverse effects:
• Disease-Modifying Anti-Rheumatic Drugs (DMARDs):
Various drugs of different categories are used as DMARDs such as methotrexate,
sulfasalazine, hydroxychloroquine and Leflunomide. Most of the DMARDs are
immunosuppressant drugs which are reported to retard joint degeneration in about
two third of patients14 . The use of MTX should be considered as anchor therapy in
patients with rheumatoid arthritis, and should be started within the first three months
of diagnosis. Each DMARDs acts by different mechanism. Methotrexate is the core
therapy for management of RA. Sulfasalazine acts by scavenging toxic oxygen
metabolites produced by neutrophils as well as by inhibiting translocation of NF-kB
resulting into inhibition of transcription of various chemokines 15. Leflunomide has a
relatively specific inhibitory effect on activated T cells. Leflunomide retards
proliferation of activated T cells in addition to inhibiting adhesion and migration of
inflammatory cells. Leflunomide give rise to a metabolite that inhibits de
novopyrimidine synthesis by inhibiting dihydroorotic acid dehydrogenase.
Leflunomide has been reported to have clinical improvement in arthritic patients16 .
Drug Regular Dose 17 Adverse drug reaction 18,19
Methotrexate 7.5–15 mg every • Nausea; vomiting and diarrhea
week • Hepatotoxicity
at doses exceeding • Alopecia
20 mg/wk the • New-onset cough or shortness
incidence and of breath
severity of toxic • Photosensitivity
reactions are • Myelosuppression.
increased

Hydroxychloroquine 5mg/kg/day • Nausea; diarrhea

• Headache
max.
• Vision changes (retinal damage)
400 mg/day • Skin pigmentation
Sulfasalazine 500–1000 mg twice • Nausea; diarrhea
daily • Headache
• Rash, yellow-orange
discoloration
• Photosensitivity
• Myelosuppression
Leflunomide 10–20 mg/day • Nausea; diarrhea and
Maximum : 20 abdominal pain
mg/day • Hepatotoxicity
• hypertension, headache
• Alopecia and rash
Biological Agents:
1. Tumor necrosis factor inhibitors (TNF-Inhibitors)
Drug Regular Dose18 Adverse drug reaction 19.20
Etanercept 50 mg subQ once • Central nervous system:
weekly Headache
• Dermatologic: Skin rash
• Gastrointestinal: Abdominal pain
, diarrhea and vomiting
• Infection: Infection
• Local: Injection site reaction:
bleeding, bruising, erythema,
itching, pain, or swelling.
• Respiratory: Upper respiratory
tract infection ,rhinitis
• Miscellaneous: Antibody
development, positive ANA titer
Adalimumab 40 mg subQ every • Central nervous system:
other week; Headache
May increase to 40 • Dermatologic: Skin rash
mg subQ every • Immunologic: Antibody
week in patients not development
receiving • Local: Injection site reaction
concomitant • Neuromuscular & skeletal:
methotrexate Increased creatine
phosphokinase
• Respiratory: Upper respiratory
tract infection and sinusitis
Infliximab 3 mg/kg IV at 0, 2, • Central nervous system:
and Headache
6 wk; then every 8 • Gastrointestinal: Abdominal pain
wk and nausea
thereafter • Hepatic: Increased serum ALT
• Immunologic: Increased ANA
titer, antibody development (anti-
infliximab)
• Infection
• Respiratory: Upper respiratory
tract infection, sinusitis, cough,
pharyngitis
• Miscellaneous: Infusion related
reaction
Certolizumab 400 mg subQ at 0, • Gastrointestinal: Nausea
2, and • Immunologic: Antibody
4 wk; then 200 mg development
every • Infection
other week or 400 • Respiratory: Upper respiratory
mg every 4 weeks tract infection

2. Interleukin-6 inhibitors:
Drug Regular Dose17 Adverse drug reaction 18,19
Tocilizumab IV infusion 4 • Endocrine & metabolic: Increased
mg/kg over 1 hour serum cholesterol (>240 mg/dL;
every 4 weeks; >1.5-2 x ULN; combination therapy)
• Hepatic: Increased serum ALT and
increase to 8
increased serum AST
mg/kg every 4 • Miscellaneous: Infusion-related
weeks based on reaction.
clinical response;
doses exceeding
800 mg per
infusion are not
recommended

SubQ dosing
(Weight less than
100 kg): 162 mg
subQ every other
week; increase to
162 mg SUBQ
every week based
on clinical
response
(Weight 100 kg or
greater) 162 mg
subQ every week
Switching from IV
to subQ, give the
first subQ dose
instead of the next
scheduled IV
dose
 3. Selective T-Cell Costimulation Blocker
Drug Regular Dose 17 Adverse drug reaction 18,19
Abatacept IV infusion: Weight • Central nervous system:
based dose every Headache
2 wk for two doses • Gastrointestinal: Nausea
and then monthly • Respiratory: Nasopharyngitis,
(i.e., 750 mg for upper respiratory tract infection
those weighing 60– • Miscellaneous: Infection,
100 kg) antibody development.
SubQ dosing with
IV loading dose:
Give weight-based
IV loading dose,
then 125 mg subQ
within 1 day of
loading dose,
followed by 125 mg
subQ once weekly
SubQ dosing
without IV loading
dose: 125 mg subQ
weekly
Transitioning from
IV to subQ therapy:
125 mg subQ in
place of next
scheduled IV dose,
followed by 125 mg
subQ once weekly

4. Anti-CD20 Monoclonal Antibody

Drug Regular Dose 17 Adverse drug reaction 18,19
Rituximab 1000 mg IV followed • Cardiovascular: Peripheral
by a second 1000- edema, hypertension
mg IV dose 2 weeks • Central nervous system: Fever,
later in combination fatigue, chills, headache,
with methotrexate insomnia, pain
every 24 weeks or • Dermatologic: Rash, pruritus,
based on clinical angioedema
evaluation;
 • Gastrointestinal: Nausea,
diarrhea, abdominal pain, weight
gain.
• Hematologic: Cytopenias
,lymphopenia, anemia ,
leukopenia, neutropenia
,neutropenic fever ,
thrombocytopenia
• Hepatic: ALT increased
• Neuromuscular & skeletal:
Neuropathy, weakness, muscle
spasm, arthralgia
• Respiratory: Cough , rhinitis,
epistaxis
• Miscellaneous: Infusion-related
reactions, human antichimeric
antibody (HACA) positive , night
sweats

• Small molecule DMARDS (sDMARDs) Janus kinase (JAK) inhibitors.

Drug Regular Dose 17 Adverse drug reaction 18,19
Tofacitinib 5 mg orally twice • Cardiovascular: Hypertension,
daily peripheral edema
• Central nervous system:
Headache, fatigue, insomnia,
paresthesia
• Dermatologic: Erythema, pruritus,
skin rash
• Endocrine & metabolic:
Dehydration
• Gastrointestinal: Diarrhea,
abdominal pain, diverticulitis,
dyspepsia, gastritis, nausea,
vomiting.
• Genitourinary: Urinary tract
infection
• Hematologic & oncologic:
Anemia, skin carcinoma
• Hepatic: Increased serum ALT ,
liver steatosis
• Infection
• Neuromuscular & skeletal:
Arthralgia, joint swelling,
musculoskeletal pain, tendonitis
 • Renal: Increased serum
creatinine
• Respiratory: Upper respiratory
tract infection, nasopharyngitis,
cough, dyspnea, sinus
congestion
• Miscellaneous: Fever

• Glucocorticoids:
Steroids have been widely used for suppressing pain and inflammation in arthritis
since many years. Corticosteroids acts by inhibiting induction of COX enzyme.
Moreover, corticosteroids also inhibits release of collagenase and lysosomal enzyme
by reducing macrophage phagocytosis and IL-1 secretion. 20
Glucocorticoids are generally better avoided on the long-run because of adverse
effects which include :
- CNS: Headache and steroid psychosis.
- Cardiovascular: hypertension.
- Skin: easy bruising, poor wound healing, skin atrophy and acne.
- Endocrine: Cushing’s syndrome, osteoporosis, diabetes, hirsutism, hypokalemia
and weight gain.
- Musculoskeletal: steroid myopathy and avascular necrosis.
- Eye: cataract and glaucoma.21

• Non-Steroidal Anti-Inflammatory Drugs (NSAIDs):

NSAIDs are pain relieving agents. They offer little protection against tissue
degeneration. NSAIDs like Ibuprofen, Diclofenac or others act non-selectively by
inhibiting both Cyclooxygenase enzymes (COX 1 and COX 2) which are responsible
for synthesis of protanoids from its precursor Arachidonic acid. COX 1 enzyme is
constitutively present in cells whereas COX 2 is inducible form and is generated at
sites of inflammation. It is reported that NSAIDs provides pain relief by reducing
prostaglandin, bradykinins and oxygen radicals.22

Initial Therapy
1-In patients with newly diagnosed early Rheumatoid Arthritis (Figure 1), start
treatment with a single csDMARD, preferably methotrexate (start with oral 7.5–15
mg/week and increase the dose to 20 mg/week for maximum response if needed.
Use subcutaneous Methotrexate, if patient had gastric intolerance to oral MTX. (LOE
low)
2-In patients with contraindication or intolerance to methotrexate, we consider
alternatives such as sulphasalazine. (LOE low)
3-As we expect DMARDs to take a few weeks to produce a therapeutic effect, we
might bridge the patients with a tapering course of corticosteroids and NSAIDs to
control the pain and inflammation.
4-In patients with moderate to high disease activity, we might consider initiating
treatment with combination DMARDs from the beginning.
5-A minimal period of 3 months is given before a major change to therapy is made.
6-Treatment target should be achieved within 6 months.

Inadequate or no response:
1-If there’s no improvement by 3 months after the initial therapy or the treatment
target wasn’t reached by 6 months we alter the therapy (Figure1)
2-In the absence of poor prognostic factors, we add a second csDMARD if we
initially started with a single agent.
3-In the presence of poor prognostic factors or in those who started initially with a
combination csDMARDs, we add a biologic DMARD or JAK inhibitor. (LOE
moderate to very low). As we have no preference to any of the biologics, the choice
will largely depend on the patient’s condition, cost ,preference and comorbidities.

Failure of biologic DMARD:

1-The general idea for primary failure of the first biologic is to switch to another
biologic with a different mechanism of action. (LOE low to very low).
2-If a patient has failed a TNFi, we switch to a NON-TNFi or JAK inhibitor. (LOE low
to very low).
3- If a patient fails a NON-TNFi, we switch to another NON-TNFi with a different
mechanism of action or a TNFi or JAK inhibitor. (LOE low to very low).

4-If a patient fails multiple biologic DMARDs, switch to JAK inhibitor, like tofacitinib,
is considered. (LOE low to very low).

Recommendations:
1.Patients presenting arthritis should be referred to, and seen by, rheumatologist,
within 6 weeks after the onset of symptoms.
2.Among the DMARDS, methotrexate is considered to be the (anchor drug) and,
unless contraindicated, should be part of the first treatment strategy.
3.Arthritis activity should be assessed at 1-month to 3-months intervals until the
treatment target has been reached.

b DMARDs Privileges of consultant Rheumatologist

Jak-I Privileges of consultant Rheumatologist
 Clinical Diagnosis of
RA

 Start methotrexate (and/or other Conventional synthetic

DMARD)
 Combination with short-term glucocorticoids.

Achieve improvement
Yes
No at 3 months and target
at 6 months

Poor
prognostic
factors Continue

Add biological DMARDs *

1-Etanercept Consider Dose
2-Adalimumab reduction in sustained
- Certolizumab (In Pregnant remission
Woman)
After failure of other biologics:
- Certolizumab
- Tocilizmab
- Abatacept
- Rituximab
- JAK-I: Tofacitinib Achieve improvement
at 3 months and target
No at 6 months Yes

Change biological
DMARDs or use a
Jak-I Continue

Figure 1:
➔ Conventional synthetic DMARDs (cs DMARDs) e.g. methotrexate, 24
leflunomida, SSZ, HCQ
Monitoring of rheumatoid arthritis:Monitoring:
➔ Targeted synthetic DMARDs (ts DMARDs) e.g. Tofacitinib
*Based on logistic issues (MOH)
* We have no preference to any of the biologics; the choice will be largely dependent on the patient's
condition, preference and comorbidities.
The following table shows the recommendations for monitoring CBC, LFT and renal
function for patients on csDMARDs therapy.
Agent < 3 months 3 – 6 months > 6 months
Leflunomide 2 – 4 weeks 8 – 12 weeks 12 weeks
Methotrexate 2 – 4 weeks 8 – 12 weeks 12 weeks
Sulfasalazine 2 – 4 weeks 8 – 12 weeks 12 weeks

Recommendations for TB screening in patients receiving biologics

or tofacitinib23

Screening for latent tuberculosis:

Screening for latent tuberculosis (TB) is mandatory for every patient
before starting a biologic DMARD. Kindly follow Pathway 1 for
screening.
Biologic therapy can be started immediately if screening was negative,
after 1 month of therapy for latent TB or after completion of course of
therapy for active TB.

PPD or IGRA
test

Negative Positive
No Latent TB Chest X ray

Start Biologic Negative Positive

Treat for Latent TB Work up for active TB

Sputum
AFB culture and smear

Positive Negative
Treat active TB Treat Latent TB
Use of biologics and DMARDs in high-risk populations:23.24.25,26
Risk factor Recommendations
Congestive Heart Failure -Use combination DMARDs or NON-
TNFi biologics (Abatacept, Rituximab,
Tocilizumab, Tofacitinib) are preferred
over TNFi in heart failure. ( LOE
moderate to very low).
-Use of TNFi should be avoided
because of the risk of worsening heart
failure.
-Choice of therapy according to patients'
co-morbidities, contraindications, cost &
convenience
Hepatitis B -Patients infected with Hepatitis B Virus
can receive immunosuppression after
receiving prophylactic antiviral therapy
for Hepatitis B.
-Same recommendations as in patients
without this condition (LOE very low)
-Choice of therapy according to
patients' co-morbidities,
contraindications, cost & convenience
Hepatitis C -Patients receiving treatment for
Hepatitis C virus infection can receive
the same treatment as in patients
without this condition. (LOE very low)
-In patients with Hepatitis C infection
that are not receiving antiviral therapy,
use of csDMARDs is preferred over
TNFi (LOE very low)
-Choice of therapy according to
patients' co-morbidities,
contraindications, cost & convenience
Previously treated or untreated Skin -csDMARDs are preferred over
Cancer biologics and tofacitinib. (LOE very
low)
-Choice of therapy according to
patients' co-morbidities,
contraindications, cost & convenience

Previously treated -Rituximab is the preferred biologic in

Lymphoproliferative Disorder these patients. (LOE very low)
-Choice of therapy according to
patients' co-morbidities,
contraindications, cost & convenience
Previously treated solid organ -Same recommendation as in patients
malignancy without this condition. (LOE very low)
-Choice of therapy according to
patients' co-morbidities,
contraindications, cost & convenience
Previous serious infections -Use combination DMARDs over TNFi
Abatacept is the preferred biologic for
these patients. (LOE very low)
-Choice of therapy according to
patients' co-morbidities,
contraindications, cost & convenience
Pregnancy The safest medication are:
Hydroxychloroquine, sulfasalazine
and among biological therapy is
certolizumab.
- Certolizumab pegol is compatible with
all three trimesters of pregnancy and
has reduced placental transfer
compared with other TNF inhibitors.
-Infliximab may be continued until 16
weeks and etanercept and
adalimumab may be continued until
the end of the second trimester.
- To ensure low/no levels of drug in
cord blood at delivery, etanercept and
adalimumab should be avoided in the
third trimester and infliximab stopped at
16 weeks. If these drugs are continued
later in pregnancy to treat active
disease, then live vaccines should be
avoided in the infant until 7 months of
age.
Lactation -Certolizumab preferred option since there
is minimal transfer into breastmilk.
-Women should not be discouraged
from breastfeeding on TNFis
(Infliximab, etanercept , adalimumab
and Certolizumab.
Vaccinations:23
Herpes zoster vaccine is recommended for Rheumatoid Arthritis
patients that are above 50 years of age before starting biologic therapy.
However, once already on a biologic this vaccine is contraindicated
because it’s a live vaccine.
All killed vaccines are recommended for Rheumatoid Arthritis patients.
Preferably they should be given before methotrexate or Rituximab
therapy, because they can blunt the immune response. These vaccines
include pneumococcal vaccine, annual flu vaccine and hepatitis B
vaccine.

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