Abdulaziz Abuhaimed

2140008317
Abdulaziz Almulhim
2140009432
Faris Alarfaj
Abdulmajeed Hasen
2140007969
Abdulilah Almulhim
Group 15
2140007071

2140008250

Table of Contents
Topic Summary........................................................................................................... ii
Theme and Topic correlation...................................................................................... iv
Introduction................................................................................................................ 1
Epidemiology.............................................................................................................. 2
Etiology and Pathogenesis.......................................................................................... 3
Pathophysiology of SLE............................................................................................... 5
SLE Signs and symptoms............................................................................................ 6
Generalized symptoms:........................................................................................... 6
Specific symptoms:................................................................................................. 6
Differential diagnosis.................................................................................................. 8
Diagnosis of SLE......................................................................................................... 9
SLE interaction with other conditions.......................................................................10
Pregnancy and lupus............................................................................................. 10
Antiphospholipid syndrome and lupus...................................................................10
Coronary artery disease and lupus........................................................................11
Infections and Immunosuppression.......................................................................11
Treatment: A multidisciplinary approach..................................................................12
1) Drugs:............................................................................................................... 12
2) Monitoring......................................................................................................... 14
3) Monitoring for Potential Risks developed by SLE Patients:................................14
4) Potential Future Therapies:............................................................................... 15
Prognosis:................................................................................................................. 15
Ethical and legal aspects:......................................................................................... 16
Impact of systemic lupus erythematosus on quality of life.......................................17
References................................................................................................................ 19
Annotated Bibliography............................................................................................ 22

Topic Summary

(SLE) is an autoimmune disease in which organs tissues, and cells

undergo damage mediated mistakenly by tissue-binding autoantibodies

and immune complexes, which can affect every aspect of life.

The prevalence of systemic lupus Erythematosus was estimated to be
19.28 per 100,000 population in Saudi Arabia, in comparison to 20 to 150

cases per 100,000 globally.

SLE occurs due to changes in the immune system leading to production of
autoantibodies. Furthermore, SLE is a multifactorial disease having both
genetic and environmental factors and is greatly associated with the X

chromosome. SLE affects more females than males (9:1).

There is around 45 predisposing genes that have been identified to be
associated with SLE (accounting only for 18% of disease susceptibility);
which suggests that exposures and epigenetics play a major role in the

disease.
SLE inflicts damage on the body through complement activation, direct
cell lysis, and causing functional imbalance affecting normal homeostatic

processes such as blood coagulation.

Clinical manifestations of SLE can vary immensely from person to person.
It can affect many systems including the dermatological, musculoskeletal,
ophthalmological, hematological, neurological, renal, gastrointestinal,

pulmonary, and cardiovascular systems.

To achieve proper diagnosis of SLE, drug induced lupus Erythematosus
must be excluded. In addition to that, there are other differentials for SLE
that should be excluded before establishing a diagnosis of SLE.
2

A proper diagnosis of SLE is established either through a biopsy confirmed

lupus nephritis or by fulfilling 4 of the 11 American College of

Rheumatology criteria in Lupus diagnosis.

Systemic Lupus Erythematosus causes complications in patients with
other underlying conditions due to its wide spectrum of manifestations.
Examples

of

these

interactions

include:

Pregnancy

and

lupus,

Antiphospholipid syndrome and lupus, Coronary artery disease and lupus.

SLE Treatment depends on non-specific immunosuppression. Main drugs
are

hydroxychloroquine,

Corticosteroids

and

Cyclophosphamide.

Furthermore, frequent clinical monitoring is essential, regarding CBC and

platelet count, Creatinine determination and urinalysis.

Uncontrolled flares inevitably leads to organ damage, most commonly in

joints and kidneys due to a spike in antibody levels.

Systemic Lupus Erythematosus has a significant and diverse impact on
the patient quality of life. The decrease in the quality of life has been
attributed to both the disease itself, and secondary complications due to
treatment. Psychological and physical improvement has been noted to

improve the overall quality of life for these patients.

Pregnancy in SLE poses a critical ethical conundrum due its possible
complications and requirement for termination of the fetus.

Theme and Topic correlation.

Topic

Introduction and
Definition of
Systemic Lupus
Erythematosus
(SLE).
Epidemiology of SLE
Etiology and
Pathogenesis of SLE
Pathophysiology of
SLE
Clinical Features and
presentation
Differential
Diagnosis
Diagnosis of SLE
Interaction of SLE
with other diseases
Treatment and
management of SLE
Prognosis of SLE
Ethical and legal
aspects of SLE
Impact of SLE on
quality of life

Theme 1
Personal
and
Professiona
l
Developme
nt

Theme 2
Population,
Society,
Health and
Disease

Theme 3
Foundation
of Medicine

Theme 4
Clinical
Skills

X
X

X
X

X
X

Introduction
Systemic lupus erythematous (SLE) is defined as an autoimmune
disease in which organs, tissues, and cells undergo damage mediated
mistakenly by autoantibodies and immune complexes. It is a chronic
inflammatory disease that has severe manifestations and follows a relapsing
and remitting course. It is characterized by an autoantibody response to
nuclear and cytoplasmic antigens, so immune system lose the ability to
differentiate between foreign cells and its own cells and tissues. SLE can
affect any organ system, but it mainly involves the skin, joints, kidneys,
blood cells, and nervous system, building antibodies in the tissue causing
inflammation, injury to the tissue and pain.

(26)

SLE can affect every aspect of life including physical, psychological,

and social functioning, and its impact can range anywhere from mild to lifethreatening. Although the cause of SLE is not yet fully elucidated, various
genes make individuals susceptible to the disease. The course of the disease
is unpredictable and can be triggered by environmental factors, such as
ultraviolet light and some drugs.
As

autoantibody

multisystem
production

autoimmune
and

disease

it

complement-fixation

is

associated
immune

with

complex

deposition. The immune system attack triggers an inflammatory process,

resulting in tissue damage. SLE is the pro-type of an autoimmune disease

that can cause a wide spectrum of symptoms and complications.

(12)

Epidemiology
The prevalence of SLE is between 500,000 to 1.5 in million Americans.
Where 80% of patients are female and 80-90% of lupus patient are between
15-45 years of age. Lupus affects more African Americans, Asian Americans,
Hispanics, and Native Americans than Caucasians.
The overall prevalence of SLE in the continental United States and
Hawaii has been reported to range between 14.6 and 122 cases per 100.000
persons. The incidence has tripled in the last 40 years, mainly due to
improved diagnosis of mild disease. Studies have varied over time and place
and used different methods of case ascertainment.
Applying prevalence rates to 2002 US, we estimate that at least
153.000 persons in the United States between the age of 15 and 64 years
have definite SLE. 11,000 white men, 78,000 white women, 7000 African
American men, 51,000 African American women, 1,000 men of other race
and 5,000 women in the other race.

(14)

A study conducted in Saudi Arabia in Jeddah city with 93 patients

treated

with

SLE

at

the

university

hospital.

Frequencies

of

clinical

manifestation, cases of admission and causes of death were analyzed. The

study population consisted of 84 female (90.3%) and 9 male (9.7%) patients

(ratio 10:1). Fifty-six percent of the patients were Saudi nationals; 69 patients
(74%) of Arabic descent, seven (8%) Africans, seven (8%) Southeast Asians
and nine (10%) originated from the Indian subcontinent. Mean age at time of
diagnosis was 24 10 years (range 755 yrs); 22% of the patients were
diagnosed as having SLE at an age older than30 years.

(15)

Another study established to determine the prevalence of SLE in AlQasem region of the Kingdom of Saudi Arabia, conducted in three phases to
determine the prevalence of systemic lupus erythematosus in the region. Of
the 10,372 studied, 2 cases of systemic lupus erythematosus were identified
using the criteria set for the diagnosis of systemic lupus erythematosus by
the American College of Rheumatology. Based on that, the prevalence of
systemic lupus erythematosus was estimated to be 19.28 per 100,000
population in the region. Conclusion was that The estimated prevalence of
systemic lupus erythematosus in Al-Qasem area is similar to that found in
western countries.

(3)

Etiology and Pathogenesis

Abnormal immunological responses can occur due to interactions
between susceptibility genes and environmental factors. Responses may
include:1-activation of innate immunity, 2-abnormal activation pathways in
3

the adaptive immune system (T and B lymphocytes).3-switching off the

effect of regulatory CD4 and myeloid derived suppressor cells,4- reduction in
the clearance of apoptotic cells and immune complexes, causing selfantigens to be recognized by the immune system in the surface of apoptotic
cells, therefore leading to creation of autoantibodies which allows SLE to
develop. Immune cell activation is accompanied by an increase in the
secretion of: proinflammatory interferons (type 1 and type 2), interleukin17,
and tumor necrosis factor A. Decrease in production of some cytokines (IL-2
and TGF-B) which normally induce sustained regulatory function of CD4, can
also contribute to the pathogenesis of SLE.(18)
SLE is a multi-genic disease, single gene defects (rare) confer high
hazard ratios, these include mutation in TREX1 gene on the X chromosome.
In most of the susceptible individuals multiple genes are affected and each
one contributed in a small degree to the abnormal immune/inflammatory
response; if there was enough predisposing gene variation SLE may result.
There are around 45 predisposing genes that have been identified (Multiple
of them can be found in the major histocompatibility complex) accounting
only for 18% of disease susceptibility; suggesting that exposures and
epigenetics play a major role in the disease. Some polymorphisms on genes
such as STAT4 contribute to multiple autoimmune disease and are associated
with severe forms of these diseases. (23)(19)

Female sex is permissive to SLE due to: 1-hormone effects; therefore,

estrogen contraceptive pills and hormone replacement therapy increase
chancers of lupus by 2 folds. 2-genes on X chromosome such as TREX1 play
a role in the increased predisposition in females because some genes on the
second X are not silent and remain active, this also explains why males with
XXY karyotype have increased risk of SLE.3-epigenetic differences between
them and the male sex. It was also observed that females of many
mammalian species make higher antibody response than males. (18)(23)
Exposure to UV light also causes flares of lupus by increasing apoptosis
and DNA alterations. some infections such as Epstein barr virus can trigger
SLE in susceptible individuals because it contains amino acids sequences
that are similar to the sequences of the human spliceosomes which gets
recognized by autoantibodies in SLE patients. (18)

Pathophysiology of SLE
SLE induces damage on the bodys cells through immune complexes
precipitating in tissues causing damage interacting with the complement
system. In SLE, autoantibodies either bind to circulating auto-antigens (Type
III hypersensitivity) or bind to antigens deposited in a specific organ (e.g.
DNA attached to the glomerular basement membrane). These processes may
occur in Lupus nephritis, vasculitis, neuritis, and other SLE manifestations.

(11)

Another mechanism is direct cell lysis by autoantibodies or by

phagocyte mediated removal of cells (type II hypersensitivity), this explains
5

the hemolytic anemia, leucopenia, and thrombocytopenia manifesting In SLE.

(7)

Moreover, serum antibodies in SLE can cause functional impairments

that can explain some symptoms. An example would be coagulopathies in
SLE, anti-phospholipid antibodies can precipitate in phospholipid-dependent
coagulation, natural anticoagulation, or both leading to phenotypic Protein C
activation defect causing increased thrombogenesis.

(7)

Another way SLE causes tissue damage is through antibodies

penetrating cells causing them to be dysfunctional. An example would be
anti-DNA antibodies penetrating cells causing them to die through apoptosis,
this will lead to more nucleosomes being exposed ultimately resulting in
more production of anti-DNA antibodies. A different example is antiribosomal P proteins antibodies directly enter hepatocytes causing them to
dysfunction which can explain the association of liver disease with SLE.

(7)(18)

SLE Signs and symptoms

Systemic Lupus Erythematous has wide range of signs and symptoms
ranging from musculoskeletal to cardiovascular. SLE symptoms are often
divided to generalized symptoms and specific symptoms.

Generalized symptoms:
Fatigue is the most common complaint in
SLE patients. It can be caused by the disease or by
other issues such as lifestyle factors (diet, sleep,
exercise, smokingetc.), depression, medication
use, or anemia.

(19)

Change in weight is common among Lupus

Table 1 different presentations of SLE (7)

patients. Some patients lose weight due to loss of

appetite, side effects of medications, or GI disease. Other patients gain

weight either by increased appetite due to Glucocorticoid use or by salt and
water retention due to Lupus attacking the kidneys.

(7)(18)

Fever is present in most SLE patients, it is usually responsive to nonsteroidal anti-inflammatory drugs.

(19)

Specific symptoms:
Joint pain and stiffness (sometimes arthritis) is usually the first specific
symptom in patients with SLE. It moves around the bodys joints (fingers,
wrist, kneeetc.).

(11)(25)

Skin manifestations is common in SLE patients. The butterfly rash is

the

most

common

skin

abnormality.

Most

patients

experience

photosensitivity. Other skin issues are discoid lesions and Raynauds

syndrome.

(7)(19)

SLE can cause Glomerulonephritis which can develop in nephrotic

syndrome (proteinuria, edema, and hypoalbuminia) ultimately leading to
renal failure if left untreated.

(11)

GI symptoms are usually due to SLE medications. However, SLE can

affect the pancreas, peritoneum, or large intestine causing nausea, vomiting,
diarrhea, and abdominal pain.

(7)(19)

The pulmonary system can be effected by SLE in a variety of ways.

Pleurisy and shortness of breath are the most common symptoms with
multiple possible causes including pleural effusion, pneumonitis, & interstitial
lung disease. (11)
Cardiovascular

manifestation

are

chest

pain

(pericarditis)

and

shortness of breath (heart valve disease). SLE also increase the risk of
Coronary artery disease.

(11)(18)

Patients with SLE can present with hemolytic anemia, leucopenia,

lymphocytopenia,

and

thrombocytopenia.

Idiopathic

thrombocytopenic

purpura (ITP) can appear years before other symptoms surface. Some
patients present with Anti-phospholipid syndrome.

(7)(18)

Inflammation of the retinal artery (retinal vasculitis) is not uncommon

in SLE patients. It presents as cotton wool spots. Sjgrens syndrome has
been associated with SLE. It affects the mucous membranes and exocrine
glands in the eyes and mouth.

(7)(19)

The nervous system is also affected by SLE (or SLE medication). It

usually causes seizure and psychosis. Many syndromes have been associated
with SLE including anxiety disorder, aseptic meningitis, cerebrovascular
disease, autonomic dysfunction, mood disorders, movement disorders
(chorea), and myasthenia gravis.(7)(18)

Differential diagnosis
Before diagnosing a patient with SLE, doctors must rule out other
possible causes. Several drugs have been linked with lupus-like symptoms
causing drug induced lupus erythematosus. Isoniazid, procainamide, and
hydralazine have been studied extensively. Patients who take these
medications have positive antinuclear antibody results and other positive
serological findings. Clinical manifestations are rare in such cases. Drug
induced lupus differs from SLE by the following features:

(5)(19)

Prevalence is nearly equal in both sexes.

Nephritis and CNS features arent common

Histone antibodies are usually found.

Antibodies to native DNA arent present.

Resolution of symptoms and lab results to normal follow

discontinuation of the drugs.(5)

Other problems that should be considered in the differential

diagnosis:

Acute Pericarditis

Antiphospholipid Syndrome

Autoimmune Hepatobilliary Disease

B-Cell Lymphoma

Fibromyalgia

Hepatitis C

Infectious Mononucleosis

Infective Endocarditis

Lyme Disease

Mixed Connective-Tissue Disease

Polymyositis

Rheumatoid Arthritis

Scleroderma

Sjogren Syndrome
10

Undifferentiated Connective-Tissue Disease

(5)

Diagnosis of SLE
According to the Systemic Lupus International Collaborating Clinics
(SLICC), SLE is diagnosed either by lupus nephritis with ANAs or anti-ds
antibodies proven by a biopsy, or by filling 4 out of 11 of the ACR (American
College of Rheumatology) criteria:

(11)

Table 2; ACR

SLE interaction with other conditions

Because of the wide array of symptoms that systemic lupus
erythematosus displays, it is logical to expect the disease to cause
complications in patients with other underlying conditions. As a result of the
interaction between SLE and underlying conditions, these patients will
require special or additional treatment. Examples of these interactions

11

include: Pregnancy and lupus, Antiphospholipid syndrome and lupus,

Coronary artery disease and lupus.

(18)

Pregnancy and lupus

Although lupus does not affect fertility in men and women, it does
increase fetal loss by 2-3 folds. the increase in fetal loss has been noted
especially in cases with high disease activity, nephritis, and/or production of
antiphospholipids antibodies. To control this interaction, the mother is usually
given Prednisolone due to the fact that it can be deactivated by 11-beta
dehydrogenase-2 in the placenta.

(6)(18)

Detection of antiphospholipid antibodies more than twice indicates

possible

hemodynamic

complications.

As

such,

in

patients

with

aforementioned type of interaction, heparin in its low molecular weight form

is given to control the coagulation, in addition to aspirin. Continuous
monitoring of fetal heart rate is essential to allow for prompt intervention.

(18)

Antiphospholipid syndrome and lupus

APS is an autoimmune syndrome that increases the blood coagulability
by producing antiphospholipid and other pro-inflammatory antibodies. APS
can be primary in patients with HLA-DR7 genetic marker, or secondary to
SLE. Primary APS rarely develops into SLE, this condition is suspected in
patients with repeated fetal losses, or increased blood clotting. Moreover, it
can be tested by finding two positive antiphospholipid antibodies tests.

12

Control of coagulation is essential for these patients, and an INR of 3.0 must
be maintained to prevent complications.

(18)

Coronary artery disease and lupus

Patients of SLE have an increased prevalence of cardiovascular
disease, ranging from double the relative risk to 55 fold risk increase in
young women. Although the pathogenesis is not fully explained, it has been
noted that the risk factors for atherosclerosis such as hyperlipidemia and
hypertension are common in patients of SLE. These conditions are either
attributed directly to the disease, or secondary due to glucocorticoids
therapy. The combination of Inflammation, vascular injury, and immune cell
activation allow for plaque formation and atherosclerosis. Control of cardiac
risk factors with appropriate assessment and application of prevention
methods can help to protect SLE patients from coronary artery disease.

(17)(21)

(22)

Infections and Immunosuppression

Immune suppression, either primary from SLE, or secondary from the
treatment, provide an environment for tuberculosis infection. As such, the
incidence of TB in SLE patients increases by 40 folds according to a study. It
has also been noted that the severity of the infection is increased, this is
shown with the higher percentage expressing extra-pulmonary infection.
Furthermore, SLE patients that develop TB have a higher incidence of

13

arthritis and renal disease, this reflects a more aggressive presentation of

the disease and requires appropriate therapeutic approach.

(2)(13)

In general, Infections by microbes have an important role in initiation

and exacerbation of SLE. This is achieved by multiple ways in which the
microbes trigger immunity and bypass tolerance. First method is association
of the microbial antigen with self-antigen. As a result, the body mounts an
immune reaction against both the bacterial antigen and the self-antigen.
Second method is the broad spectrum of bacterial and viral products which
might active nonselective polyclonal B-cells and produce non-selective
antibodies as a result. Third method of bypassing tolerance is through
mimicry, where the microbe antigen resembles a protein found normally in
the body. These include just some examples on how infections, and their
associated microbes can both initiate and complicate SLE and its associated
autoimmunity.

(2)

Treatment: A multidisciplinary approach

SLE treatment is dependent on non-specific immunosuppression. SLE
management is various, especially in its mild form. Referring suspected SLE
patients to Rheumatology clinic is the routine procedure. There, the doctor
will construct the treatment plan depending on the case. (9)

14

1) Drugs:
Hydroxychloroquine (Antimalarial drugs)
Antimalarials are the first-line treatment for patients with mild SLE
along with NSAIDs. They inhibit phagosomes, therefore inhibit TLR activation,
which suppresses IFN- (decreases autoantigen processing).

(4)

Corticosteroids
Especially useful in the onset flares. By inhibiting nuclear factor B,
they suppress B and T cells activities. And also alter the function of
monocytes and neutrophils. Glucocorticoids are administered orally on a
daily basis. If greater than 60 mg/d, IV methylprednisolone pulse is given.

(4)

Cyclophosphamide
The

standard

treatment

for

lupus

nephritis,

usually

given

in

combination with corticosteroids. The side effects may include infertility,

malignancy, hemorrhagic cystitis and infection.

(4)

Mycophenolate Mofetil (MMF)

Mycophenolate Mofetil (MMF) inhibits lymphocytes proliferation by
controlling the synthesis of guanosine nucleotides enzyme, which is essential
for DNA synthesis in lymphocytes. MMF is considered more suitable in
treating lupus nephritis than azathioprine. Some studies state that MMF has

15

almost the same efficacy to Cyclophosphamide for lupus nephritis, while

other studies claim that MMF is superior.

(4)

Azathioprine
Used as a corticosteroid-sparing agent, mechanism of action similar to
MMF. Has a moderate effect in treating lupus nephritis.

16

(4)

Methotrexate
A steroid-sparing agent inhibits the synthesis of DNA and RNA.
Effective in resistant arthritis and skin disease, not in major organ
involvement.

(4)

2) Monitoring
Frequent visits are crucial to detect the flares early. Also helps to
assess organs damage and adverse drug reactions. At each visit, the patient
is asked about different symptoms (alopecia, rash, fatigue of unknown origin,
etc...). Physical examination pays attention to joint problems, edema and
ulcers among other problems.

(9)

The following should be assessed regularly:

* CBC and platelet count
* Creatinine determination
* Urinalysis.
3) Monitoring for Potential Risks developed by SLE Patients:
Premature atherosclerosis
The risk is directly correlated with disease duration. Minimizing
corticosteroid use or maximizing the use of corticosteroid-sparing agents is a
priority in patients with SLE with hypercholesterolemia. Dietary advice and
lipid-lowering agents are usually necessary as well.
17

(9)

Hypertension and Renal Disease

Uncontrolled Blood Pressure will reduce kidney function, therefore
increasing

the

overall

mortality.

Tight

hypertension is an important aspect of SLE.

monitoring

and

treatment

of

(9)

4) Potential Future Therapies:

In 2012, Belimumab (a monoclonal antibody) was officially approved in
the treatment of mild SLE cases. The unresponsive sever cases indicate that
other cytokines may play a role in the disease. They act by disrupting certain
cellular communication.

(24)

Inhibiting mediators can also be used in treatments. Complements are

activated in regions where Immune Complexes are deposited, causing organ
damage. Therefore, inhibiting the Complement Cascade can be an adjunct
therapy to prevent organ damage.

(24)

Prognosis:
In modern day, short and medium term survival has substantially
improved in SLE patients. Although the long term prognosis is still poor due
to disease and treatment complications.

(10)

SLE affects females more than males in a 9:1 ratio, mainly females at
child-bearing age. The disease has various manifestations, severity and

18

treatment response, hence being defines as a syndrome rather than a

single disease.

(16)

Flares are intercepted with periods of remission, which if left

uncontrolled will inevitably lead to organ damage, most commonly in joints
and kidneys. Thats why its important that SLE patients have to go through
immunosuppression therapy, which will help stop/decrease the auto organattack phases and inflammations.

(16)

Differences in prognosis and severity are attributed to ethnicity, sex

and the age of onset. The apparent manifestation in young women and the
frequent exacerbation during pregnancy suggests the role of hormones,
mainly estrogen as possible factor. In 3-18% of cases, its diagnosed in a
later life stage Late SLE onset, in the age of 50 and older.

(16)

There are contradictory findings as to whether Late or Early onset SLE

has a severer prognosis. Though it was believed that the late-onset is more
benign, recent studies suggest that the late-onset has a worse prognosis
than the early one, with more exacerbation of the diseases symptoms.

(16)

Ethical and legal aspects:

Female patients constitute 80% of lupus. Women diagnosed with lupus
should be counselled in regards of the possible risks that are associated with
SLE in pregnancy; they can be assured that if the disease is in a quiescent

19

phase without renal or antiphospholipid involvement that the risk of

miscarriage is not significantly increased.(14)
The most difficult issue is when to advice a woman with SLE to not get
pregnant or to terminate a pregnancy. Maternal mortality rates in Women
with SLE and associated arterial pulmonary hypertension have been quoted
as high as 40%, and the prevalence of arterial pulmonary hypertension is
around 4.2% in Lupus patients. Such a high mortality rate indicates the
importance

of

screening

women

for

underlying

arterial

pulmonary

hypertension prior to pregnancy. Female patients should be also advised not

to conceive during an active period of the disease. (8)
Termination of the pregnancy or preterm delivery should be considered
in case the patient was suffering from uncontrolled hypertension or
worsening renal function despite proper treatment. In such cases we will be
facing a legal/ethical issue, that is whether the mother has full right to
terminate the baby/fetus in order to protect herself or whether the
baby/fetus should be considered a person and there is a conflict of interest
so the mothers right for a decision should be revoked. (8)

Impact of systemic lupus erythematosus on quality of life

SLE has a significant but diverse effect on patient's quality of life (QoL).
SLE patients scored less compared to their healthy counterparts in health,

20

work, and active recreation quality assessment, it has also been noted that
the drop in quality of life score is not explained by disease activity alone, as
treatment regime and accumulated damage also have an impact on the
patient's quality of life. (1)(20)
Improvement in physical and mental health has been associated with
higher quality of life scores, and these improvements are usually intertwined.
Better self-image and higher socioeconomic status has also been associated
with improvement in score. (1)
Due to the fact that SLE is a chronic disease, maintaining a good
quality of life score, and empowering the patient through education is very
essential for the control of it. Emphasizing the importance of medication
adherence and follow-up checkups can improve the patient compliance.
Furthermore, the patient can also be taught to monitor their own symptoms,
as for SLE patients even a fever might indicate a disease flare. Stressing on
the benefit of risk factor control and lifestyle changes is also very beneficial
in the long term complication control for these patients. (5)

21

Word Count: 3490

Excluding: Cover page, Table of content, Topic summary, Citations,
References, Annotated bibliography, Plagiarism cover sheet, and Flowchart.

22

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Annotated Bibliography
1. Wallace D, Hahn B, Dubois E. Dubois' lupus erythematosus and related
syndromes. Philadelphia, PA: Elsevier/Saunders; 2013.
Studies have varied over time and place for checking prevalence and used
different methods of case ascertainment. The study conducted in different
USA states used both inpatient and outpatient records for case validation the
major different were the sampling frame, and racial composition of the
population.
2. Ginzler E. Systemic Lupus Erythematosus, An Issue of Rheumatic
Disease Clinics. London: Elsevier Health Sciences; 2010.
Articles covering specific features of SLE and their relationship to therapy
include those by Klein, Morgan Roth, and Werth regarding cutaneous
manifestation and the newly validated instrument, also showing differences
between pediatric and adult lupus with Specify survival rates in developing
countries and developed countries.
3. Al-Arfaj AS e. Prevalence of systemic lupus erythematosus in central
Saudi Arabia. - PubMed - NCBI [Internet]. Ncbi.nlm.nih.gov. 2015 [cited
29

November

2015].

Available

from:

http://www.ncbi.nlm.nih.gov/pubmed/11938371
Used a systemic approach assessing people with SLE in Saudi Arabia (AlQaseem)

, and conducted the study with a 3 phases to determine the

26

prevalence of systemic lupus erythematous in the region.

Identifying the

cases was by using the criteria set for the diagnosis of systemic lupus
erythematous by the American college of Rheumatology. At the end of the
study in Al-Qaseem they reached to an estimated prevalence which was
reveling a similar one in the western countries.
4. Bijlsma J. EULAR textbook on rheumatic diseases. London: BMJ / EULAR;
2012.
This

textbook

provides

sufficient

and

illuminating

information

on

rheumatic diseases with an emphasis of Systemic lupus Erythematosus. It

helped us especially in pathophysiology and complications of SLE. In
addition, it conveyed a very lucid picture of possible clinical manifestation
of SLE.

27