Autoimmune diseases are an umbrella term that encompasses a wide variety of illnesses that share one

thing in common, the occurrence whereby the body’s own immune system attacks healthy and fully
functioning cells resulting in long lasting damage if left unmanaged. For this report, Systemic Lupus
Erythematosus and Progressive Systemic Sclerosis will be discussed. These conditions are also known as
connective tissue disorders due to the pathological characteristics of the diseases causing connective
tissues such as the skin, ligaments, fascia, tendons, and bones to deteriorate.

SLE is a disease that is often times long standing in nature, and affects various systems, organs, tissues,
and cells. The damage done is initially mediated by specific immune complexes and tissue binding
autoantibodies. In most cases, these autoantibodies exist in the patients for years before the initial onset
of signs and symptoms of the disease. (1) This disease has a higher prevalence in females who are of child
bearing age, and has a ratio of 9:1 female to male ratio (2). Some studies suggest that this can be due to
the different hormone levels that are present in both genders. (5)

Although there are very distinct clinical manifestations for SLE, it can still prove to be a challenge
diagnosing the disease due to the similar nature of connective tissue diseases in general. Not all patients
with SLE will present with a cookie cutter symptom and no two cases are the same. The diagnosis of
systemic lupus erythematosus, requires laboratory investigations, detailed history taking, and comparing
these findings to the diagnosis criteria. The diagnostic criteria contain common symptoms such as
hyperpyrexia, an increase in blood pressure, malaise, arthralgia, and inflammation. Other SLE distinct
symptoms include but are not limited to topical changes (malar and discoid rash), photo sensitivity,
presence of anti-dsDNA, anti- SM, or antiphospholipid antibody. (3-4) SLE also manifests neurologically
(Psychosis, convulsions), renally (proteinuria, red blood cell cast), and haematologically (anaemia,
leukopenia, thrombocytopenia). (2-4)

The aetiological mechanism of this disease varies tremendously on a wide variety of factors. From
hormone levels as stated previously (5), infections from viruses such as the cytomegalovirus or Epstein-
Bar virus, and even ultraviolet rays can be a potential trigger (6).

Since inflammation is a hallmark when it comes to causation of symptoms in Systemic Lupus, it is only
logical that non-steroidal anti-inflammatory drugs and corticosteroids are a large part of the medical
management for the connective tissue disease. Besides that, an accommodation of lifestyle to work
around the symptoms are needed. From little things such as putting on sunscreen to controlling diet and
physical activity they all cumulatively help improve the symptoms of this currently uncurable disease (7).
Progressive Systemic Sclerosis which is also known as Scleroderma much like systemic lupus, is also an
autoimmune connective tissue disease that occurs more often in females than males with a 4:1 ratio (10).
this disease affects multiple bodily systems and can be described by pathological changes in vascular
tissues, fibrosis in dermal tissues, internal organs, and virtually every bodily organ. (8-9)

Progressive systemic sclerosis can be categorized into diffuse cutaneous and limited cutaneous with the
former presenting with thickening of the skin on the arms and legs, both dorsal and ventral aspects of the
elbow and knees. The latter on the other hand, skin thickening often occurs only on the dorsal aspect of
the elbows and knees. Other than location of cutaneous changes, diffuse cutaneous scleroderma
progresses and recedes faster than the limited cutaneous variety.

To this date, there is no one laboratory test that confirms progressive system sclerosis. Akin to SLE,
diagnosis of this disease is done by carefully taking a patient’s history, performing a physical examination,
and taking a look for autoantibodies that are present in almost everyone who suffer from this disease.
However, these autoantibodies are not scleroderma specific and can be found in other connective tissue
diseases. That is the very reason why detailed history taking and a physical examination should be done
properly and prior to laboratory investigation. (13)

Much like Systemic Lupus Erythematosus, the disease is idiopathic (11). That being said there are evidence
that suggests that genetics and environmental factors play a role in the occurrence of scleroderma. (12)
Patients with progressive systemic Sclerosis can present an array of signs and symptoms such as initial
Raynaud’s phenomenon, inflammation of soft tissue, puffing of the digits, and pruritus. Carpal tunnel
syndrome pain, hyperpigmentation of the skin, malaise, muscle weakness, and a reduced in range of
motion are also common clinical manifestations present. As the disease progresses, it goes from an
oedematous phase to a fibrotic phase whereby dry skin, hair loss, reduced perspiration, and fibrosis of
the articulating structures of the joints starts to affect the joints making them stiff. While all this is
happening, without patients noticing, the disease has started to affect the function of their internal
organs. (9)

The exact mechanism on how scleroderma affects its patients varies upon which organ is in question.
Generally, this disease causes an increase in fibroblast activity which produces an excess of extracellular
matrix and deposition of collagen by activation of T-lymphocytes, damage to microvascular tissues, and
altered connective tissue synthesis. The drug management also still much like SLE, is based on the
symptoms the patient is presented with. (14)
As chiropractors in the making, there should be a competent level of understanding of these diseases as
patients that we get in the future may present themselves with symptoms of systemic lupus
erythematosus or progressive systemic sclerosis. By doing so, they will get diagnosed and treated earlier
giving them a chance at a better prognosis.
1. https://accessmedicine-mhmedical-
com.ezp2.imu.edu.my/content.aspx?sectionid=192284866&bookid=2129&Resultclick=2#11566
06477
2. https://elearn.imu.edu.my/pluginfile.php/212842/mod_resource/content/1/Reference%20SLE_
2.pdf
3. https://elearn.imu.edu.my/pluginfile.php/212841/mod_resource/content/1/Reference%20SLE_
1.pdf
4. Renz H. Autoimmune diagnostics. Berlin: de Gruyter; 2011.
5. https://lupusnewstoday.com/2016/01/21/the-immune-system-is-a-natural-target-for-estrogen-
action-opposing-effects-of-estrogen-in-two-prototypical-autoimmune-diseases/
6. https://www.ncbi.nlm.nih.gov/pubmed/24763542
7. http://www.scielo.br/scielo.php?pid=S0482-50042012000300009&script=sci_arttext&tlng=en
8. https://elearn.imu.edu.my/pluginfile.php/212843/mod_resource/content/1/Reference%20Scler
osis_1.pdf
9. https://accessmedicine-mhmedical-
com.ezp2.imu.edu.my/content.aspx?sectionid=159214725&bookid=2129&Resultclick=2
10. https://www.orpha.net/consor/cgi-bin/OC_Exp.php?Lng=GB&Expert=220402
11. https://www.jci.org/articles/view/31139
12. https://emedicine.medscape.com/article/331864-overview
13. https://accessmedicine-mhmedical-
com.ezp2.imu.edu.my/content.aspx?sectionid=42584910&bookid=506&Resultclick=2#5727258
5
14. https://accessmedicine-mhmedical-
com.ezp2.imu.edu.my/content.aspx?sectionid=42584910&bookid=506&Resultclick=2#5727265
9
15.