 Staphylococcus aureus

SOFT TISSUE ABSCESS  Streptococcus species

such as streptococcus
pyogenes
IDEAL PATHOPHYSIOLOGY  Serratia marcescens
 Pseudomonas aeruginosa
Precipitating Factors:  Mycobacteria
Predisposing factors:
(avium/tuberculosis)
Bacterial infection
 Nocardia spp.
All age groups Foreign bodies  fungi

Autoimmune disorder Compromised Immune System

(Dermatomyositis, calcinosis)  Ulcer (soft tissue)
Chronic Skin Condition  Osteomyelitis
 Cellulitis
Trauma  Pyomyositis
Blocked Glands (Environmental)  Infective endocarditis

Poor circulation (Environmental)

Invasive medical procedure
Underlying medical conditions (environmental)

Activation of the immune system response at site of injury

Mast cells at injured site Disrupted endothelial cells release Disrupted endothelial cells release
release histamine pro-inflammatory cytokines leukocytosis-inducing factors
(e.g IL’s, TNFa) and chemokines

 circulating WBC’s
vessel permeability: Vasodilation:
extravasation of immune  blood flow to Chemotaxis:
cells/mediators (e.g., injured site Immune cells migrate
WBC’s, complement to injury site
proteins, platelets

INFLAMMATION

Cardinal signs of the inflammatory response

Redness (rubor), Heat (color), Pain (dolor), Swelling (Tumor)

Continued Innate Immunity Acquired Immunity Recruitment

Phagocytosis: Complement System: Natural Killer Cells: Humoral: Cell-mediated:

(*main mechanism) Opsonize pathogen Perforin-mediated wall (B cell response) (T cell response)
Neutrophils and (tag for destruction), promote breakdown (puncture production of antibodies  helper cell and
macrophages engulf inflammation holes), enzyme- activation of cytotoxic cell activity
foreign pathogens and mediated destruction) complementary system
dead tissue

Breakdown of
proteins

Formation
Accumula Pressure Abscess Release
of Tissue Necrosis (cell
tion of build-up Rupture of PUS
ABSCESS weakening death)
PUS

Disruption of
collagen fibers
Healing Process
Textual Discussion of the Disease Process (Ideal)

According to Feger, 2022, Soft tissue abscesses are focal or localized collections
of pus caused by an immune response to pathogenic microorganisms. They are
surrounded by a peripheral rim or abscess membrane and can be found within the soft
tissues in any part of the body. Soft tissue abscesses include subcutaneous abscesses,
intramuscular abscesses and intermuscular abscesses or abscesses located in the
deep soft tissues within the fascial planes. Following are the contributing factors that
can lead to soft tissue abscess.

In predisposing factor soft tissue abscess occurred in all age groups. According
to Skin and Soft Tissue Infections, skin and soft tissue infections are prevalent across all
age ranges, affecting both active youngsters and less mobile elderly individuals. It's
crucial for clinicians to skillfully categorize these infections to ensure patients receive
timely and suitable treatment (Skin and Soft Tissue Infections, n.d.)

Calcinosis cutis, a rare complication of dermatomyositis are predisposing factors

that is notably in cases positive for anti- NXP2 (Nuclear Matrix Protein 2 ) antibodies, is
infrequently documented for its associated complications. However, in a handful of
instances, it has resulted in skin ulcerations and subsequent bacterial infections. As
seen in the current case, ulcerative calcinosis cutis can escalate to cellulitis, further
complicated by subcutaneous abscess formation and the advancement of lymphangitis,
potentially necessitating urgent debridement (Takimiya et al., 2022). In addition, it
characterized by the accumulation of calcium salts within cells, impacts around 40% of
patients and may result in skin ulcers, recurrent infections, joint stiffness, and nerve
compression (Pinotti et al., 2023).

Under precipitating factors, abscesses are commonly triggered by bacterial

infections, with the majority caused by Staphylococcus bacteria. When bacteria invade
the body, the immune system responds by dispatching white blood cells to combat the
infection. This immune response leads to inflammation, resulting in the death of
surrounding tissue. As a consequence, a cavity forms and becomes filled with pus,
giving rise to an abscess (Professional, 2022).

In addition, According to Rehmus, 2023, abscesses found on the torso, limbs,

underarms, or in the head and neck area are often caused by Staphylococcus aureus
bacteria, with methicillin-resistant strains (MRSA) being prevalent in the United States.
Additionally, Streptococci bacteria are commonly associated with these types of
infections.

Bacteria commonly infiltrate the skin through openings like hair follicles, puncture
wounds, or cuts. Occasionally, abscesses develop in the vicinity of foreign objects
embedded in the skin, such as splinters or shards of glass (Cpt, 2024).

Skin and soft tissue infections (SSTIs) occur when the skin's defense
mechanisms are compromised, permitting bacterial infiltration and interaction in the
affected region. Trauma and surgical interventions frequently compromise the skin's
protective barrier. Primary SSTIs arise from the invasion of healthy skin, while
secondary SSTIs emerge in already compromised skin, such as from trauma or
underlying health issues. Although typically localized, these infections can also spread
via the bloodstream or lymphatic system (Silverberg, 2021).

When even minor trauma, tears, or inflammation disrupt our skin's natural
protective barrier, bacteria have an opportunity to enter. This can lead to the formation
of an abscess as the body's immune response, involving white blood cells, attempts to
combat these invading germs. Additionally, blockages in sweat or oil glands, sebaceous
glands, hair follicles, or existing cysts can also initiate abscess formation (Abscess,
2023). In addition, Hidradenitis suppurativa, often referred to as acne inversa, is a
persistent skin condition marked by recurring nodules beneath the skin's surface. These
nodules are similar to boils, causing inflammation and discomfort. Eventually, they
rupture, forming abscesses that release fluid and pus. The healing process leads to
substantial scarring of the skin ((Hidradenitis Suppurativa: MedlinePlus Genetics, n.d.)

Abscesses can also stem from blockages in the apocrine and sebaceous glands.
Sebaceous glands are present throughout the body, while apocrine glands are primarily
located in the armpits and genital areas. Cysts often develop in these glands, increasing
the likelihood of abscess formation (Guha et al., 2022).

In peripheral vascular disease (PVD), plaque accumulation narrows the blood

vessels, particularly affecting the legs and feet. This condition is common among
individuals with diabetes. Due to the restricted blood flow caused by narrowed vessels,
the skin may become thin and unhealthy, making it prone to tearing. This heightened
vulnerability to skin damage increases the risk of developing abscesses (William
Campbell, DO, FAAFP, n.d.).

Invasive procedures can potentially lead to skin abscesses due to various

factors. Firstly, the procedure itself may introduce bacteria into the skin, especially if
proper aseptic techniques are not followed [1]. Additionally, the trauma caused by the
procedure can compromise the skin's integrity, creating openings for bacteria to enter
and cause infection (Types of Healthcare-associated Infections | HAI | CDC, n.d.).

Other factors that remain incompletely understood may also influence the
development of soft tissue abscesses. Additionally, the multitude of microorganisms
present within the abscess, along with the presence of antibiotic-resistant enzymes,
hostile anaerobic microbial environments, and the protective capsule surrounding the
abscess, contribute to persistent infections despite antibiotic therapy and necessitate
drainage procedures. It is important to consider both aerobic and anaerobic organisms
when selecting antibiotics to treat such infections (Radhi et al., 2021).

In summary, the pathophysiology of soft tissue abscesses involves a complex interplay of

various factors. Typically, these abscesses arise due to a localized bacterial infection in the soft
tissues of the body. The process often begins with the introduction of bacteria into the skin or
soft tissue through breaks in the skin barrier, such as cuts, wounds, or punctures. Once bacteria
enter the soft tissue, they can proliferate and evade the body's immune defenses, leading to
infection. Factors such as compromised immunity, poor circulation, and underlying medical
conditions like diabetes can increase the risk of infection and abscess formation. As the bacterial
population grows, the body mounts an inflammatory response, resulting in the classic signs of
inflammation such as redness, swelling, heat, and pain at the site of infection. In severe cases,
the inflammatory response may lead to tissue necrosis (death of tissue) and the formation of a
pocket of pus within the affected area, known as an abscess. The bacteria commonly implicated
in soft tissue abscesses include Staphylococcus aureus and Streptococcus species, although
other pathogens may also be involved depending on the specific clinical scenario (Mandell et
al., 2020)

Certainly! Abscess rupture occurs when pressure builds up within the abscess cavity due
to the accumulation of pus and inflammatory fluids. This pressure weakens the surrounding
tissue, leading to breach of the skin barrier. Eventually, the combination of increased pressure
and tissue damage causes the abscess to burst, releasing pus, bacteria, and debris. Rupture
typically provides immediate relief from pain and pressure, allowing for drainage of the abscess
contents. Following rupture, the body initiates the healing process to repair the damaged tissue
and resolve the infection. Proper wound care is essential for complete healing and to prevent
complications (Carpenter & Brady, 2023).

Types of healthcare-associated infections | HAI | CDC. (n.d.).

https://www.cdc.gov/hai/infectiontypes.html

Mandell, G. L., Bennett, J. E., Dolin, R., & Blaser, M. J. (Eds.). (2020). Mandell, Douglas, and
Bennett's Principles and Practice of Infectious Diseases (9th ed.). Elsevier.

William Campbell, DO, FAAFP. (n.d.). Most common causes of abscesses: Health solutions:

Board certified family medicine. https://www.hstinleypark.com/blog/most-common-

causes-of-abscesses#:~:text=Because%20your%20blood%20vessels%20are,at%20risk

%20for%20an%20abscess.

Hidradenitis suppurativa: MedlinePlus Genetics. (n.d.).

https://medlineplus.gov/genetics/condition/hidradenitis-suppurativa/

Radhi, M. M., Al-Rubea, F. M., Hindi, N. K. K., & Al-Jubori, R. H. K. (2021). Bacterial skin

abscess. In Infectious diseases. https://doi.org/10.5772/intechopen.91657

Guha, N., Paul, A., Islam, J., Das, M. K., & Zaman, K. (2022). Phytosomes in functional

cosmetics. In Elsevier eBooks (pp. 237–275). https://doi.org/10.1016/b978-0-323-91077-

4.00001-6

Abscess. (2023, October 8). WebMD. https://www.webmd.com/a-to-z-guides/abscess

Silverberg, B. (2021). A structured approach to skin and soft tissue infections (SSTIs) in an

ambulatory setting. Clinics and Practice, 11(1), 65–74.

https://doi.org/10.3390/clinpract11010011

Carpenter, R., & Brady, M. F. (2023, January 30). BAX gene. StatPearls - NCBI Bookshelf.

https://www.ncbi.nlm.nih.gov/books/NBK555927/

Cpt, S. C. (2024, March 26). What to know about skin abscesses.

https://www.medicalnewstoday.com/articles/skin-abscess#causes

Rehmus, W. E. (2023, June 8). Cutaneous abscess. MSD Manual Professional Edition.

https://www.msdmanuals.com/professional/dermatologic-disorders/bacterial-skin-

infections/cutaneous-abscess

Professional, C. C. M. (n.d.-a). Abscess. Cleveland Clinic.

https://my.clevelandclinic.org/health/diseases/22876-abscess

Pinotti CS, Cannon L, Dvergsten JA, Wu EY. Calcinosis in juvenile dermatomyositis:

Updates on pathogenesis and treatment. Front Med (Lausanne). 2023 Mar 2;10:1155839.
doi: 10.3389/fmed.2023.1155839. PMID: 36936211; PMCID: PMC10017873.
Takimiya, R., Fujikawa, H., Shirasawa, S., & Muranaka, K. (2022). Calcinosis cutis causing

cutaneous ulceration and secondary bacterial infection in a patient with antinuclear

matrix protein 2 antibody–positive dermatomyositis. Acute Medicine & Surgery, 9(1).

https://doi.org/10.1002/ams2.810

Soft tissue abscesses are common and can occur in all age groups 2.
Feger, J. (2022). Soft tissue abscess. Radiopaedia.org. https://doi.org/10.53347/rid-97517

Skin and soft tissue infections. (n.d.). McGraw Hill Medical.

https://accessmedicine.mhmedical.com/content.aspx?bookid=2816§ionid=240348
 SOFT TISSUE ABSCESS

ACTUAL PATHOPHYSIOLOGY

Predisposing factors: Precipitating Factors:

Autoimmune disease (Diagnosed: Diagnosed of Pneumonia, 2007

Dermatomyositis, calcinosis, 2010) Diagnosed of Rheumatoid Heart
Skin Inflammation Disease, 2007
(DERMATITIS)
Extrapulmonary Tuberculosis, 2020
Muscle Inflammation
(MYOSITIS)

TISSUE DAMAGE

CALCINOSIS Dysregulation of Immune System

Methicillin-
Mycobacterium Lead: to Skin Ulceration sensitive
tuberculosis, Group Staphylococcus
aureus
A Streptococcus
Bacterial invasion

Inflammatory response Lab test

Hematology (04/05/24):
 Lymphocytes: 0.23
 Monocytes: 0.13
Continued Innate Immunity

Vital Signs (04/05/24):

PR: 107 bpm
RR: 22 cpm

Phagocytosis:
(*main mechanism)
Neutrophils and Accumulation Pressure Healing Process
Abscess Release of PUS
macrophages engulf of PUS build-up
Formation
foreign pathogens
and dead tissue
Wound care
dressing performed
(04/05/2024)

Roentgenological Report Microbiology (04/05/24):

(04/05/24): Rare Epithelial cells
CxR AP (Consider pleural plaque, Few Pus Cells Administered
bilateral left axilla and arm 1+ Gram positive cocci in Medication:
calcified lymph nodes singles 04/05/24:
Ampicillin +sulbactam
1.5g IVTTq6H
04/08/24:
LEGEND: Shift ampicillin
+sulbactam to
Predisposing factor Signs & Symptoms cloxacillin 500 mg 1
tab q6Hrs.
Precipitating factor 04/08/24:
Complication Decontamination
Compensatory
Response
procedure performed
Outcome (Bleach 1 TSR +1
Progression gallon water.
Intervention 04/08/24:
Bacteria Mupirocin ointment.
04/08/24:
Vitamin C, 1 cap OD.
Diagnostic Test
Textual Discussion of the Disease Process (Actual)

A soft tissue abscess refers to a localized collection of pus within the body's soft
tissues. These abscesses typically occur as a result of bacterial infection, often
stemming from a break in the skin, such as a cut or wound. The bacteria enter the body
through the break and multiply, leading to inflammation and the formation of pus. The
abscess may present as a painful, swollen, and warm area on the skin, sometimes
accompanied by redness. In more severe cases, there may be fever and systemic
symptoms (Brown, D. L., & Bulger, E. M., 2019).

The predisposing factors that increased patient risk of the patient in developing
soft tissue abscess where he was diagnosed of dermatomyositis, calcinosis at the age
of 6 years old last 2010, where in dermatomyositis is a rare autoimmune condition
affecting connective tissue, marked by distinctive skin rashes and inflammation of
muscles. A serious consequence of the disease is calcinosis, where insoluble calcium
salts build up in the skin and other tissues. This calcinosis can take different forms: it
may appear superficially as sponge-like patches or nodular deposits, or deeper as
tumoral masses affecting muscles or fascia, and in severe cases can extend over a
large area like an exoskeleton. Commonly affected areas include the extremities and
pressure points. Complications include ulcers, recurrent infections, and limited joint
movement, leading to significant health challenges (Davuluri et al., 2022).

Among the precipitating factors, the patient's history includes a pneumonia diagnosis in
2007 at the age of 4, which poses susceptibility to skin abscess formation, as observed in the
patient's experience. Staphylococcus aureus, including methicillin-resistant strains (MRSA), is
recognized as a prevalent pathogen in such cases. Staphylococcal pneumonia is a serious
condition requiring immediate diagnosis due to its potential complications, including severe
necrotizing pneumonia, bacteremia, or sepsis, which can progress to shock. Staphylococcus
aureus, historically associated with sepsis and abscess development since the 1800s, can lead to
bacteremia during pneumonia episodes, facilitating the spread of bacteria from the lungs to
distant sites, potentially resulting in abscess formation, such as in the skin (Clark & Hicks, 2023).

Another contributing factor is the patient's diagnosis of rheumatic heart disease in 2007.
Rheumatic fever typically emerges from an untreated or poorly treated strep throat infection,
often stemming from an unusual strain of streptococcus bacteria. While the precise mechanism
behind this strain's ability to trigger the characteristic inflammatory reaction of rheumatic fever
remains unclear, it's theorized that antibodies, designed to combat strep bacteria, mistakenly
attack healthy tissues in the heart muscle, valves, joints, brain, and skin. This erroneous immune
response results in widespread inflammation and tissue damage across the body (Philadelphia,
n.d.).

In addition the patient was diagnosed of extrapulmonary tuberculosis last 2020,

Mycobacterium tuberculosis a bacteria from the lungs can travel through the bloodstream to
distant organs, including the skin, where they can cause localized infections and abscess
formation. The immune response to TB infection involves the formation of granulomas, which
can sometimes break down, releasing TB bacteria into surrounding tissues and leading to
abscess formation. Additionally, TB infection in nearby structures or tissues, such as lymph
nodes or bones, can extend into the skin, resulting in secondary abscess formation (Esmail, H.,
& Barry, C. E., 2018).

All of these predisposing factors and precipitating factors specifically the

dermatomyositis, calcinosis are high risk of developing soft tissue abscess. These all can
dysregulate the immune system of our body leading to skin ulceration. Skin ulceration provides
a pathway for bacteria to enter the body due to the compromised integrity of the skin barrier.
When the skin is ulcerated, whether due to trauma, infection, or underlying medical conditions,
it creates an open wound that exposes the underlying tissues to the external environment.
Bacteria, particularly opportunistic pathogens like Staphylococcus aureus and Streptococcus
pyogenes, can then colonize and infect these exposed tissue.

Once bacteria enter the body, the inflammatory response is triggered, as indicated by
the patient's hematology test results last April 04, 2024 showing decreased lymphocytes of 0.23
and increased monocytes of 0.13, along with the elevated vital signs taken in same day of pulse
rate of 107 beats per minute and respiratory rate of 22 cycle per minute. The ongoing response
to continued innate immunity leading to phagocytosis the main mechanism where neutrophils
and macrophages engulf foreign pathogens and dead tissue leading to accumulation of pus, as
the immune system fights off the bacteria, dead immune cells, bacteria, and tissue debris
accumulate, forming pus. Pus is a mixture of dead cells, bacteria, and fluid, and it serves as a
medium for trapping and isolating the bacteria within the abscess cavity. Over time, as pus
accumulates, it creates a localized pocket of infection within the skin tissue, leading to the
formation of an abscess. The abscess may enlarge and become fluctuant (soft and fluid-filled) as
pus accumulates within it, the patient undergone chest x-ray for further confirmatory last April
05, 2024 with the result of consider pleural plaque, bilateral left axilla and arm calcified lymph
nodes. The abscess may resolve spontaneously as the body's immune system successfully clears
the infection. However, if the abscess continues to enlarge or if it comes under pressure, it may
rupture, releasing pus and bacteria into the surrounding tissue and potentially leading to
secondary infections or complications, as the patient undergone microbiology laboratory test
last April 05, 2024 with the remarks of rare epithelial cells, few pus cells, 1+ gram positive cocci
in singles.

Following the resolution of the infection, the healing process commences, with the body
activating tissue repair mechanisms. This includes the formation of granulation tissue, which
comprises new blood vessels, fibroblasts, and extracellular matrix components. Granulation
tissue fills the void left by the abscess and serves as a scaffold for new tissue formation. On April
5, 2024, the patient underwent wound dressing, followed by administration of medication as
prescribed by the physician, initially with Ampicillin + Sulbactam intravenously every 6 hours. On
April 8, 2024, the medication regimen was switched to Cloxacillin 500mg orally every 6 hours.
Additionally, on the same day, a decontamination procedure was performed using a bleach
solution as per specific time, solution, and ratio guidelines, along with the application of
Mupirocin ointment and vitamin C supplementation as directed by the physician. As of April 10,
2024, the patient is alert, oriented, and positioned supine, undergoing observation for recovery.
 Esmail, H., & Barry, C. E. (2018). Chapter 8 - Tuberculosis and Other Mycobacterial
Infections. In J. Cohen, J. Powderly, & D. Opal (Eds.), Infectious Diseases (Fourth Edition) (pp. 65-
74). Content Repository Only!Mycobacterium tuberculosis

Philadelphia, C. H. O. (n.d.). Rheumatic fever and rheumatic heart disease. Children’s Hospital

of Philadelphia. https://www.chop.edu/conditions-diseases/rheumatic-fever-and-

rheumatic-heart-disease

Clark, S. B., & Hicks, M. A. (2023, August 8). Staphylococcal pneumonia. StatPearls - NCBI

Bookshelf. https://www.ncbi.nlm.nih.gov/books/NBK559152/

Davuluri, S., Duvvuri, B., Lood, C., Faghihi-Kashani, S., & Chung, L. (2022c). Calcinosis in

dermatomyositis: Origins and possible therapeutic avenues. Baillière’s Best Practice and

Research in Clinical Rheumatology/BaillièRe’s Best Practice & Research. Clinical

Rheumatology, 36(2), 101768. https://doi.org/10.1016/j.berh.2022.101768

Brown, D. L., & Bulger, E. M. (2019). Soft Tissue Infections: Abscesses, Cellulitis, and
Necrotizing Fasciitis. In Rosen's Emergency Medicine: Concepts and Clinical Practice
(9th ed., Vol. 1, pp. 1351–1372). Elsevier.
s

Textual Discussion of the Disease Process (Actual)

Juvenile Dermatomyositis with Calcinosis

 Juvenile dermatomyositis (JDM) is a rare condition characterized by both muscle
inflammation and a distinctive skin rash, setting it apart from other muscular disorders.
Typically emerging in children aged 5 to 10, JDM manifests with weakness in muscles
surrounding the neck, shoulders, and hips. Additionally, affected children develop a rash
in specific areas like the eyelids, knuckles, and finger joints. (Articles, n.d.)

In terms of predisposing factors, dermatomyositis was diagnosed in the patient at

the age of 6, a period when the immune system is still maturing and may not function
optimally. Additionally, a familial history of psoriasis on the patient's paternal side could
contribute to the autoimmune response seen in dermatomyositis.

Regarding precipitating factors, the exact cause of dermatomyositis is often

unknown, although it is categorized as one of the idiopathic inflammatory myopathies.
It's believed to arise from either a viral infection affecting the muscles or an immune
system dysfunction.

The patient's medical history includes pneumonia diagnosed at 4 years old,

followed by diagnoses of rheumatoid heart disease in the same year, and both
pulmonary and extrapulmonary tuberculosis in subsequent years. These conditions, all
involving immune system dysregulation, could exacerbate existing autoimmune
conditions like dermatomyositis. The inflammatory and immune response triggered by
pneumonia, in particular, may heighten the risk of complications such as calcinosis in
dermatomyositis.

Dermatomyositis arises from dysregulated immune responses, characterized by

the infiltration of autoreactive T lymphocytes into muscle and skin tissues. This
infiltration triggers the release of pro-inflammatory cytokines like interferon-gamma,
tumor necrosis factor-alpha (TNF-alpha), and interleukins (IL-1, IL-6, IL-17). In the skin,
interleukins prompt the infiltration of immune cells into the dermis and epidermis,
causing inflammation (dermatitis), while in muscles, they attract CD4+ T cells and
macrophages, leading to muscle fiber damage (myositis).

Manifestations of dermatomyositis include skin redness and muscle pain and

weakness, as seen in the patient's experience. Vasculopathy ensues, involving
inflammation and damage to blood vessels, resulting in vasoconstriction and impaired
blood flow. Perifascicular atrophy, where muscle fibers waste away at the periphery of
muscle fascicles, is also observed. Chronic inflammation may worsen dermatomyositis
severity.

Ongoing inflammation, confirmed through recent hematology lab results showing

decreased lymphocytes and elevated monocytes, leads to tissue damage. Low creatine
and potassium levels reflect tissue destruction and altered calcium metabolism. Calcium
deposits within affected tissues cause dystrophic calcification, potentially exacerbating
inflammation and impairing wound healing.

The presence of calcinosis exacerbates inflammation and may hinder wound

healing, as indicated by laboratory and radiological findings. Ultrasound results revealed
additional abdominal complications, including fatty liver, cholecystitis, and renal disease.

The disease mechanism involves the activation of C3 by putative antibodies or

factors, leading to the formation of C3b and C4b fragments, which contribute to the
formation of C3bNEO and membrane attack complex (MAC) deposited in the
endomysial vasculature. As the disease progresses, capillaries are destroyed, and
muscles undergo microinfarction. Perifascicular atrophy initiates the process, with
necrotic and degenerative fibers present as the disease advances.

The pathogenesis of dermatomyositis' cutaneous component remains poorly

understood, with some studies suggesting similarities to muscle involvement. While
complement-mediated vascular inflammation may drive muscle pathology, direct
cytotoxic effects of CD8+ lymphocytes are implicated in polymyositis. However, cytokine
studies suggest overlapping inflammatory processes, with abnormalities in tumor
necrosis factor (TNF) linked to dermatomyositis.

Femia, A. N., MD. (n.d.-b). Dermatomyositis: practice essentials, background,

pathophysiology. https://emedicine.medscape.com/article/332783-overview?
form=fpf
Dermatomyositis - symptoms, causes, treatment | NORD. (n.d.-b). National
Organization for Rare Disorders.
https://rarediseases.org/rare-diseases/dermatomyositis/

Davuluri, S., Duvvuri, B., Lood, C., Faghihi-Kashani, S., & Chung, L. (2022b). Calcinosis
in dermatomyositis: Origins and possible therapeutic avenues. Baillière’s Best
Practice and Research in Clinical Rheumatology/BaillièRe’s Best Practice &
Research. Clinical Rheumatology, 36(2), 101768.
https://doi.org/10.1016/j.berh.2022.101768

Peravali, R., Acharya, S., Raza, S. H., Pattanaik, D., & Randall, M. B. (2020b).
Dermatomyositis developed after exposure to Epstein-Barr virus infection and
antibiotics use. ˜the œAmerican Journal of the Medical Sciences, 360(4), 402–
405. https://doi.org/10.1016/j.amjms.2020.05.011
Qudsiya, Z., & Waseem, M. (2023c, August 7). Dermatomyositis. StatPearls - NCBI
Bookshelf.
https://www.ncbi.nlm.nih.gov/books/NBK558917/#:~:text=Dermatomyositis%20is
%20thought%20to%20be,which%20forms%20C3b%20and%20C4b

https://emedicine.medscape.com/article/332783-overview?form=fpf

https://rarediseases.org/rare-diseases/dermatomyositis/

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10269219/#:~:text=Dermatomyositis
%20(DM)%20is%20a%20rare,debilitating%20sequela%20of%20the%20disease.

https://www.sciencedirect.com/science/article/abs/pii/S0002962920301841

https://www.ncbi.nlm.nih.gov/books/NBK558917/#:~:text=Dermatomyositis%20is
%20thought%20to%20be,which%20forms%20C3b%20and%20C4b.