Mastitis pathophysiology

Mastitis Microchapters
Home
Patient Information
Overview
Historical Perspective
Classification
Pathophysiology
Causes
Differentiating Mastitis from other Diseases
Epidemiology and Demographics
Risk Factors
Screening
Natural History, Complications, and Prognosis
Diagnosis
History and Symptoms
Physical Examination
Laboratory Findings
Electrocardiogram
X Ray
CT
MRI
Ultrasound
Other Imaging Findings
Other Diagnostic Studies
Treatment
Medical Therapy
Surgery
Primary Prevention
Secondary Prevention
Case Studies
Case #1
Mastitis pathophysiology On the Web
Most recent articles
Most cited articles
Review articles
CME Programs
Powerpoint slides
Images
American Roentgen Ray Society Images of Mastitis pathophysiology All Images X-rays Echo & Ultrasound CT Images MRI
Ongoing Trials at Clinical Trials.gov
US National Guidelines Clearinghouse
NICE Guidance
FDA on Mastitis pathophysiology
CDC on Mastitis pathophysiology
Mastitis pathophysiology in the news
Blogs on Mastitis pathophysiology
Directions to Hospitals Treating Mastitis
Risk calculators and risk factors for Mastitis pathophysiology

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Prince Tano Djan, BSc, MBChB [2]

Please help WikiDoc by adding content here. It's easy! Click here to learn about editing.

Pathophysiology

Nonpuerperal Mastitis: Pathogenesis

Most clinically significant cases of nonpeurperal mastitis start as inflammation of the ductal and lobular system (galactophoritis) and possibly the immediately surrounding tissue.

Development of Nonpeurperal mastitis is the result of Secretory stasis about 80% of cases. The retained secretions can get infected or lead to inflammation by causing mechanical injury leading to leakage of the lactiferous ducts. Autoimmune reaction to the secretions may also be a factor.

Several mechanisms are thought to lead to the pathogenesis of mastitis are shown below:

• Secretory disease or galactorrhea.
• Changes in permeability of lactiferous ducts (retention syndrome).
• Blockage of lactiferous ducts, for example duct plugging caused by squamous metaplasia of lactiferous ducts.
• Trauma, injury.
• Mechanical irritation caused by retention syndrome or Fibrocystic Condition.
• Infection.
• Autoimmune reaction to luminal fluid.

About 25% of patients may be hyperprolactinemic and significant coincidence with fibrocystic condition and thyroid anomalies has been documented (Peters & Schuth 1989, Goepel & Pahnke 1991). Up to 50% of patients experience transient hyperprolactinemia possibly caused by the inflammation or treatment and most had abnormally high Prolactin reserve (Goepel & Pahnke 1991).

Prolactin, IGF-1 and TSH are important sytemic factors in galactopoiesis, their significance in secretory disease is not documented but it has been asserted that the mechanisms of secretory disease and galactopoiesis are closely related.

Permeability of the alveolar and ductal epithelia is mostly controlled by tight junction regulation and is closely linked to galactopoiesis and possibly secretory disease. The tight junctions are regulated by a multitude of systemic (prolactin, progesterone, glucocorticoids) and local (intramammary pressure, TGF-beta, osmotic balance) factors.

Current smokers have the worst prognosis and highest rate of recurrent abscesses.

Acromegaly may present with symptoms of non-puerperal mastitis.

Terminology

Depending on appearance, symptoms, aetiological assumptions and histopathological findings a variety of terms has been used to describe mastitis and various related aspects.

• Galactopoiesis: milk production

• Secretory disease: aberrant secretory activity in the lobular and lactiferous duct system, believed to be the most frequent factor causing galactophoritis. The secretions may be milk like or apocrine luminal fluid.

• Retention syndrome (aka retention mastitis): accumulation of secretions in the ducts with mainly intraductal inflammation.

• Galactostasis: like retention syndrome where the secret is known to be milk.

• Galactophoritis: inflammation of the lobular and lactiferous duct system, mainly resulting from secretory disease and retention syndrome.

• Plasma cell mastitis: plasma cells from the intraductal inflammation infiltrate surrounding tissue.

• Duct ectasia: literally widening of lactiferous ducts - relatively common finding in breast exams, increase with age. Strongly correlated with cyclic and very strongly with noncyclic breast pain. Correlation with mastitis is of anecdotal quality and has been questioned by recent research.

• Duct ectasia syndrome: in older literature this was used as synonym for nonpuerperal mastitis with recurring breast abscess, nipple discharge and possibly associated fibrocystic condition with blue dome cysts. Recent research shows that duct ectasia is only very weakly correlated with mastitis symptomes (inflammation, breast abscess). The use of the terms Duct Ectasia and Duct Ectasia Syndrome is inconsistent throughout the literature.

• Squamous metaplasia of lactiferous ducts: cuboid cells in the epithelial lining of the lactiferous ducts transform (squamous metaplasia) to squamous epithelial cells. Present in many cases of subareolar abscesses.

• Subareolar abscess: abscess bellow or in close vicinity of the areola. Mostly resulting from galactophoritis.

• Retroareolar abscess: deeper (closer to chest) than the lobular ductal system and thus deeper than a subareolar abscess.

• Periductal inflammation (aka periductal mastitis): inflammation infiltrated tissue surrounding lactiferous ducts. Almost synonym for subaerolar abscess. May be just a different name for plasma cell mastitis.

• Fistula: fine channel draining an abscess cavity

• Zuska's disease: periareolar abscess associated with squamous metaplasia of lactiferous ducts. Some authors also associate this with nipple discharge.