Mastitis pathophysiology: Difference between revisions

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Latest revision as of 22:39, 29 July 2020

Mastitis Microchapters

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

Overview

Most clinically significant cases of non-puerperal mastitis start as inflammation of the ductal and lobular system and possibly the immediate surrounding tissue. Development of non-puerperal mastitis is the result of secretory stasis whereas puerperal mastitis occurs when bacteria, often from the patient's skin or the baby's mouth/nostrils,[1] enters a milk duct through a crack in the nipple.

Pathophysiology

Anatomy of the breast

The images below show a general overview of breast anatomy.

Cross-section of the breast - By Original author: Patrick J. Lynch. Reworked by Morgoth666 to add numbered legend arrows. - Patrick J. Lynch, medical illustrator, CC BY 3.0, https://commons.wikimedia.org/w/index.php?curid=2676813

1) Chest wall
2) Pectoralis muscles
3) Lobules
4) Nipple
5) Areola
6) Milk duct
7) Fatty tissue
8) Skin


Surface anatomy of the breast


Surface anatomy of the breast - By Original: Ralf RoletschekDerivative: علاء نجار - Derivative from this file, CC BY-SA 3.0, https://commons.wikimedia.org/w/index.php?curid=46044299

Pathogenesis

Non-puerperal Mastitis

Most clinically significant cases of non-puerperal mastitis start as inflammation of the ductal and lobular system and possibly the immediate surrounding tissue.

Development of non-puerperal mastitis is the result of secretory stasis in 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.


Puerperal Mastitis

Development of puerperal mastitis occurs when bacteria, often from patients skin or the baby's mouth/nostrils,[2] enters a milk duct through a crack in the nipple.

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

Approximately a quarter of patients may be hyperprolactinemic. There has been a strong association with fibrocystic condition and thyroid conditions. Up to 50% of patients may experience transient hyperprolactinemia possibly caused by inflammation or treatment and a significant number of patients may have abnormally high prolactin reserve.[3][4]

TSH, prolactin, and IGF-1 are important systemic factors in galactopoiesis. The significance of these factors in secretory disease is not well documented but it has been asserted that the mechanisms of secretory disease and galactopoiesis are closely related.

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

Acromegaly may present with symptoms of non-puerperal mastitis.

Microscopic pathology

Histopathology of granulomatous mastitis shows characteristic distribution of granulomatous inflammation which remains the gold standard for diagnosis.[5]

Histologically, lupus mastitis is seen as lymphocytic lobular panniculitis and hyaline sclerosis of the adipose tissue. This histologic finding is required to make an accurate diagnosis.[6]

References

  1. Amir LH, Garland SM, Lumley J. (2006). "A case-control study of mastitis: nasal carriage of Staphylococcus aureus". BMC Family Practice. 7: 57. doi:10.1186/1471-2296-7-57.
  2. Amir LH, Garland SM, Lumley J. (2006). "A case-control study of mastitis: nasal carriage of Staphylococcus aureus". BMC Family Practice. 7: 57. doi:10.1186/1471-2296-7-57.
  3. Peters F, Schuth W (1989). "Hyperprolactinemia and nonpuerperal mastitis (duct ectasia)". JAMA. 261 (11): 1618–20. PMID 2918655.
  4. Kutsuna S, Mezaki K, Nagamatsu M, Kunimatsu J, Yamamoto K, Fujiya Y; et al. (2015). "Two Cases of Granulomatous Mastitis Caused by Corynebacterium kroppenstedtii Infection in Nulliparous Young Women with Hyperprolactinemia". Intern Med. 54 (14): 1815–8. doi:10.2169/internalmedicine.54.4254. PMID 26179543.
  5. Ocal K, Dag A, Turkmenoglu O, Kara T, Seyit H, Konca K (2010). "Granulomatous mastitis: clinical, pathological features, and management". Breast J. 16 (2): 176–82. doi:10.1111/j.1524-4741.2009.00879.x. PMID 20030652.
  6. Summers TA, Lehman MB, Barner R, Royer MC (2009). "Lupus mastitis: a clinicopathologic review and addition of a case". Adv Anat Pathol. 16 (1): 56–61. doi:10.1097/PAP.0b013e3181915ff7. PMID 19098467.

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