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Subareolar abscess

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Also called Zuska's disease (only nonpuerperal case), subareolar abscess is a subcutaneous abscess of the breast tissue beneath the areola of the nipple. It is a frequently aseptic inflammation and has been associated with squamous metaplasia of lactiferous ducts.

Subareolar abscess can develop both during lactation or extrapuerperal, the abscess is often flaring up and down with repeated fistulation.

90% of cases are smokers, however only a very small fraction of smokers appear to develop this lesion. It has been speculated that either the direct toxic effect or hormonal changes related to smoking could cause squamous metaplasia of lactiferous ducts. It is not well established whether the lesion regresses after smoking cessation.

Extrapuerperal cases are often associated with hyperprolactinemia or with thyroid problems.[citation needed]

Treatment is problematical unless an underlying endocrine disorder can be successfully diagnosed and treated.

The inflammation should be controlled by bromocriptine even in absence of hyperprolactinemia.[1]

Antibiotic treatment is given in case of acute inflammation. However, this alone is rarely effective, and the treatment of a subareaolar abscess is primarily surgical. In case of an acute abscess, incision and drainage are performed, followed by antibiotics treatment. However, in contrast to peripheral breast abscess which often resolves after antibiotics and incision and drainage, subareaolar breast abscess has a tendency to recur. In many cases, in particular in patients with recurrent subareolar abscess, the excision of one or several ducts is indicated, together with the excision of any chronic abscess or fistula. This can be performed using radial or circumareolar incision.[2]

Duct resection has been traditionally used to treat the condition, the original Hadfield procedure has been improved many times but long term success rate remains poor even for radical surgery.[3] Petersen even suggests that damage caused by previous surgery is a frequent cause of subareolar abscesses.[4] Goepel and Pahnke and other authors recommend performing surgeries only with concomitant bromocriptine treatment.[1]

Squamous metaplasia of lactiferous ducts

Micrograph of squamous metaplasia of lactiferous ducts. H&E stain.

Squamous metaplasia of lactiferous ducts - abbreviated SMOLD is a change where the normal double layer cuboid epithelium of the lactiferous ducts is replaced by squamous keratinizing cell layers. The resulting epithelium is very similar to normal skin, hence some authors speak of epidermalization. SMOLD is rare in premenopausal women (possibly 0.1-3%) but more frequent (possibly up to 25%) in postmenopausal women where it does not cause any problems at all.

SMOLD appears to be a completely benign lesion and may exist without causing any symptoms. In principle it ought to be completely reversible as the classification as metaplasia would suggest. Because of difficulties in observing the actual changes and rare incidence of the lesion this does not appear to be documented.

The last section of the lactiferous ducts is always lined with squamous keratinizing epithelium which appears to have important physiological functions. For example the keratin forms plugs sealing the duct entry and has bacteriostatic properties. In SMOLD the keratinizing lining which is supposed to form only the ends of the lactiferous ducts extends deep into the ducts.

SMOLD is distinct from squamous metaplasia that may occur in papilomatous hyperplasia. It is believed to be unrelated to squamous cell carcinoma of the breast which probably arises from different cell types.

The keratin plugs (debris) produced by SMOLD have been proposed as the cause for recurrent subareolar abscesses by causing secretory stasis. The epidermalized lining has also different permeability than the normal lining, hindering resorption of glandular secretions. The resorption is necessary to dispose of stalled secretions inside the duct - and at least equally important it affects osmotic balance which in turn is an important mechanism in the control of lactogenesis (this is relevant both in puerperal and nonpuerperal mastitis).

While in lactating women this would appear to be a very plausible pathogenesis, there is some uncertainty about the pathogenesis in non-lactating women where breast secretions should be apriori minimal. It appears pathologic stimulation of lactogenesis must be present as well to cause subareolar abscess and treatment success with bromocriptin appears to confirm this[1] as compared to poor success rate of the usual antibiotic and surgical treatments documented by Hanavadi et al.[3]

Further uncertainty in the relation of SMOLD and the subareolar abscess is that squamous metaplasia is very often caused by inflammatory processes. SMOLD could be the cause of the inflammation - or the result of a previous or longstanding inflammation.

SMOLD usually affects multiple ducts and frequently (relative to extremely low absolute prevalence) both breasts hence it is very likely that systemic changes such as hormonal interactions are involved.

At least the following factors have been considered in the aetiology of SMOLD: reactive change to chronic inflammation, systemic hormonal changes, smoking, dysregulation in beta-catenin expression, changes in retinoic acid and vitamin D metabolism or expression.

Vitamin A deficiency may cause epidermilization of the ducts and squamous metaplasia and likely also contributes to infection.[5] Vitamin A deficiency has been observed to cause squamous metaplasia in many types of epithelia. However supplementation with Vitamin A would be beneficial only in exceptional cases because normally the local catabolism of vitamin A will be the regulating factor.

Squamous metaplasia of breast epithelia is known to be more prevalent in postmenopausal women (where it does not cause any problems at all). Staurosporine, a nonspecific protein kinase C inhibitor can induce squamous metaplasia in breast tissue while other known PKC inhibitors did not show this effect. cAMP stimulation can also induce squamous metaplasia.[6]

References

  1. ^ a b c Goepel E, Pahnke VG (1991). "[Successful therapy of nonpuerperal mastitis – already routine or still a rarity?]". Geburtshilfe Frauenheilkd (in German). 51 (2): 109–16. doi:10.1055/s-2007-1023685. PMID 2040409.
  2. ^ Michael S. Sabel (2009). Essentials of Breast Surgery. Elsevier Health Sciences. pp. 85–88. ISBN 0-323-03758-5.
  3. ^ a b Hanavadi S, Pereira G, Mansel RE (2005). "How mammillary fistulas should be managed". Breast J. 11 (4): 254–6. doi:10.1111/j.1075-122X.2005.21641.x. PMID 15982391.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  4. ^ Petersen EE (2003). Infektionen in Gynäkologie und Geburtshilfe. Thieme Georg Verlag. ISBN 3-13-722904-9.
  5. ^ Michael S. Sabel (2009). Essentials of Breast Surgery. Elsevier Health Sciences. p. 86. ISBN 0-323-03758-5.
  6. ^ Heffelfinger SC, Miller MA, Gear R, Devoe G (1998). "Staurosporine-induced versus spontaneous squamous metaplasia in pre- and postmenopausal breast tissue". J. Cell. Physiol. 176 (2): 245–54. doi:10.1002/(SICI)1097-4652(199808)176:2<245::AID-JCP3>3.0.CO;2-O. PMID 9648912.{{cite journal}}: CS1 maint: multiple names: authors list (link)
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