A detailed history is obtained from each patient. This history should include risk factors for the development of breast cancer. Following this, a thorough clinical examination is performed. It is policy in our unit to perform mammography in all women over the age of 35 years. Women with a discrete lump will undergo ultrasound examination of the questionable area and then either fine-needle aspirate biopsy (FNAB) or core biopsy.
Symptomatic discrete cystic lesions will be aspirated. Patients less than 35 years of age will undergo ultrasound examination of discrete lesions and a similar management protocol as outlined above. In some rare cases, magnetic resonance imaging (MRI) is performed in addition to mammography and ultrasound in order to establish the diagnosis.
Once a firm diagnosis is established and a management plan instituted, the patient is reassured and discharged.
It is useful to provide both general practitioner and patient with detailed information leaflets that outline the unit’s management protocols. In general, it is our policy not to excise benign breast lumps once a clear diagnosis is established. Instead, our unit practices the philosophy that these lesions have little, if any, premalignant potential and symptoms will most likely improve over the passage of time.
Most benign lesions can actually be regarded as aberrations of normal processes. It has been presented that the borderline between a normal change and a disease should be more defined in relation to their clinical aspects than to histologic findings (Hughes 1991).
The most common benign disorder, fibrocystic change, affects 40–50% of premenopausal women (Sohn et al. 1999). It is a unified term for several proliferative, but nonneoplastic parenchymal alterations, which are usually bilateral and multifocal (Tavassoli 1992). The histologic pattern in each case is varying and may include pure fibrocystic lesions (duct ectasia, cysts, fibrosis, adenosis, ductal epithelial proliferation), focal fibrosis, ductal and lobular epithelial hyperplasia (also atypical) and microcystic and fibrous mastopathy due to involutional change (Sohn et al. 1999).
Fibroadenoma is the most common tumor in young and adolescent women. It arises as a localized hypertrophy of the TDLU and contains structures resembling terminal ducts and expanded stromal tissue (Sewell 1995). Both the stroma cellularity and the epithelial component of fibroadenoma varies, which may lead to misinterpretations in differential diagnosis between fibroadenoma and phyllodes tumor or carcinoma (Rosen 2001). After menopause, fibroadenomas degenerate and may develop large, coarse calcifications. Multiple tumors occur in about 15% of cases, and sometimes the tumor may grow to involve the whole breast, known as adolescent giant fibroadenoma (Rosen 2001). Carcinoma may develop in a fibroadenoma in 1–2% of cases (Sohn et al. 1999).
Phyllodes tumor, previously known as cystosarcoma phyllodes, arises from periductal stroma and contains sparse lobular elements (Rosen 2001). Increased cellularity of the stromal components is characteristic and separates phyllodes tumor from fibroadenoma. Although usually benign, some tumors show increased mitotic activity, pronounced overgrowth of the stroma and aggressive peripheral growth, turning it into malignancy (Sewell 1995).
Papilloma arises in the duct epithelium as papillary projections with or without fibrous cores (Rosen 2001). It is usually a solitary tumor, but may also present as multiple lesions (Sewell 1995). The term intraductal papilloma refers to a lesion in a cystically dilated duct (Rosen 2001). Clinically, papilloma often becomes evident because of nipple discharge, which may be bloody or non-bloody (Rosen 2001). It is a low-risk lesion, but may develop atypical and precancerous cell populations (Sewell 1995).
Radial sclerosing lesion, also known as radial scar is usually an incidental finding at mammography and presents as a stellate lesion mimicking cancer. It is a benign lesion with a central fibrous core surrounded by contracted ducts and lobules, which may show different types of proliferation including atypic and precancerous changes (Rosen 2001). The etiology is unproved, but it has been presented that it might be due to an inflammatory process resulting in scar formation or slow infarction (Sewell 1995).
Ductal hyperplasia has no specific clinical or pathologic features, and it does not usually present as a palpable tumor. Microscopically, there is epithelial proliferation in the ductal system and it is often present in tissue with fibrocystic changes (Rosen 2001). Atypical ductal hyperplasia refers to a monoclonal neoplastic proliferation within a ductus already occupied by ordinary hyperplasia (Sewell 1995). It is close to intraductal carcinoma, but does not fulfill all the criteria (Rosen 2001).
In puerperal mastitis, accumulation of milk provides a microenvironment for bacterial (usually Staphylococcus aureus) growth. Without treatment it may lead to abscess formation. In chronic state, fistulas are seen. The pathogenesis is uncertain and histologic findings depend on chronicity of the process (Rosen 2001). Plasma cell mastitis is a form of periductal mastitis characterized by an intense plasmasytic reaction to retained secretion in the ducts. Histologically, there is hyperplasia of duct epithelium surrounded by plasma cell infiltrate. Both the acute and mature phases may be difficult to distinguish from carcinoma. (Rosen 2001.)
- Roberts MM, Elton RA, Robinson SE et al. Consultations for breast disease in general practice and hospital referral patterns. Br J Surg 1987; 74:1020-1022.
- Cochrane RA, Singhal H, Monypenny IJ et al. Evaluation of general practitioner referrals to a specialist breast clinic according to the UK national guidelines. Eur J Surg Oncol 1997; 23:198-201.
- Hughes LE, Mansel RE, Webster DJT. Aberrations of normal development and involution (ANDI): A new perspective on pathogenesis and nomenclature of benign breast disorders. Lancet 1987; 2:1316-1319.
- Minton JP, Foecking MK, Webster DJ et al. Response of fibrocystic disease to caffeine withdrawal and correlation of cyclic nucleotides with breast disease. Am J Obstet Gynecol 1979; 135:157-158.
- Boyd NF, McGuire V, Shannon P et al. Effect of a low-fat high-carbohydrate diet on symptoms of cyclical mastopathy. Lancet 1988; 2:128-32.
- Horrobin DF. The effects of gamma-linolenic acid on breast pain and diabetic neuropathy: possible noneicosanoid mechanisms. Prostaglandins Leuko Essent Fatty Acids 1993; 48:101-104.
A.D. Purushotham, P. Britton and L. Bobrow
A prospective study of benign breast disease and the risk of breast cancer. JAMA 2002