adenosis sklerosis

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1. Adenosis Nama lain: hiperplasi duktus, papillomatosis duktus, sclerosing adenosis, adenomatosis. Kelainan utama yang tampak ialah dominasi daripada hiperplasi epitel, tetapi dapat juga ditemukan fibrosis dan kelainan kistik. Kelainan ini sering ditemukan pada usia 35 - 45 tahun. Makroskopik tampak suatu daerah yang konsistensinya keras, tidak berbatas jelas, pada penampang dapat ditemukan kista-kista.Gambaran tumor dengan konsistensi keras ini harus dibedakan dengan karsinoma. Pada penampang karsinoma payudara dapat ditemukan chalk streaks, yaitu daerah keputih-putihan yang terjadi karena nekrosis sel-sel. Chalk streaks tidak ditemukan pada adenosis. Gambaran mikroskopik menunjukkan: 1. hiperplasi intraduktus. 2. papilomatosis intraduktus. 3. reduplikasi dan proliferasi kelenjar. 4. pertambahan stroma. Jaringan ikat dapat menekan duktus sehingga lumennya menghilang dan yang tampak hanya gencel-gencel epitel di antara stroma yang padat, dinamai sclerosing adenosis. Gambaran ini menyerupai infiltrasi sel karsinoma. Gambaran serupa, sehingga sukar dibedakan antara hiperplasi epitel duktus dan karsinoma duktus, menyebabkan adanya pendapat bahwa jenis mammary dysplasia golongan ini mempunyai

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Page 1: Adenosis Sklerosis

1. Adenosis

Nama lain: hiperplasi duktus, papillomatosis duktus, sclerosing adenosis,

adenomatosis. Kelainan utama yang tampak ialah dominasi daripada hiperplasi

epitel, tetapi dapat juga ditemukan fibrosis dan kelainan kistik. Kelainan ini sering

ditemukan pada usia 35 - 45 tahun. Makroskopik tampak suatu daerah yang

konsistensinya keras, tidak berbatas jelas, pada penampang dapat ditemukan kista-

kista.Gambaran tumor dengan konsistensi keras ini harus dibedakan dengan

karsinoma.

Pada penampang karsinoma payudara dapat ditemukan chalk streaks, yaitu

daerah keputih-putihan yang terjadi karena nekrosis sel-sel.

Chalk streaks tidak ditemukan pada adenosis. Gambaran mikroskopik

menunjukkan:

1. hiperplasi intraduktus.

2. papilomatosis intraduktus.

3. reduplikasi dan proliferasi kelenjar.

4. pertambahan stroma.

Jaringan ikat dapat menekan duktus sehingga lumennya menghilang dan yang

tampak hanya gencel-gencel epitel di antara stroma yang padat, dinamai sclerosing

adenosis. Gambaran ini menyerupai infiltrasi sel karsinoma. Gambaran serupa,

sehingga sukar dibedakan antara hiperplasi epitel duktus dan karsinoma duktus,

menyebabkan adanya pendapat bahwa jenis mammary dysplasia golongan ini

mempunyai incidence yang lebih tinggi ke arah perubahan menjadi ganas.

Kepentingan klinik mammary dysplasia. Berbagai gambaran patologik pada

mammary dysplasia secara klinik penting karena 2 hal, yaitu:

kelainan ini mengakibatkan tonjolan yang harus dibedakan dengan karsinoma.

predisposisi untuk terjadinya karsinoma.

Adenosis sklerosa ditandai dengan fibrosis intralobuler dan proliferasi saluran epitelial

kecil dan sel myoepitel. Lesi tersebut dapat disangka karsinoma invasif, tetapi

kecenderungannya untuk mempertahankan posisi sel epitel dan sel myoepitel yang

Page 2: Adenosis Sklerosis

saling berhadapan dan pola pertumbuhan lobulernya merupakan kunci untuk mengenali

sifat jinaknya.

Penyakit fibrokistik Payudara

Ada sejumlah perubahan jaringan payudara yang berhubungan dengan penyakit

fibrokistik. Yang termasuk didalamnya adalah pembentukan kista, proliferasi duktus epitalia,

papilomatosis difusa, dan adenosis duktus dengan pembentukan jaringan fibrosa. Secara klinis,

perubahan-perubahan ini dapat menimbulkan nodula yang teraba, massa, dan keluarnya cairan

dari puting. Penyakit fibrokistik payudara terjadi pada masa dewasa; penyebab kemungkinan

besar berhubungan dengan kelebihan estrogen dan defisiensi progesteron selama fase luteal

siklus menstruasi. Sekitar 50% perempuan mengalami penyakit fibrokistik payudara. Keadaan

ini biasanya terjadi bilateral.

Sekitar 30% perempuan dengan penyakit fibrokistik yang terbukti dengan biopsi,

mengalami hiperplasia proliferatif; hal ini penting karena jenis perubahan ini berkaitan dengan

peningkatan resiko berkembangnya karsinoma di masa yang akan datang. Untuk pasien dengan

hiperplasia epitelial sederhana (sekitar 25% dari semua kasus penyakit fibrokistik) resiko

berkembangnya karsinoma selanjutnya adalah dua kali lebih besar. Pada kasus lain, terdapat

beberapa abnormalitas dalam sitologi sel dan arsitekturnya, namun tidak semua gambaran

karsinoma in situ menggunakan istilah atipikal hirperplasia. Pada perempuan dengan atipikal

hiperplasia (sekitar 5% dari kasus), resiko berkembangnya karsinoma selanjutnya adalah lima

kali lebih besar.

Gejala-gejalanya berupa pembengkakan dan nyeri tekan pada payudara menjelang

periode menstruasi. Tanda-tandanya adalah teraba massa yang bergerak bebas pada payudara,

terasa granularitas pada jaringan payudara, dan kadang-kadang keluar cairan yang tidak berdarah

dari puting. Banyak perempuan tidak mengeluhkan gejala dan baru mencari pemeriksaan

kesehatan setelah meraba adanya massa.

Penanganannya adalah meredekan gejala nyeri tekan payudara dengan analgetik ringan

dan pemanasan lokal. Perbaikan dapat dicapai dengan menghindari kopi, teh, cola, dan coklat

(mengandung metilxantin); keju, minuman anggur, kacang-kacangan, jamur, dan pisang

(mangandung tiramin); dan tembakau (mengandung nikotin). Kira-kira 30% perempuan dengan

penyakit fibrokistik yang terbukti dengan biopsi mengalami hiperplasia proliferatif, yang

Page 3: Adenosis Sklerosis

meningkatkan resiko kanker payudara hingga tiga kali resiko pada umumnya. Masalah utama

bagi ahli kesehatan adalah membedakan massa yang disebabkan penyakit fibrokistik keganasan.

Hubungan Kelainan Fibrokistik dengan Karsinoma Payudara

Hubungan perubahan fibrokistik dengan karsinoma payudara merupakan suatu masalah

medis yang kontroversial. Di buku ini hanya dapat diajukan beberapa pernyataan ringkasan yang

cukup memiliki dasar. Secara klinis, meskipus beberapa gambaran tertentu pada perubahan

fibrokistik cenderung membedakannya dengan kanker, satu-satunya cara pasti untuk membuat

pembedaan ini adalah denan biopsi dan pemeriksaan histologik. Dalam kaitannya dengan

hubungan berbagai pola perubahan fibrokistik dengan kanker, pernyataan berikut saat ini

merupakan opini yang paling memiliki dasar.

Tidak ada atau sangat sedikit peningkatan risiko karsinoma payudara; fibrosis, perubahan

kistik (mikro atau makroskopik), metaplasia apokrin, hiperplasia ringan.

Sedikit peningkatan risiko (1,5 hingga 2 kali): hiperplasia sedang sampai subur,

papilomatosis duktus, adenosis sklerotikans, fibroadenoma, terutama jika berkaiitan dengan

perubahan fibrokistik, penyakit payudara proliferatif, atau riwayat kanker payudara dala

keluarga.

Peningkatan risiko yang bermakna (5 kali): hiperplasia atipikal, duktulus atau lobulus.

Lesi proliferatif mungkin multifokal, dan risiko karsinoma berikutnya berlaku untuk kedua

payudara.

Riwayat kanker payudaa dalam keluarga dapat meningkatkan risiko pada semua kategori

(misal, menjadi sekitar sepuluh kali lipat pada hiperplasia atipikal).

Hanya sekitar 15% spesimen bipsi memperlihatkan hiperplasia epitel atipikal. Oleh karena

itu, sebagian besar perempuan yang memiliki benjolan terkait dengan perubahan fibrokistik

dapat diyakinkan bahwa hanya sedikit atau tidak ada peningkatan kerentanan terhadap kanker.

Jelas tampak bahwa berbagai varian perlu dibedakan. Selain itu, terdapat ketidakpuasan dengan

istilah perubahan fibrokistik tanpa kualifikasi atau, yang lebih buruk, penyakit fibrokistik. Resiko

inheren untuk berbagai pola diperlihatkan pada Gambar 7.

Page 4: Adenosis Sklerosis

slerosing adenosis occurs as part of a spectrum of proliferative abnormalities referred to as fibrocystic changes (1). Although sclerosing adenosis may manifest as a clinically palpable mass (adenosis tumor), it is more commonly detected only at mammography.

Sclerosing adenosis may be focal or diffuse at mammography; that is, it may appear as a focal cluster of microcalcifications or as diffuse calcifications. A focus of sclerosing adenosis may be associated with a nodule or with a spiculated lesion, as in this case (1–3).

As the name implies, sclerosing adenosis is a combination of stromal sclerosis and proliferative adenosis pathologically (Fig 2a). Adenosis manifests as a lobulocentric lesion that is largely derived from the terminal ductal lobular unit (TDLU) (1). This condition involves proliferation of ductules and lobules in the TDLU. Both epithelial and myoepithelial cells proliferate. In florid adenosis, hyperplasia of epithelial and myoepithelial cells is associated with distortion and effacement of the underlying lobules. Nuclear pleomorphism and an increase in cell size occur, and the TDLU enlarges (1). In sclerosing adenosis, there is stromal sclerosis involving half or more of the TDLU (4), which is elongated, distorted, and compressed by the sclerosis. Myoepithelial proliferation is a prominent finding (Fig 2b). Sclerosing adenosis contains calcifications in about 50% of cases (5). Calcifications are more common and extensive in sclerosing adenosis than in florid adenosis (1).

Figure 2a.  (a) Low-power photomicrograph (original magnification, ×40; hematoxylin-eosin stain) shows glandular structures of varying sizes (adenosis) with the smaller glands compressed by surrounding stromal sclerosis. (b) Low-power photomicrograph (original magnification, ×40; immunoperoxidase stain with monoclonal antibody HHF-35) demonstrates a layer of cells immunoreactive for muscle actin around each of the small glands. The presence of these myoepithelial cells suggests a benign process (adenocarcinoma of the breast usually has no myoepithelium).

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Page 5: Adenosis Sklerosis

Figure 2b.  (a) Low-power photomicrograph (original magnification, ×40; hematoxylin-eosin stain) shows glandular structures of varying sizes (adenosis) with the smaller glands compressed by surrounding stromal sclerosis. (b) Low-power photomicrograph (original magnification, ×40; immunoperoxidase stain with monoclonal antibody HHF-35) demonstrates a layer of cells immunoreactive for muscle actin around each of the small glands. The presence of these myoepithelial cells suggests a benign process (adenocarcinoma of the breast usually has no myoepithelium).

Sclerosing adenosis may present a diagnostic dilemma for the pathologist because stromal sclerosis and elastosis may mimic infiltrating carcinoma (3). Tubular carcinoma in particular presents a difficulty in differential diagnosis. Absence of the basement membrane and of myoepithelial cells in tubular carcinoma (and their presence in sclerosing adenosis) is helpful in differentiation (5,6). The pathologist must also differentiate sclerosing adenosis from radial scar, which is characterized by more extensive sclerosis with a central fibrocollagenous scar (5).

At mammography, sclerosing adenosis forms part of a differential diagnosis for spiculated lesions that includes both malignant lesions (eg, infiltrating ductal carcinoma, infiltrating lobular carcinoma, tubular carcinoma, ductal carcinoma in situ) and benign lesions (eg, postoperative scar, radial scar, fat necrosis, tuberculosis) (3).

The mammographic differentiation of benign from malignant spiculated lesions is not reliable. Infiltrating carcinoma tends to have a denser center than either sclerosing adenosis or radial scar (3). Microcalcifications are often present in association with spiculated breast carcinomas but may also occur in benign lesions, including sclerosing adenosis (as in this case), radial scar, and fat necrosis.

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Page 6: Adenosis Sklerosis

Histologic features that are useful for the pathologist usually do not aid in mammographic differential diagnosis of spiculated lesions. With the exception of cases involving clear-cut postoperative scarring or fat necrosis (wherein mammographic-clinical correlation may be sufficient), biopsy is mandatory.

Carcinoma in situ rarely develops in an area of sclerosing adenosis but may mimic invasive carcinoma at pathologic examination (7). The presence of an intact basement membrane and myoepithelial cells, both of which are absent in invasive cancer, aids in differential diagnosis (7). In addition, the underlying architecture of adenosis is not altered when ductal or lobular carcinoma in situ develops. Lobular carcinoma in situ is found more often than ductal carcinoma in situ in areas of sclerosing adenosis (1).

Several studies have addressed whether sclerosing adenosis is a precursor lesion or a risk factor for carcinoma. In 1945, Foote and Stewart (8) studied the frequency of fibrocystic changes in patients with and without breast carcinoma and concluded that adenosis, especially sclerosing adenosis, is neither a precursor nor a risk factor. However, subsequent authors have reported an overall relative risk ranging from 1.7 to 2.5 (4,9,10). In and of itself, sclerosing adenosis appears to cause only a mild increase in the risk of infiltrating breast cancer. When atypical hyperplasia is also present, the relative risk rises markedly to as much as 6.7 (4).

In this case, results of both stereotactically guided core needle biopsy and mammographic needle localization with open surgical biopsy confirmed florid sclerosing adenosis. The patient was followed up for 3 years and is presently doing well.

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Page 7: Adenosis Sklerosis
Page 8: Adenosis Sklerosis

Sclerosing adenosis is a benign (i.e., non-cancerous) condition of the breast in which extra tissue develops within the breast lobules, the small portions of the glands that can produce milk.

In women with sclerosing adenosis, multiple small, firm, tender lumps (called nodules); fibrous tissue; and sometimes small cysts (i.e., sacs filled with fluid or semi-solid material) form in the breast. Many women with sclerosing adenosis experience recurring pain that tends to be linked to the menstrual cycle.

In most cases, sclerosing adenosis is detected during routine mammograms or following breast surgery. Usually, a biopsy (i.e., examination of a sample of tissue under the microscope) is required to confirm the diagnosis, because the condition is otherwise difficult to distinguish from breast cancer.

Clinical research suggests that women with sclerosing adenosis may have 1.5 times to twice as high a risk of developing breast cancer than do other women. If you have been diagnosed with sclerosing adenosis, it is especially important to be aware of any future changes or developments in your breasts. As with all matters of the breasts, vigilant attention is key.

Sclerosing adenosis is a type of adenosis, Adenosis is a proliferative lesion of the terminal duct lobular unit characterized by an

increased number of acini that may either produce a mass (florid adenosis, or the extreme, adenosis tumor) or become surrounded by stromal sclerosis (sclerosing adenosis).

Adenosis represents a spectrum of benign alterations of breast tissue. Patients with sclerosing adenosis have an increased risk of breast cancer ranging from

1.7- to 3.7-fold has been reported in most series.

Adenosis and sclerosing adenosis retain the lobular architecture, but it becomes exaggerated and distorted.

The involved lobules show an increased number of acini, which become compressed and obliterated by stromal fibrosis in sclerosing adenosis.

Sclerosing adenosis can be seen as a component of other proliferative lesions, such as intraductal and/or sclerosing papilloma and complex sclerosing lesion, and can be present within fibroadenomas.

Sclerosing adenosis can coexist with both invasive and in situ cancers. Sclerosing adenosis can manifest as a palpable mass or as a suspicious finding at

mammography that consists of architectural distortion, indeterminate microcalcifications, or both.

Page 9: Adenosis Sklerosis

Imaging Findings for Sclerosing adenosis At mammography, sclerosing adenosis may consists of architectural distortion,

indeterminate microcalcifications, or both. Sclerosing adenosis can be difficult to distinguish from infiltrating carcinoma.