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    Hormon-hormon glucocorticoid bertanggung jawab untuk pengembangan stretch mark mempengaruhi

    dermis dengan mencegah fibroblast dari pembentukan serat kolagen dan elastin, yang diperlukan untuk

    menjaga kulit cepat tumbuh kencang. Hal ini menciptakan kurangnya materi pendukung, seperti kulit

    ditarik dan menyebabkan merobek dermal dan epidermal.

    Pada rongga tubuh dan peritoneum, kortisolmenghambatproliferasifibroblasdansintesissenyawainterstitialsepertikolagen.

    Kelebihanglukokortikoidtermasuk kortisol dapat mengakibatkan penipisan

    lapisankulitdanjaringan penghantaryang menopangpembuluh darahkapiler. Hal ini dapat

    membuat tubuh menjadi lebih rentan dan mudahcedera.

    Elastosis fokus linear, juga dikenal sebagai striae elastotic, adalah gangguan elastotic jarang ditandai

    dengan teraba, putih / kuning / merah band linear dan plak klinis, dan peningkatan jaringan elastis tidak

    teratur histologis. Gangguan ini pertama kali dijelaskan dalam tiga pria Kaukasia tua yang disajikan

    dengan garis kuning, teraba, dan simetris pada kedua sisi bagian belakang (Burket, Zelickson, & Padilla,

    1989). Ada sekitar 20 kasus elastosis fokus linear dijelaskan dalam literatur. Ini memiliki dominasi laki-

    laki sedikit dan telah dilaporkan di Afrika-Amerika, Kaukasia, dan orang Asia berkisar dari 7 sampai 89

    tahun usia.

    Penyebab elastosis fokus linear tidak diketahui. Namun, telah dihipotesiskan bahwa gangguan ini

    mungkin merupakan hasil dari proses degeneratif-regeneratif ekstrim mirip dengan "keloid serat elastis"

    (Hashimoto, 1998). Lesi akut dapat muncul untuk tumbuh, berwarna merah muda, dan pada elastolysis

    menunjukkan biopsi, sedangkan lesi kronis tetap stabil, memiliki eritema tidak ada, dan menunjukkan

    elastogenesis pada biopsi (Choi et al., 2000). Selain itu, belum ada asosiasi yang dikenal antara gangguan

    dan infeksi atau gangguan autoimun.

    http://id.wikipedia.org/wiki/Proliferasihttp://id.wikipedia.org/wiki/Proliferasihttp://id.wikipedia.org/wiki/Fibroblashttp://id.wikipedia.org/wiki/Fibroblashttp://id.wikipedia.org/wiki/Fibroblashttp://id.wikipedia.org/wiki/Sintesishttp://id.wikipedia.org/wiki/Sintesishttp://id.wikipedia.org/wiki/Senyawa_organikhttp://id.wikipedia.org/wiki/Senyawa_organikhttp://id.wikipedia.org/wiki/Cairan_tubuhhttp://id.wikipedia.org/wiki/Cairan_tubuhhttp://id.wikipedia.org/wiki/Cairan_tubuhhttp://id.wikipedia.org/wiki/Kolagenhttp://id.wikipedia.org/wiki/Kolagenhttp://id.wikipedia.org/wiki/Kolagenhttp://id.wikipedia.org/wiki/Glukokortikoidhttp://id.wikipedia.org/wiki/Glukokortikoidhttp://id.wikipedia.org/wiki/Kulithttp://id.wikipedia.org/wiki/Kulithttp://id.wikipedia.org/wiki/Kulithttp://id.wikipedia.org/w/index.php?title=Jaringan_penghantar&action=edit&redlink=1http://id.wikipedia.org/w/index.php?title=Jaringan_penghantar&action=edit&redlink=1http://id.wikipedia.org/w/index.php?title=Jaringan_penghantar&action=edit&redlink=1http://id.wikipedia.org/wiki/Pembuluh_darahhttp://id.wikipedia.org/wiki/Pembuluh_darahhttp://id.wikipedia.org/wiki/Pembuluh_darahhttp://id.wikipedia.org/wiki/Cederahttp://id.wikipedia.org/wiki/Cederahttp://id.wikipedia.org/wiki/Cederahttp://id.wikipedia.org/wiki/Cederahttp://id.wikipedia.org/wiki/Pembuluh_darahhttp://id.wikipedia.org/w/index.php?title=Jaringan_penghantar&action=edit&redlink=1http://id.wikipedia.org/wiki/Kulithttp://id.wikipedia.org/wiki/Glukokortikoidhttp://id.wikipedia.org/wiki/Kolagenhttp://id.wikipedia.org/wiki/Cairan_tubuhhttp://id.wikipedia.org/wiki/Senyawa_organikhttp://id.wikipedia.org/wiki/Sintesishttp://id.wikipedia.org/wiki/Fibroblashttp://id.wikipedia.org/wiki/Proliferasi
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    PEMERIKSAAN PENUNJANG

    1. Uji supresi deksametason.

    Mungkin diperlukan untuk membantu menegakkan diagnosis peyebabsindrom cushingtersebut,

    apakahhipopisis atau adrenal.

    2. Pengambilan sampele darah.

    Untuk menentukan adanya varyasi diurnal yang normal pada kadar kortisol, plasma.

    3. Pengumpulan urine 24 jam.

    Untuk memerikasa kadar 17 hiroksikotikorsteroid serta 17ketostoroid yang merupakan

    metabolik kortisol dan androgen dalam urine.

    4. Stimulasi CRF.Untuk membedakan tumor hipofisis dengan tempattempat tropi.

    5. Pemeriksaan radioimmunoassay

    Mengendalikan penyebabsindrom cushing

    6. Pemindai CT, USG atau MRI.

    Untuk menentukan lokasi jaringan adrenal dan mendeteksi tumor pada kelenjar adrenal.

    Kolagen: protein rantai panjang yang tersusun lagi atas asam amino alanin, arginin, lisin, glisin, prolin,

    serta hiroksiproline daya regang yang tinggi

    Elastin: protein jaringan penunjang kaya glisin dan alanin elastisitas tinggi

    Alanin adlah asam amino

    kehamilan Kategori

    A: Umumnya diterima. Studi terkontrol pada wanita hamil tidak menunjukkan bukti risiko janin.

    B: Mungkin diterima. Entah studi hewan tidak menunjukkan risiko tetapi penelitian manusia studi tidak

    tersedia atau hewan menunjukkan risiko kecil dan studi manusia dilakukan dan menunjukkan tidak ada

    resiko.

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    C: Gunakan dengan hati-hati jika manfaat lebih besar daripada risiko. Penelitian terhadap hewan

    menunjukkan penelitian risiko dan manusia tidak tersedia atau tidak hewan atau studi manusia

    dilakukan.

    D: Gunakan dalam KEHIDUPAN-MENGANCAM darurat ketika tidak ada obat yang lebih aman tersedia.

    Positif bukti risiko janin manusia.

    X: Jangan gunakan pada kehamilan. Risiko lebih besar daripada manfaat potensial. Ada alternatif yang

    lebih aman.

    NA: Informasi tidak tersedia.

    BIOCUTIS

    Are you wondering what causes and how to prevent and treat stretch marks?

    You can wisely choose how to prevent and treat them once you understand that the skin is

    composed of the intercellular elements that serve as scaffolds for the different structural elements

    of the skin. These elements are in charge of the skins mechanical properties: firmness, strength,

    suppleness, and elasticity.

    Stretch marks affect skin that is subjected to continuous and progressive stretching; increased

    stress is placed on the connective tissue due to increased size of the various parts of the body.

    It occurs on the abdomen and the breasts of pregnant women, on the shoulders of body builders, in

    adolescents undergoing their growth spurt, and in individuals who are overweight.

    It has also been suggested that they develop more easily in skin that has a high proportion of rigid

    cross-linked collagen, as occurs in early adult life.

    Prolonged use of oral or topical corticosteroids or Cushing syndrome (increased adrenal cortical

    activity) leads to the development of stretch marks. Genetic factors could certainly play a role,

    although this is not fully understood.

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    The most commonly affected areas of the body include the abdominal area, thighs, upper arms,

    breasts, hips, and lower back.

    Causes of stretch marks (stria)

    Dermal inflammation and dilated capillaries mark the initial presentation, which results in anerythematous appearance with characteristic pink, lavender, and purple hues. Later, striae appear

    hypopigmented and fibrotic. Pathogenesis remains unclear, although estrogen and mast cell

    degranulation with elastolysis may be contributing factors.

    Skin distension apparently leads to excessive mast cell degranulation with subsequent immoderate

    inflammation that damages collagen and elastin connective skin tissues.

    It has been postulated that stretch marks may result from an exaggerated wound healing process,

    and, clinically in pregnancy at least the severity of stetch marks appears to be related to a

    younger maternal age, although the age of onset of stretch marks was not recorded bySalteret

    al. (2006). Of further interest is a significantly higher occurrence of varicosities in those individualsalso presenting with stretch marks. It is plausible that these phenomena describe a generalized

    deterioration of extracellular matriz structures that could result from a number of biological events.

    Mast cell degranulation and elastolysis in the early stage of striae distensae.

    1.- A mast cell is a free cell of the connective tissue. This means it is able to migrate through

    surrounding extracellular matrix using its pseudopodes (or filopodes) which are several

    micrometers long and motile. The mast cell cytoplasma contains several hundred vesicles

    (granules). Mast cells are a normal component of body tissues that play a role in the process of

    tissue repair by releasing inflammatory mediators such as histamine, proteoglycans, and cytokines.

    Mast-cell activation also stimulates the arrival of other inflammatory cellsa critical step in local

    inflammation.

    They start their lives in the bone marrow, leaving it as monocytes released into the bloodstream.

    But the monocyte is really just a transit stage: fairly rapidly a monocyte will find a place to exit the

    vascular system, because theyre really a conective tissue cell. They enter intercellular spaces,

    where they settle down and complete their final differentiation into the definitive mast cell

    morphology. Mast cells are involved in allergy, acute and chronic inflammation processes, T-cell

    activation and tissue defense of parasites. Their function is improper in many deseases of the skin

    e.g., psoriasis, chronic eczema, sclerodermia, lichen simplex and planus.

    2.- Elastolysis is characterized by degenerative changes in the elastic fibers resulting in loose,

    pendulous skin. The skin is sagging, redundant, and stretchable, with reduced elastic recoil.

    Alterations in the quantity or the morphology of elastin in which fragmentation or a loss of elastic

    fibers is present. Abnormal cross-linking of elastin may also exist.

    http://www.nature.com/jid/journal/v126/n8/full/5700316a.htmlhttp://www.nature.com/jid/journal/v126/n8/full/5700316a.htmlhttp://www.nature.com/jid/journal/v126/n8/full/5700316a.htmlhttp://www.nature.com/jid/journal/v126/n8/full/5700316a.htmlhttp://www.nature.com/jid/journal/v126/n8/full/5700316a.htmlhttp://www.nature.com/jid/journal/v126/n8/full/5700316a.htmlhttp://www.nature.com/jid/journal/v126/n8/full/5700316a.htmlhttp://www.nature.com/jid/journal/v126/n8/full/5700316a.html
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    Studies have shown that several factors, such as copper deficiency, lysyl oxidase, elastases, and

    elastase inhibitors, contribute to abnormal elastin degradation. Lysyl oxidase, a copper-dependent

    enzyme, is important in the synthesis and cross-linking of elastin and collagen. Therefore, low levels

    of serum copper could lead to diminished elastin synthesis. However, only a few patients with cutis

    laxa (elastolysis) have demonstrated low serum copper levels. Defective copper utilization may also

    lead to decreased activity of elastase inhibitor alpha-1 antitrypsin, resulting in destruction of elastic

    fibers.

    Cultured dermal fibroblasts from patients with cutis laxa (elastolysis) have shown increased

    elastolytic activity compared with healthy skin, and elastolysis has been suggested to result from

    increased elastase activity.

    Inflammatory cells or their mediators might damage elastic fibers. Polymorphonuclear leukocytes

    and macrophages release elastases, which could damage elastic fibers with subsequent

    phagocytosis.

    Excessive loss of cutaneous elastin in one patient with cutis laxa (elastolysis) appeared to be related

    to the combined effects of low lysyl oxidase activity with high levels of cathepsin G, an elastolytic

    protease. However, variations in the morphology of the elastic fibers among skin samples from

    individuals with cutis laxa (elastolysis) suggest that the biochemical basis of the disorder may be

    heterogeneous. Indeed, cutis laxa (elastolysis) could result from mutations that affect the synthesis,

    the stabilization, or the degradation of elastic fibers.

    3.- According to Sheu HM, Yu HS, Chang CH. Department of Dermatology, Kaohsiung Medical

    College, Taiwan, R.O.C.Journal of Cutaneous Pathology01/01/1992; 18(6):410-6. ISSN: 0303-

    6987: The lesions of nine patients with early striae distensae (SD = stretch marks) during puberty

    were examined by light and electron microscopy. Specific changes were seen in very early stage SD,

    and in clinically uninvolved skin 0.5 to 3 cm remote from the edge of the long axis of the stretch

    mark lesions.

    Sequential changes of elastolysis accompanied by mast cell degranulation appeared first,followed

    by an influx of activated macrophages that enveloped fragmented elastic fibers. The relationships

    among elastic fibers, mast cells, and macrophages seen suggest their critical roles in the process of

    stretch marks formation, especially in the early stage.

    Our results also indicate that the elastic fiber is the primary target of the pathological process, and

    the abnormalities extend as far as 3 cm beyond the lesion into normal skin.

    Stretch marks can vary in appearance however; many are much like scars as they take on a shiny,

    depressed texture and redish color. Over time it is possible that this appearance can fade. The scar

    can be reduced and the reddish lines can become lighter in color.

    Pregnancy: the main occasion of stretch marks

    https://www.researchgate.net/journal/0303-6987_Journal_of_Cutaneous_Pathologyhttps://www.researchgate.net/journal/0303-6987_Journal_of_Cutaneous_Pathologyhttps://www.researchgate.net/journal/0303-6987_Journal_of_Cutaneous_Pathologyhttps://www.researchgate.net/journal/0303-6987_Journal_of_Cutaneous_Pathology
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    Pregnancy is a beautiful time with a number of ugly consequences. Many of those occur with the

    skin due to hormonal changes as well as the physical changes the body undergoes when expecting.

    The most commonly experienced consequence is stretch marks. Skin becomes thinner during

    pregnancy because of high hormone levels that disrupt the skins equilibrium. By the third

    trimester, about 90 % of women have experienced stretch marks. These marks could be disgusting,

    but luckily there are options available for stretch mark removal.

    Stretch Mark Removal by Surgery

    A popular way to get rid of stretch marks is by surgery. Tummy tucks, or more medically known as

    abdominoplasties remove skin in the area under the belly button. During pregnancy, this is where

    the majority of stretch marks appear. Removal of this area eliminates stretch marks entirely.

    No matter where you experience stretch marks the surgery can be done as long as there is an

    excess of skin. Surgeries always come with the risk of scarring as well. However, these will be low

    enough to cover up with clothing. And with proper care and treatment, they can be completely

    faded within the first year after surgery.

    Seek Natural Alternatives

    Are you determined to do something about your stretch marks before they get worse?

    Unfortunately, health insurance does not always cover aesthetic surgeries such as this one. The cost

    depends on where you get the procedure done. An estimated price could range from 4000 to 7500

    dollars. Therefore, it is in your best interest to evade stretch marks all together by preventing their

    appearance by using particular natural products.

    You dont have to pay for expensive treatments. Instead, why not try a more natural approach that

    is helping thousands of people forget their stretch marks.

    The best way to treat stretch marks is with natural products. Bio Body Cream eliminates stretch

    marks by dissolving and renewing damaged tissues. This stretch mark scar removal cream is able to

    digest scar tissue and moisturize your skin with its specially formulated biological ingredients.

    Avoid expensive plastic surgeries and get rid of stretch marks the natural way with effective and

    organic Biocutis skin treatment products.