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Ophthalmology 2011-Jun

Histologic assessment of dermatochalasis: elastolysis and lymphostasis are fundamental and interrelated findings.

يمكن للمستخدمين المسجلين فقط ترجمة المقالات
الدخول التسجيل فى الموقع
يتم حفظ الارتباط في الحافظة
Kundandeep S Nagi
J Andrew Carlson
Edward J Wladis

الكلمات الدالة

نبذة مختصرة

OBJECTIVE

To determine the presence, degree, and extent of lymphatic, elastic, and collagen fiber alterations in dermatochalasis (DC) specimens.

METHODS

Case control study of patients with DC compared with age-, gender-, and site-matched controls.

METHODS

A total of 25 eyelid specimens were studied; 15 of these were blepharoplasty specimens (experimental) and 10 were entropion/ectropion specimens of patients without DC (controls).

METHODS

The number and maximal dilation of lymphangiectasia was measured by light microscopy, immunohistochemistry with lymphatic marker D2-40, and elastic tissue content by Verhoeff-van Gieson histochemistry. The number of macrophages was compared between patients with DC and controls in CD68 immunostained specimens.

METHODS

Lymphatic density, edema, and inflammation.

RESULTS

Dermatochalasis eyelid specimens showed increased lymphangiectasia density (5.6 vs. 2.4 lymphatics/high power field; P<0.05), maximal lymphatic dilation (127 vs. 51.5 μm; P<0.05), loss of elastic fibers (2.2 vs. 8.9 fibers/high power field; P<0.05), and greater disruption of collagen networks and edema compared with controls (increased stromal collagen bed of 752 vs. 269 μm; P<0.05; increased intercollagen space of 32.5 vs. 11.8 μm; P<0.05). Macrophages were present in greater quantities in DC specimens (28.6 vs. 11.9 macrophages/high power field; P<0.05).

CONCLUSIONS

Patients with DC show an increase in number and maximal dilation of lymphatic vessels in conjunction with widely spaced collagen bundles. This finding coexists with loss of elastic fibers, components known to be essential to the structure and function of the lymphatic system. Governed by macrophages, the pathogenesis of DC may begin with subclinical inflammation leading to elastolysis and secondary lymphostasis.

BACKGROUND

The author(s) have no proprietary or commercial interest in any materials discussed in this article.

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