2004, Número 3
<< Anterior Siguiente >>
Med Cutan Iber Lat Am 2004; 32 (3)
Estudios histopatológicos en la lipodermatoesclerosis asociada a hipertensión venosa: consideraciones fisiopatológicas
Vignale R, Panuncio A, Saralegui P, Di Matteo C, Civila E
Idioma: Ingles.
Referencias bibliográficas: 38
Paginas: 111-116
Archivo PDF: 754.00 Kb.
RESUMEN
La lipodermatoeslerosis (LDS) o paniculitis esclerosante es una induración del dermis, hipodermis y en ocasiones de la fascia superficial. Es un proceso inflamatorio crónico relacionado a una patología venosa, con neovascularización, necrosis grasa y fibrosis. Se postulan varias hipótesis patogénicas, pero el mecanismo exacto se desconoce. En este trabajo estudiamos 6 biopsias cutáneas de 6 pacientes portadores de lipodermatosclerosis crónica. Realizamos estudios inmunohistoquímicos para metaloproteinasas 1, 2 y 3; CD68, actina alfa de musculo liso y cortes semifinos de material incluído en plástico. Nuestros principales hallazgos fueron: los vasos venosos estaban alterados, con luces estrechadas con hiperplasia y fibrosis intimal, algunos vasos arteriales también mostraron fragmentación y reduplicación de la capa elástica interna con fibrosis subintimal. Se encontró una marcada desorganización de la dermis reticular e hipodermis debido a la intensa fibrosis. Se observó asimismo, necrosis grasa pseudomembranosa y pseudoquistes con un infiltrado inflamatorio mixto de disposición parcheada. Las metaloproteinasas 1, 2 y 3 fueron positivas en la epidermis, células endoteliales, algunas células dérmicas e hipodérmicas, alrededor de los pseudoquistes y de necrosis grasa pseudomembranosa. En cortes semifinos de plástico, se observó la presencia de gotas lipídicas entre las fibras colágeno, inclusive en la dermis superficial.
REFERENCIAS (EN ESTE ARTÍCULO)
Jorizzo JL, White WL, Zanolli MD, Greer KE, et al. Sclerosing panniculitis. A clinicopathologic assesment. Arch Dermatol 1991; 127: 554-8.
Kirsner RS, Pardes JB, Eagelstein WH, Falange V. The clinical spectrum of lipodermatosclerosis. J Am Acad Dermatol 1993; 28: 623-7.
Nazchitz JE, Yeshurun D, Misselevich I, Boss JH. The pathogenesis of lipodermatosclerosis: facts, uncertainties amd theories. J Eur Acad Dermatol Venereol 1997; 9: 209-14.
Greemberg AS, Hasan A, Montalvo BM, Falabella A, et al.Acute lipodermatosclerosisis associated with venous insufficiency. J Am Acad Dermatol 1996; 35: 566-8.
Bruce AJ, Bennett DD, Lohse ChM, Rooke TW, et al. Lipodermatosclerosis: Review of cases evaluated at Mayo Clinic. J Am Acad Dermatol 2002; 46: 187-92.
Herouy Y, May AE, Pornschlegel G, Stetter Ch, et al. Lipodermatosclerosis is characterized by elevated expression and activation of matrix metalloproteinases: implications for venous ulcer formation. J Invest Dermatol 1998; 111: 822-7.
Diaz Cascajo C, Borghi S. Subcutaneous pseudomembranous fat necrosis: new observations J Cutan Pathol 2002; 29: 5-10.
Valencia IC, Falabella A, Kirsner RS, Eagelstein WH. Chronic venous insufficiencyand venous ulceration. J Am Acad Dermatol 2001; 44: 401 -21.
Shi SR, Key ME, Kalkra KL. Antigen retrieval in formalin fixed and paraffin embedded tissues. An enhancement method for immunohistochemical staining on microwave oven heating of tissue section. J Histochem Cytochem 1991; 39: 741-8.
Coleridge Smith PD. Deleterious effects of white cells in the course of skin damage in CVI. Int Angiol 2002; 21: 26-32.
Oda M, han JY, Nakamura M. Endothelial cell dysfunction in microvasculature: relevance to disease processes. Clin Hemorheol Microcirc 2000; 23: 199-211.
Leu HJ. Morphology of chronic venous insufficiency- Light and electron microscopic examination. Vasa 1991; 20: 330-42.
Sahary M, Shields DA, Porter JB, Scurr JM, et al. Leucocyte activity in the microcirculation of the legs in patients with chronic venous disease. J Vasc Surg 1997; 26: 265-73.
Carpentier PH. Role of leukocytes in the pathogenesis of trophic venous disorders. J Mal Vasc 1998; 23: 274-6.
Bergan JJ, Schmif-Schonbein GW, Takase S. Therapeutic approach to chronic venous insufficiency and its complications: place of Daflon 500 mg. Angiology 2001; 52: 43-7.
Herouy Y, Aizpurua J, Stetter C, Dichmann S, et al. The role of the urokinase-type plasminogen activator (uPA) and its receptor (CD87) in lipodermatosclerosis. J Cutan Pathol 2001; 28: 291-7.
Chabrier PE. Growth factors and vascular wall. Int Angiol 1996; 15: 100-3.
Peschen M, Grenz H, Grothe C, Schöpf E, et al. Patterns of epidermal growth factor receptor, basic fibroblast growth factor and transforming growth factor-Beta 3 expression in skin with chronic venous insufficiency. Eur J Dermatol 1998; 8: 334-8.
Naschitz JE, Sabo E, Yeshurun D, Gilhar A, et al. An experimental model of fascitis-panniculitis. Induction of chronic fibrosis panniculitis in the rat by subcutaneous injections of lipase. Isr J Med Sci 1996; 32: 1078-85.
Naschitz JE, Bejar J, Mogilner J, Misselevich I, et al. Acute lipase-induced panniculitis in rats with ligated veins of the hindlimb: a contribution of the role of acute panniculitis as a precursor of lipodermatosclerosis of venous disease. J Dermatol Sci 1999; 19: 9-16.
Cornelius LA, Nehring LC, Roby JD, Parlos WC, et al. Human dermal microvascular endothelial cells produce matrix metalloproteinases in response to angiogenic factors and migration. J Invest Dermatol 1995; 105: 170-6.
Tamai K, Ishikawa H, Mauviel A, Uitto J. Interferon-Gama coordinately upregulates matrix metalloproteinases (MMP) -1 and MMP-3, but not tissue inhibitor of metalloproteinases (TIMP), expression in cultured keratinocytes. J Invest Dermatol 1995; 104: 384-90.
Vaalamo M, Weckroth M, Poulakkainen P, Kere J, et al. Patterm of matrix metalloproteinases and TIMP-1 expression in chronic and normally healing human cutaneous wounds. Br J Dermatol 1996; 135: 52-9.
Kähäri VM, Saarialho-Kere U. Matrix metalloproteinases in skin. Exp Dermatol 1997; 6: 199-213.
Herouy Y, Trefzer D, Zimpfer U, Schöpf E, et al. Matrix metalloproteinases and venous leg ulceration. Eur J Dermatol 2000; 9: 173-80.
Herrick SE, Sloan P, McGurk M, Freak L, et al.Sequential changes in histologic pattern and extracellular matrix deposition during the healing of chronic venous ulcers. Am J Pathol 1992; 141: 1085-95.
Knauper V, Murphy G, Tschesche H. Activation of human neutrophil procollagenase by stromelysin 2. Eur J Biochem 1996; 15: 187-91.
Wysocki AB, Staiano-Coico L, Grinnell F. Wound fluid from chronic leg ulcers contains elevated levels of metalloproteinases MMP-2 and MMP-9. J Invest Dermatol 1993; 101: 64-8.
Konttinen YT. Matrix metalloproteinases, gelatinases and collagenases in chronic leg ulcers. J Invest dermatol 1996; 106: 1119-24.
Herouy Y, Nochowschi P, Schöpf E, Norgauer J. Lipodermatosclerosis and the significance of proteolytic remodeling in the pathogenesis of venous ulceration. Int Mol Med 1999; 3: 511-5.
Norgauer J, Hildenbrand T, Idzko M, Panther E, et al. Elevated expression of extracellular matrix metalloproteinases inducer (CD147) and membrane-type matrix metalloproteinases in venous leg ulcers. Br J Dermatol 2002; 147: 1180-6.
Brinckmann J, Notbohm H, Tronnier M, Acil Y, et al. Overhydroxylation of lysil residues in the initial step for altered collagen cross-links and fibril architectures in fibrotic skin. J Invest Dermatol 1999; 113: 617-21.
Brinckmann J, Neess CM, Gaber Y, Sobhi H, et al. Diferent pattern of collagen cross-links in two sclerotic diseases: lipodermatosclerosis and circumscribed scleroderma. J Invest Dermatol 2001; 117:269-73.
Kim CS, Kawada T, Yoo H, Kwon BS, et al. Macrophage inflammatory protein-related-2, a novel CC chemolineca regulate preadipocyte migration and adipocyte differentiation. FEBS Lett 2003; 549: 125-30.
Chaldakov GN, Stankulov IS, Hristova M, Ghenev PI. Adipobiology of disease: adipokines and adipokine-targeted pharmacology. Curr Phar Des 2003; 9:1023-31.
Hausman DB, DiGirolamo M, Bartness TJ, Hausman GJ, et al. The Biology of White Adipocyte Proliferation. Obesity Rev 2001; 2: 239-54.
Lilla J, Stickens D, Werb Z. Metalloproteases and adipogenesis: a weighty subject. Am J Pathol 2002; 160: 1551-4.
Sanchez Yus E, Huarte S, Sanz Vico MD. ¿Vena o Arteria? Una cuestión decisiva en la patología hipodérmica. Piel 1987; 2: 213-7.