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and cardiac ultrasound revealed no systemic alterations&#46; The patient was diagnosed with predominantly lymphatic combined vascular malformation associated with TSC caused by <span class="elsevierStyleItalic">TSC2</span> mutation&#46; At age 11 years the patient began treatment with oral rapamycin &#40;0&#46;8&#160;mg&#47;m<span class="elsevierStyleSup">2</span>&#47;12&#160;h&#41; for 6 months&#46; Because no decrease in the circumference of the affected arm was observed and the patient showed no systemic signs&#44; rapamycin treatment was discontinued&#46; Since the age of 14 years the patient&#39;s superficial capillary malformations have been treated with pulsed dye laser &#40;PDL&#41; &#40;10<span class="elsevierStyleHsp" style=""></span>mm&#44; 10<span class="elsevierStyleHsp" style=""></span>ms&#44; 6<span class="elsevierStyleHsp" style=""></span>J&#47;cm<span class="elsevierStyleSup">2</span>&#41;&#44; and the superficial venous malformations have been treated with multiplex neodymium-doped yttrium aluminum garnet &#40;Nd&#58;YAG&#41; laser &#40;PDL &#91;10<span class="elsevierStyleHsp" style=""></span>mm&#44; 10<span class="elsevierStyleHsp" style=""></span>ms&#44; 6<span class="elsevierStyleHsp" style=""></span>J&#47; cm<span class="elsevierStyleSup">2</span>&#93; followed after a 1-s delay by Nd&#58;YAG laser &#91;10<span class="elsevierStyleHsp" style=""></span>mm&#44; 15<span class="elsevierStyleHsp" style=""></span>ms&#44; 70<span class="elsevierStyleHsp" style=""></span>J&#47;cm<span class="elsevierStyleSup">2</span>&#93;&#41; &#40;<a class="elsevierStyleCrossRef" href="#fig0015">Fig&#46; 3</a>A and B&#41;&#46;</p><elsevierMultimedia ident="fig0005"></elsevierMultimedia><elsevierMultimedia ident="fig0010"></elsevierMultimedia><elsevierMultimedia ident="fig0015"></elsevierMultimedia><p id="par0015" class="elsevierStylePara elsevierViewall">The phosphatidylinositol 3-kinase &#40;PI3K&#47;AKT&#41;&#47;phosphatase and tensin homolog&#40;PTEN&#41;&#47;mammalian target of rapamycin &#40;mTOR&#41; pathway is implicated in the pathogenesis of hamartomatous syndromes such as TSC&#44; vascular anomalies&#44; overgrowth&#44; and malignant tumors&#46;<a class="elsevierStyleCrossRefs" href="#bib0060"><span class="elsevierStyleSup">2&#44;4&#8211;6</span></a> mTOR&#44; a kinase belonging to the phosphatidyl-3-inositol family&#44; consists of 2 multiprotein complexes &#40;mammalian target of rapamycin complex &#91;mTORC&#93;1 and mTORC2&#41; and is involved in the regulation of multiple processes associated with growth&#44; cell differentiation&#44; angiogenesis&#44; and modulation of the inflammatory response&#46;<a class="elsevierStyleCrossRef" href="#bib0085"><span class="elsevierStyleSup">7</span></a> The angiogenic activity of mTOR is mediated primarily via the translation and activation of hypoxia-inducible factor 1 &#40;HIF-1&#41;&#44; which in turn is implicated in VEGF expression in situations of cellular hypoxia and suppresses mTORC1 activity&#46;<a class="elsevierStyleCrossRef" href="#bib0085"><span class="elsevierStyleSup">7</span></a> The fact that TSC is one of the diseases most clearly associated with dysregulation of the mTOR pathway explains the appearance of different types of vascular malformations in this disease&#44; although these alterations are rarely reported&#46;<a class="elsevierStyleCrossRef" href="#bib0060"><span class="elsevierStyleSup">2</span></a> Vascular anomalies described in TSC include angiomyolipomas&#44; lymphatic malformations&#44; and&#44; less commonly&#44; arterial anomalies &#40;occlusion&#44; stenosis&#44; aneurysms&#41;&#44; which are likely related to alterations of the vasa vasorum caused by hamartomas&#46;<a class="elsevierStyleCrossRef" href="#bib0060"><span class="elsevierStyleSup">2</span></a> Lymphedema in TSC<a class="elsevierStyleCrossRef" href="#bib0090"><span class="elsevierStyleSup">8</span></a> may be the result of lymphatic malformations&#46; It has been proposed that congenital and acquired lymphedema are more frequent in TSC&#46;<a class="elsevierStyleCrossRef" href="#bib0060"><span class="elsevierStyleSup">2</span></a></p><p id="par0020" class="elsevierStylePara elsevierViewall">The involvement of an entire body segment&#44; as in the present case&#44; may be due to the loss of heterozygosity during early fetal development&#44;<a class="elsevierStyleCrossRef" href="#bib0060"><span class="elsevierStyleSup">2</span></a> combined with the germinal mutation&#46; Postzygotic mosaic mutations that affect cell signaling pathways regulating cell growth&#44; apoptosis&#44; or migration can give rise to regional alterations&#44; in some cases accompanied by overgrowth&#44; which can compromise the skin&#44; subcutaneous tissue&#44; muscle&#44; bone&#44; and&#47;or nerves&#46; In terms of severity&#44; overgrowth can be variable&#44; stable&#44; or progressive&#46;<a class="elsevierStyleCrossRef" href="#bib0095"><span class="elsevierStyleSup">9</span></a> When monitoring these patients&#44; it should be borne in mind that alterations in these pathways can also increase the likelihood of developing various malignant tumors&#46;<a class="elsevierStyleCrossRefs" href="#bib0060"><span class="elsevierStyleSup">2&#44;4</span></a></p><p id="par0025" class="elsevierStylePara elsevierViewall">In TSC patients&#44; mTOR inhibitors such as rapamycin &#40;sirolimus&#41; have shown beneficial effects on neurological signs&#44; but no clear effects on overgrowth and&#47;or vascular malformations&#46;<a class="elsevierStyleCrossRef" href="#bib0060"><span class="elsevierStyleSup">2</span></a> Good results have been reported in other patients with vascular malformations&#46;<a class="elsevierStyleCrossRef" href="#bib0100"><span class="elsevierStyleSup">10</span></a> Further studies with better dose control and longer periods of administration are likely needed to determine its true efficacy&#46; Blockade of the mTOR pathway could play a fundamental role in the development of vascular lesions in TSC patients&#46;</p><span id="sec0005" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0005">Conflicts of Interest</span><p id="par0030" class="elsevierStylePara elsevierViewall">The authors declare that they have no conflicts of interest&#46;</p></span></span>"
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Case and Research Letters
Tuberous Sclerosis Complex Associated with Hemihypertrophy and Combined Vascular Malformations
Complejo de esclerosis tuberosa asociado a hemihipertrofia y malformaciones vasculares combinadas
M.Á. Flores-Terrya,
Autor para correspondencia
miguelterry85@hotmail.com

Corresponding author.
, A. Alegre-Sánchezb, P. Boixedab, J.C. López-Gutiérrezc
a Servicio de Dermatología Médico-Quirúrgica y Venereología, Hospital General Universitario de Ciudad Real, Ciudad Real, España
b Servicio de Dermatología Médico-Quirúrgica y Venereología, Hospital Ramón y Cajal, Madrid, España
c Servicio de Cirugía Pediátrica, Hospital Infantil La Paz, Madrid, España
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who was diagnosed with TSC at 9 years of age&#44; was followed from birth for hypertrophy and combined vascular malformations of the left arm&#46; The diagnosis of TSC was confirmed upon identification of the c&#46;235G&#62;T mutation in <span class="elsevierStyleItalic">TSC2</span> in heterozygosis&#44; in the absence of any clinical signs of the disease&#46; The patient&#39;s mother carried the same mutation and presented clinical signs of TSC&#46; A physical examination carried out during the first months of life revealed telangiectatic and purpuric vascular lesions &#40;<a class="elsevierStyleCrossRef" href="#fig0005">Fig&#46; 1</a>A&#41; accompanied by multiple visible capillaries and venous vessels &#40;<a class="elsevierStyleCrossRef" href="#fig0005">Fig&#46; 1</a>B and C&#41; on the left arm&#44; the diameter of which was enlarged&#46; No skin lesions indicative of TSC were observed&#46; Doppler ultrasound performed at 20 days of age revealed no alterations of the arterial or deep venous systems&#46; At 4 months of age&#44; a deep skin biopsy&#44; which included muscle&#44; showed enlargement of the blood vessels in the dermis and subcutaneous tissue suggestive of capillary and venous malformations&#44; in addition to ectasia of the lymphatic vessels&#46; Immunohistochemistry revealed positive staining for D2-40 and negative staining for GLUT1 and WT1&#46; No alterations in muscle tissue were observed&#44; and atypia and mitotic figures were absent&#46; Hypopigmented macules on the thighs&#44; facial angiofibromas &#40;<a class="elsevierStyleCrossRef" href="#fig0010">Fig&#46; 2</a>&#41;&#44; and periungual fibromas on the hands and feet became more evident once the patient reached 8 years of age&#44; and were accompanied by Shagreen patches on the trunk that were compatible with TSC&#44; which was confirmed by genetic study&#46; A general physical examination and imaging techniques including conventional radiology&#44; abdominal and pelvic ultrasound&#44; brain magnetic resonance imaging&#44; and cardiac ultrasound revealed no systemic alterations&#46; The patient was diagnosed with predominantly lymphatic combined vascular malformation associated with TSC caused by <span class="elsevierStyleItalic">TSC2</span> mutation&#46; At age 11 years the patient began treatment with oral rapamycin &#40;0&#46;8&#160;mg&#47;m<span class="elsevierStyleSup">2</span>&#47;12&#160;h&#41; for 6 months&#46; Because no decrease in the circumference of the affected arm was observed and the patient showed no systemic signs&#44; rapamycin treatment was discontinued&#46; Since the age of 14 years the patient&#39;s superficial capillary malformations have been treated with pulsed dye laser &#40;PDL&#41; &#40;10<span class="elsevierStyleHsp" style=""></span>mm&#44; 10<span class="elsevierStyleHsp" style=""></span>ms&#44; 6<span class="elsevierStyleHsp" style=""></span>J&#47;cm<span class="elsevierStyleSup">2</span>&#41;&#44; and the superficial venous malformations have been treated with multiplex neodymium-doped yttrium aluminum garnet &#40;Nd&#58;YAG&#41; laser &#40;PDL &#91;10<span class="elsevierStyleHsp" style=""></span>mm&#44; 10<span class="elsevierStyleHsp" style=""></span>ms&#44; 6<span class="elsevierStyleHsp" style=""></span>J&#47; cm<span class="elsevierStyleSup">2</span>&#93; followed after a 1-s delay by Nd&#58;YAG laser &#91;10<span class="elsevierStyleHsp" style=""></span>mm&#44; 15<span class="elsevierStyleHsp" style=""></span>ms&#44; 70<span class="elsevierStyleHsp" style=""></span>J&#47;cm<span class="elsevierStyleSup">2</span>&#93;&#41; &#40;<a class="elsevierStyleCrossRef" href="#fig0015">Fig&#46; 3</a>A and B&#41;&#46;</p><elsevierMultimedia ident="fig0005"></elsevierMultimedia><elsevierMultimedia ident="fig0010"></elsevierMultimedia><elsevierMultimedia ident="fig0015"></elsevierMultimedia><p id="par0015" class="elsevierStylePara elsevierViewall">The phosphatidylinositol 3-kinase &#40;PI3K&#47;AKT&#41;&#47;phosphatase and tensin homolog&#40;PTEN&#41;&#47;mammalian target of rapamycin &#40;mTOR&#41; pathway is implicated in the pathogenesis of hamartomatous syndromes such as TSC&#44; vascular anomalies&#44; overgrowth&#44; and malignant tumors&#46;<a class="elsevierStyleCrossRefs" href="#bib0060"><span class="elsevierStyleSup">2&#44;4&#8211;6</span></a> mTOR&#44; a kinase belonging to the phosphatidyl-3-inositol family&#44; consists of 2 multiprotein complexes &#40;mammalian target of rapamycin complex &#91;mTORC&#93;1 and mTORC2&#41; and is involved in the regulation of multiple processes associated with growth&#44; cell differentiation&#44; angiogenesis&#44; and modulation of the inflammatory response&#46;<a class="elsevierStyleCrossRef" href="#bib0085"><span class="elsevierStyleSup">7</span></a> The angiogenic activity of mTOR is mediated primarily via the translation and activation of hypoxia-inducible factor 1 &#40;HIF-1&#41;&#44; which in turn is implicated in VEGF expression in situations of cellular hypoxia and suppresses mTORC1 activity&#46;<a class="elsevierStyleCrossRef" href="#bib0085"><span class="elsevierStyleSup">7</span></a> The fact that TSC is one of the diseases most clearly associated with dysregulation of the mTOR pathway explains the appearance of different types of vascular malformations in this disease&#44; although these alterations are rarely reported&#46;<a class="elsevierStyleCrossRef" href="#bib0060"><span class="elsevierStyleSup">2</span></a> Vascular anomalies described in TSC include angiomyolipomas&#44; lymphatic malformations&#44; and&#44; less commonly&#44; arterial anomalies &#40;occlusion&#44; stenosis&#44; aneurysms&#41;&#44; which are likely related to alterations of the vasa vasorum caused by hamartomas&#46;<a class="elsevierStyleCrossRef" href="#bib0060"><span class="elsevierStyleSup">2</span></a> Lymphedema in TSC<a class="elsevierStyleCrossRef" href="#bib0090"><span class="elsevierStyleSup">8</span></a> may be the result of lymphatic malformations&#46; It has been proposed that congenital and acquired lymphedema are more frequent in TSC&#46;<a class="elsevierStyleCrossRef" href="#bib0060"><span class="elsevierStyleSup">2</span></a></p><p id="par0020" class="elsevierStylePara elsevierViewall">The involvement of an entire body segment&#44; as in the present case&#44; may be due to the loss of heterozygosity during early fetal development&#44;<a class="elsevierStyleCrossRef" href="#bib0060"><span class="elsevierStyleSup">2</span></a> combined with the germinal mutation&#46; Postzygotic mosaic mutations that affect cell signaling pathways regulating cell growth&#44; apoptosis&#44; or migration can give rise to regional alterations&#44; in some cases accompanied by overgrowth&#44; which can compromise the skin&#44; subcutaneous tissue&#44; muscle&#44; bone&#44; and&#47;or nerves&#46; In terms of severity&#44; overgrowth can be variable&#44; stable&#44; or progressive&#46;<a class="elsevierStyleCrossRef" href="#bib0095"><span class="elsevierStyleSup">9</span></a> When monitoring these patients&#44; it should be borne in mind that alterations in these pathways can also increase the likelihood of developing various malignant tumors&#46;<a class="elsevierStyleCrossRefs" href="#bib0060"><span class="elsevierStyleSup">2&#44;4</span></a></p><p id="par0025" class="elsevierStylePara elsevierViewall">In TSC patients&#44; mTOR inhibitors such as rapamycin &#40;sirolimus&#41; have shown beneficial effects on neurological signs&#44; but no clear effects on overgrowth and&#47;or vascular malformations&#46;<a class="elsevierStyleCrossRef" href="#bib0060"><span class="elsevierStyleSup">2</span></a> Good results have been reported in other patients with vascular malformations&#46;<a class="elsevierStyleCrossRef" href="#bib0100"><span class="elsevierStyleSup">10</span></a> Further studies with better dose control and longer periods of administration are likely needed to determine its true efficacy&#46; Blockade of the mTOR pathway could play a fundamental role in the development of vascular lesions in TSC patients&#46;</p><span id="sec0005" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0005">Conflicts of Interest</span><p id="par0030" class="elsevierStylePara elsevierViewall">The authors declare that they have no conflicts of interest&#46;</p></span></span>"
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2022 Agosto 93 44 137
2022 Julio 65 45 110
2022 Junio 56 31 87
2022 Mayo 119 52 171
2022 Abril 122 33 155
2022 Marzo 147 70 217
2022 Febrero 151 37 188
2022 Enero 184 38 222
2021 Diciembre 159 44 203
2021 Noviembre 126 45 171
2021 Octubre 188 55 243
2021 Septiembre 130 39 169
2021 Agosto 137 35 172
2021 Julio 121 25 146
2021 Junio 142 37 179
2021 Mayo 236 44 280
2021 Abril 189 86 275
2021 Marzo 74 23 97
2021 Febrero 72 32 104
2021 Enero 47 16 63
2020 Diciembre 44 13 57
2020 Noviembre 35 19 54
2020 Octubre 33 18 51
2020 Septiembre 32 11 43
2020 Agosto 15 25 40
2020 Julio 21 7 28
2020 Junio 25 24 49
2020 Mayo 20 15 35
2020 Abril 20 15 35
2020 Marzo 19 5 24
2020 Febrero 3 0 3
2019 Mayo 1 0 1
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¿Es usted profesional sanitario apto para prescribir o dispensar medicamentos?

Are you a health professional able to prescribe or dispense drugs?