Cutaneous spider Nevi in liver cirrhosis: Capillary microscopical and hormonal investigations

Pirovino, M; Linder, Ralph E.; Boss, Ch.; Köchli, H. P.; Mahler, F

doi:10.1007/bf01727516

Cited by 61 publications

(30 citation statements)

References 15 publications

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“…Given the synchronized nature of neovascularization in this cyclical process, it is assumed that angiogenic growth factor expression is induced by steroid hormones and regulates blood vessel formation in reproductive organogenesis. [113][114][115][116] Indeed, physiological changes in the reproductive tract during the normal menstrual cycle 28 as well as physiological and pathological symptoms, including telangiectasia of pregnancy 117 and telangiectasia in postsclerotherapy patients receiving gonadal hormones, 118 are all associated with elevated levels of serum estradiol.…”

Section: Hormone-regulated Neovascularizationmentioning

confidence: 99%

Estrogen and Angiogenesis

Losordo

Isner

2001

ATVB

301

194

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Abstract-Multiple lines of evidence suggest that estrogen directly modulates angiogenesis via effects on endothelial cells.Under physiological conditions, angiogenesis is routinely observed in the uterus in association with fluctuations in the levels of circulating estradiol and other sex steroids. In pathological circumstances, such as breast cancer, a clear association between estrogen, estrogen receptor expression by endothelial cells, angiogenic activity, and/or tumor invasiveness has been made. Studies performed in our laboratory have revealed that estradiol accelerates functional endothelial recovery after arterial injury. Despite these consistent observations, the mechanisms by which estrogen regulates angiogenesis under physiological and pathological circumstances have not been defined. Key Words: estrogen Ⅲ angiogenesis Ⅲ vasculogenesis Ⅲ endothelium Ⅲ endothelial progenitor cells I n adult organisms, angiogenesis is virtually absent under normal conditions, except in the female reproductive tract. This observation suggests the potential for sex steroids to influence neovascularization. Several other associations, including the predilection of certain diseases (such as Takayasu's arteritis and lupus, both of which involve endothelial cell proliferation) for premenopausal females, also imply the potential role of estrogen in angiogenesis. 1,2 The role of estradiol in uterine angiogenesis, mediated by at least 1 of the estrogen receptors, has been further suggested by findings in the estrogen receptor-␣ knockout mouse, in which angiogenesis is impaired, 3 and by the demonstration that estrogen receptor antagonists can inhibit angiogenesis. 4 The positive correlation between estrogen receptor expression, angiogenic activity, and breast tumor invasiveness also supports the angiogenic effect of estrogen mediated by the estrogen receptor(s). [5][6][7][8] Finally, some reports suggest that the antitumor effect of tamoxifen may in fact relate to an antiangiogenic action of this estrogen receptor agonist/antagonist. 9 Several additional lines of experimental evidence suggest that estrogen and other sex steroids play important roles in physiological and pathological angiogenesis. One of the first observations suggesting a hormonal influence on angiogenesis was an inhibitory effect on tumor vascularization by medroxyprogesterone. 10 Subsequent studies have indicated that the mechanism of this inhibition may relate to the regulation of thrombospondin-1, an angiogenesis inhibitor, by this hormone. 11 Angiogenesis has been noted to be a prognostic marker in breast cancer, 12 and inhibition of angiogenesis in these tumors has been effected by antiestrogens. 4 In addition, the estrogen metabolite 2-methoxyestradiol has been shown to be a potent antiangiogenic agent 13 mediated by actions on cytoskeletal structure 14 and by increasing endothelial cell apoptosis. 15,16 Vascular Endothelial Cell Proliferation and Migration Are Enhanced by EstradiolEstradiol induces endothelial proliferation and migration 17 mediated by t...

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Section: Hormone-regulated Neovascularizationmentioning

confidence: 99%

Estrogen and Angiogenesis

Losordo

Isner

2001

ATVB

301

194

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“…In addition, feminization of male cirrhotic patients is a well-known phenomenon 7,8 . The hypothesis is further supported by the finding of an increased serum estradiol/free testosterone ratio in male cirrhotic patients with spiders 19 , although controversy exists 13 and additional humoral factors could be involved 24 . In our study, there was a trend towards a higher prevalence of spiders in female than in male alcoholics, although this trend was attenuated after adjusting for underlying liver disease (data not shown).…”

Section: Discussionmentioning

confidence: 93%

“…However, the study included only males and only a small number of patients with alcoholic hepatitis. The potential role of gender may be important because sex hormones are implicated in the pathogenesis of vascular spiders 5,18,19 . The inclusion of patients with alcoholic hepatitis is important because it is an inflammatory disease with significant mortality and pre-cirrhotic potential 7,8 .…”

Section: Galicia Clin 2014; 75 (1): 7-11mentioning

confidence: 99%

Precisión diagnóstica de las arañas vasculares para detectar enfermedad hepática en alcohólicos

2014

Gal. Clin.

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Introduction: Spider naevi are traditionally considered a sign of liver cirrhosis, particularly in patients with alcoholism. However, systematic evaluation of their diagnostic value in alcoholic patients has been scarcely performed. The aim of this study was to determine the diagnostic accuracy of the presence of spider neavi for liver disease detection in alcoholics using percutaneous liver biopsy as the reference standard.

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“…Common sequelae of the disease, such as jaundice, gynecomastia, ascites, cutaneous lesions, and variceal vessel formation can be evident to the examiner. Spider telangiectasias, palmar erythema, and gynecomastia are thought to occur due to an increase in the estradiol to free testosterone ratio [9,10]. Pulmonary manifestations of chronic liver disease tend to be severe.…”

Section: Declarationmentioning

confidence: 99%

Acquired Lower Extremity Arteriovenous Malformation: A Rare Case in an Adult with End-Stage Alcoholic Liver Cirrhosis

J¹,

N²,

C³

et al. 2018

Int J Radiol Imaging Technol

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patients. With an inadequately understood pathogenesis, acquired vascular malformations should be considered in the differential diagnosis for high-flow lesions found in patients with end-stage systemic manifestations of decompensated liver failure. Case ReportA 53-year-old man with a past medical history of alcoholic liver cirrhosis and portal hypertension presented with confusion, weakness, and ascites. He also presented with left knee pain accompanied by a large palpable mass that had developed along the medial aspect of the left knee. The patient reported he first noted the painful mass at the onset of his liver failure, 8 to 12 months prior to the current presentation. He stated the mass had continued to slowly grow in size. He asserted no history of surgery or prior mass in this location predating the liver failure. He recalled a minor "injury" to the left knee as a child that subsequently resolved with conservative management and no further work-up or intervention. The patient has no family history of an angiomatous syndrome. He had been admitted two months prior for the emergent banding of bleeding esophageal varices. On physical examination, the patient was cachectic and jaundiced. He had multiple sequelae of cirrhosis, including spider angiomata, hepatosplenomegaly, caput medusae, and palmar erythema. Diffuse lower extremity edema and ascites was also noted. A round, pulsatile, partially compressible mass was found on the left anteromedial distal thigh/knee (Figure 1). Laboratory results revealed thrombocytopenia (93 L/uL), hyponatremia AbstractA 53-year-old male with end-stage alcoholic liver cirrhosis and portal hypertension presented with hepatic encephalopathy as well as painful ambulation due to a mass on the medial aspect of his knee. The mass was first noted several months prior, concomitant with his presentation of decompensated liver failure. As a part of the pre-transplant workup, multimodality imaging evaluation of the medial knee mass was completed and revealed a high-flow vascularized soft tissue lesion. Biopsy performed to exclude malignancy confirmed a high-flow vascular malformation, presumably acquired as a sequela of the patient's liver disease. While arteriovenous malformations (AVMs) are common congenital phenomena, this case represents one of the first reported instances of an acquired lower extremity AVM in a patient with end-stage liver disease.

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Cutaneous spider Nevi in liver cirrhosis: Capillary microscopical and hormonal investigations

Cited by 61 publications

References 15 publications

Estrogen and Angiogenesis

Estrogen and Angiogenesis

Precisión diagnóstica de las arañas vasculares para detectar enfermedad hepática en alcohólicos

Acquired Lower Extremity Arteriovenous Malformation: A Rare Case in an Adult with End-Stage Alcoholic Liver Cirrhosis

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