scholarly journals Porto-Sinusoidal Vascular Disease Associated to Oxaliplatin: An Entity to Think about It

Cells ◽  
2019 ◽  
Vol 8 (12) ◽  
pp. 1506 ◽  
Author(s):  
Angela Puente ◽  
Jose Ignacio Fortea ◽  
Carmen Del Pozo ◽  
Patricia Huelin ◽  
Maria Luisa Cagigal ◽  
...  
Keyword(s):  
Portal Hypertension ◽  
Vascular Disease ◽  
Chronic Hypoxia ◽  
Glutathione Transferase ◽  
Portal Pressure ◽  
Unknown Etiology ◽  
Sinusoidal Obstruction Syndrome ◽  
Nodular Regenerative Hyperplasia ◽  
Blood Capillaries ◽  
Sinusoidal Cells

Portal sinusoidal vascular disease is a presinusoidal cause of portal hypertension (PHT) of unknown etiology, characterized by typical manifestations of PHT (esophageal varices, ascites, portosystemic collaterals), plaquetopenia and splenomegaly with a gradient of portal pressure slightly increased, according to the presinusoidal nature of the PHT. A few cases in the literature have shown a relationship between oxaliplatin and the development of presinusoidal portal hypertension, years after the chemotherapy for colorectal cancer (therefore, different to sinusoidal obstruction syndrome). There are three mechanisms through which oxaliplatin can cause sinusoidal damage: (1) damage at the level of endothelial cells and stimulates the release of free radicals and depletion of glutathione transferase, with altering the integrity of the sinusoidal cells. The damage in the endothelial sinusoidal cells allows to erythrocytes to across into the Dissé space and formation of perisinusoidal fibrosis, (2) the appearance of nodular regenerative hyperplasia is favored by the chronic hypoxia of the centrilobular areas and, finally, (3) oxaliplatin can generate an obliteration of the blood capillaries and zones of parenchymal extinction. These three facts can develop, in a minority of cases, the appearance of a presinusoidal increase of portal pressure, which typically appears years after the completion of chemotherapy and sometimes is underdiagnosed until variceal bleeding, ascites or encephalopathy appear. The knowledge of this pathology is essential to be able to perform an early diagnostic and consult to the hepatologist.

scholarly journals Refractory Hepatic Hydrothorax: A Rare Complication of Systemic Sclerosis and Presinusoidal Portal Hypertension

2018 ◽  
Vol 2018 ◽  
pp. 1-4 ◽  
Author(s):  
Gary A. Abrams ◽  
Robert Chapman ◽  
Samuel R. W. Horton
Keyword(s):  
Pulmonary Hypertension ◽  
Portal Hypertension ◽  
Liver Biopsy ◽  
Rare Complication ◽  
Portal Pressure ◽  
Nodular Regenerative Hyperplasia ◽  
Hepatic Hydrothorax ◽  
Noncirrhotic Portal Hypertension ◽  
Portal Systemic Shunt ◽  
Hypertension Portal

We report on a rare case of refractory hepatic hydrothorax in an individual with Scleroderma/CREST syndrome and noncirrhotic portal hypertension. Portal pressure measurements revealed a normal transjugular hepatic venous portal pressure gradient, mild pulmonary hypertension, and an unremarkable liver biopsy except for mild sinusoidal dilation. Pulmonary hypertension, cardiac diastolic dysfunction, and chronic kidney disease were determined to be the causes of his refractory pleural effusions and ascites. Over the year, he underwent 50 thoracenteses and 20 paracenteses averaging 10–12 liters/week. Repeat pulmonary evaluation determined his pulmonary pressures to be normal and a secondary review of the “unremarkable” liver biopsy noted mild venous outflow obstruction and possibly Nodular Regenerative Hyperplasia (NRH). Repeat portal pressures indirectly and directly confirmed the existence of presinusoidal portal hypertension that has been associated with NRH. A transjugular intrahepatic portal systemic shunt (TIPS) was placed and he has not required thoracentesis or paracentesis over the past 18 months.

Randomised clinical study: acute effects of metformin versus placebo on portal pressure in patients with cirrhosis and portal hypertension

2021 ◽  
Author(s):  
Nikolaj Rittig ◽  
Niels Kristian Aagaard ◽  
Gerda Elisabeth Villadsen ◽  
Thomas Damgaard Sandahl ◽  
Niels Jessen ◽  
...  
Keyword(s):  
Portal Hypertension ◽  
Clinical Study ◽  
Portal Pressure ◽  
Acute Effects

Electroacupuncture attenuates vascular hyporeactivity in a rat model of portal hypertension induced by bile duct ligation

2021 ◽  
pp. 096452842110392
Author(s):  
Yu-Sheng Chen ◽  
Chorng-Kai Wen ◽  
Geng-Hao Liu ◽  
Tzung-Yan Lee
Keyword(s):  
Portal Hypertension ◽  
Growth Factor ◽  
Bile Duct ◽  
Bile Duct Ligation ◽  
Portal Pressure ◽  
Contractile Responses ◽  
Hyperdynamic Circulation ◽  
Duct Ligation ◽  
Tnf Α ◽  
Cox 1

Background: A hyperdynamic circulation and impaired vascular responsiveness to vasoconstrictors are observed in portal hypertension (PHT) rats. Inflammation is a major contributor to the hyperdynamic circulation state in murine models of PHT. Electroacupuncture (EA) may ameliorate the inflammatory response and limit arterial vasodilatation and portal pressure. This study investigated the possible mechanisms underlying putative hemodynamics effects of EA in normal and PHT rats. Methods: PHT was induced by bile duct ligation (BDL) surgery over 4 weeks in rats. Sham-operated and BDL rats were treated with low-frequency EA (2 Hz) at ST36 10 min three times weekly for one or two consecutive weeks (for a total of 3 or 7 treatments, respectively). Serum tumor necrosis factor-α (TNF-α), nitrite/nitrate (NOx) and 6-keto-prostaglandin F1α (6-keto-PGF1α) were analyzed, and hemodynamic variation and contractile responses to phorbol-12,13-dibutyrate and phenylephrine in aortic and superior mesenteric arterial rings were recorded. Inducible (i) and endothelial (3) nitric oxide synthase (NOS), cyclooxygenase-1 (COX-1), and protein kinase C-α (PKC-α) levels were determined by Western blotting. Results: EA significantly reduced portal pressure and serum TNF-α, NOx and 6-keto-PGF1α levels compared to the untreated BDL group, enhanced maximum contractile responses in the aorta, up-regulated PKC-α, and down-regulated iNOS and COX-1 levels. In addition, EA decreased the aortic angiogenesis signaling cascade, reflected by down-regulation of vascular endothelial growth factor (VEGF) abundance and transforming growth factor β receptor (TGFβR)I/II expression, as assessed by immunostaining. Conclusion: EA attenuates TNF-α, NO and 6-keto-PGF1α overproduction, modulates the vascular levels of constitutive NOS and PKC-α, blunts the development of the angiogenesis cascade, and enhances vascular contractile force in PHT rats.

Portal Angiogenesis in Chronic Liver Disease Patients Correlates with Portal Pressure and Collateral Formation

2019 ◽  
Vol 37 (6) ◽  
pp. 498-508 ◽  
Author(s):  
Carolina A. Serrano ◽  
Simon C. Ling ◽  
Sofia Verdaguer ◽  
Miguel León ◽  
Nicolás Jarufe ◽  
...  
Keyword(s):  
Liver Transplantation ◽  
Portal Hypertension ◽  
Liver Disease ◽  
Chronic Liver Disease ◽  
Venous Pressure ◽  
Portal Pressure ◽  
Peripheral Circulation ◽  
Chronic Liver ◽  
Noninvasive Markers ◽  
Collateral Formation

Background/Aims: One hallmark of chronic liver disease in patients with portal hypertension is the formation of portal-systemic collaterals in which angiogenesis has a fundamental role. We studied patients with chronic liver disease undergoing liver transplantation to correlate levels of circulating angiogenic factors in portal and peripheral circulation with portal pressure and portal-systemic collaterals. Methods: Sixteen patients who underwent liver transplantation were enrolled. During transplant surgery, we determined portal venous pressure and portal-systemic collateral formation. We determined angiogenics mediator levels in systemic and portal plasma. Peripheral plasma from healthy donors was measured as controls. Results: Vascular endothelial growth factor (VEGF)-R1 and 2, Ang-1 and 2, Tie2, FGF- 1 and 2, CD163, PDGFR-β, PDGFsRα, PDGF-AB and BB, CD163, TGF-β VASH-1 levels were significantly different in the controls in comparison to cases. Significantly decreased portal venous levels of Ang-1, FGF-1, PDGF-AB/BB, and CC were observed in patients with higher portal pressure. Peripheral VEGF, Ang-1, pPDGF-AB, BB, and CC were significantly decreased in patients with more severe collateral formation. While peripheral VEGF-R1 was higher in patients with severe collateral formation. For portal circulation, VEGF, Ang-1, ­pPDGF-AB, BB, and CC were significantly decreased in patients with more severe collateral formation Conclusions: Angiogenesis factors correlated with portal pressure and collateral formation and different patterns of circulating angiogenesis mediators were found in peripheral and portal blood of patients with chronic liver disease. These results support the importance of angiogenic pathways in cirrhosis and portal hypertension and highlight areas for further study to identify clinically useful noninvasive markers of portal pressure and collateral formation.

scholarly journals Failure of Splenectomy to Ameliorate Portal Hypertension in Myeloproliferative Disorders

1994 ◽  
Vol 8 (2) ◽  
pp. 97-100
Author(s):  
Samuel S Lee ◽  
Guido Van Rosendaal ◽  
Thomas E Lay ◽  
James K Kelly ◽  
Graham F Pineo
Keyword(s):  
Portal Hypertension ◽  
Portal Pressure ◽  
Myeloproliferative Disorders ◽  
Myeloproliferative Disorder ◽  
Correct Treatment ◽  
Forward Flow ◽  
Optimum Treatment ◽  
Flow Component ◽  
Significant Amelioration

The correct treatment of portal hypertension associated with myeloproliferative disorders remains uncertain. Splenectomy has been advocated by some to eliminate the forward flow component of the portal hypertension and thus reduce portal pressure. The authors describe three recent cases of myeloproliferative disorder in whom splenectomy failed to achieve any significant amelioration of portal hypertension, with in-depth hemodynamic studies in one patient. Based on these experiences, the authors suggest that splenectomy is not the optimum treatment of the portal hypertension associated with myeloproliferative disorders.

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