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IDIOPATHIC PORTAL HYPERTENSION: A LITERATURE REVIEW
Tutchenko M.
MD, DM, full professor, Bogomolets National Medical University,
Department of Surgery, Ukraine, Kyiv
Chub S.
MD, PhD student, Bogomolets National Medical University, Department of Surgery, Ukraine, Kyiv Roshchin G. MD, Dr. Sc., Full Professor, Shupyk National Medical Academy of Postgraduate Education, Kyiv
Abstract
Idiopathic portal hypertension is a rare pathology that is not associated with liver fibrosis and cirrhosis. However, it can lead to the development of ascites and varicose bleeding of the esophagus and stomach. The article provides generalized information on the diagnosis and treatment of this pathology, which may be useful for patients suffering from bleeding from varicose veins of the esophagus without cirrhotic liver changes.
Keywords: Idiopathic portal hypertension, non-cirrhotic portal hypertension, porto-sinusoidal vascular disease.
For the first time in 1889 Guido Banti, an Italian pathologist, described a disease with splenomegaly and hypersplenism not associated with any known hematological disease [1], which today is classified as idio-pathic non-cirrhotic portal hypertension.
In the Western world, terms such as hepatoportal sclerosis, idiopathic portal hypertension, incomplete septal cirrhosis, and nodular regenerative hyperplasia (NRH) have been used for many years, and finally, in 2011, a group of European experts on portal hypertension suggested using the term idiopathic non-cirrhotic portal hypertension (INCPH) [2].
In contrast to the significant prevalence of the disease in India, idiopathic non-cirrhotic portal hypertension is not a common disease in the Western world [3].
The term non-cirrhotic portal hypertension (NCPH) refers to a heterogeneous group of liver disorders that primarily affect the vascular system of the liver and are anatomically classified based on the site of blood flow resistance as prehepatic, hepatic (pre-si-nusoidal, sinusoidal, post-sinusoidal), and posthepatic [2,4].
The European Association for the Study of the Liver has proposed new diagnostic criteria for vascular liver disease, which determine the diagnosis of porto-
sinusoidal vascular disease (PSVD) in the presence of one of three features [5]. The first is the absence of cirrhosis confirmed by histological examination and at least one sign of portal hypertension. The second is the absence of cirrhosis confirmed by histological examination and at least one specific histological sign of porto-sinusoidal vascular disease. The third is the absence of cirrhosis confirmed by histological examination and at least one nonspecific sign of portal hypertension and at least one nonspecific histological sign of porto-sinusoidal vascular disease.
In patients with PSVD changes in liver tests are characterized by a slight increase in ALT and AST, an increase in alkaline phosphatase in 2 times, which are not associated with signs of portal hypertension [5,6].
PSVD should also be suspected in patients with unexplained portal hypertension with elevated transam-inases, when the synthetic capacity of the liver is preserved, as evidenced by normal bilirubin and albumin, but there is anemia, leukopenia and thrombocytopenia as a consequence of hypersplenism [7].
Elastography helps in the differential diagnosis, and if there is a low density (<10 kPa) in patients with clinical manifestations of portal hypertension, the likelihood of cirrhosis is low [8]. Determination of liver density is appropriate for the differentiation of patients with portal vein thrombosis (PVT) and PSVD [9,10].
More than half of patients with PSVD have associated diseases [11].
A biopsy remains mandatory to confirm the diagnosis of NCPH, and the optimal sample for examination should be longer than 20 mm and contain at least 10 portal sites [12].
Doppler ultrasound is often the first examination in patients with suspected NCPH, and computed tomography may be useful to assess the presence of benign hypervascular nodules [13, 14].
Because patients with PSVD have a presinusoidal type of portal hypertension, intrahepatic pressure is normal or slightly elevated, often <10 mm Hg. [15,16]
In most patients with portal vein thrombosis (PVT) without underlying liver disease (cirrhosis or PSVD), risk factors for PVT are divided into local and systemic, and in 25% the etiological factors are not identified [17].
Sonographic diagnosis of PVT is based on the absence of blood flow in the portal vein and the presence of numerous vascular channels in the liver veins corresponding to the portal cavern [18,19,20]. After the detection of portal cavernoma, ultrasound should perform CT or MRI to more accurately determine the spread of thrombosis and detect signs of portal hypertension.
In cases of isolated portal vein thrombosis, liver biopsy indicates its normal structure, while liver tests and liver elastometry indicate pathology (cirrhosis and PSVD) [21, 22, 23].
In patients with porto-sinusoidal vascular disease (PSVD) and chronic portal venous thrombosis (PVT), the outcome of treatment is determined by age and the course of the underlying disease. In the treatment of such patients the leading point is the treatment of the disease that led to the development of portal hypertension.
The main complication of the disease is bleeding from varicose veins of the esophagus and stomach. It is established that bleeding in non-cirrhotic pathology occurs more often, as well as the occurrence of varicose veins in the esophagus and stomach [7].
However, in the absence of a convincing number of studies in patients with non-cirrhotic portal hypertension, the current approach in the treatment of vascular liver disease is to treat complications according to the protocols used in the treatment of portal hypertension in patients with cirrhosis [21,24].
Regarding the type of prophylaxis, one study compared endoscopic varicose vein ligation and endoscopic varicose vein ligation with the use of nonselective beta-blockers for primary prophylaxis [25], and two studies performed the same comparison against secondary prophylaxis for varicose vein bleeding. [25, 26] in patients with porto-sinusoidal vascular disease (PSVD).
Transjugular intrahepatic portosystemic shunt (TIPS) is acceptable for patients with varicose veins that are not controlled by medication and endoscopic treatment. In this situation, the results are favorable for patients with PSVD [27]. An international multicenter retrospective study showed 80% two-year survival in patients with PSVD who underwent TIPS [28]. At the same time, in the case of cavernous transformation of veins, stent placement is not effective [29,30]. Mortality in idiopathic portal hypertension is 3% lower within 6 weeks compared with patients with liver cirrhosis [31].
In patients with chronic portal vein thrombosis, as-cites develops with prolonged biliopathy and such patients usually have a reduced mass of liver cells and their synthetic dysfunction [32]. In ascites, TIPS is less effective than in patients with varicose veins because the presence of comorbidities and renal impairment (creatinine > 1.13 mg / dL) is associated with high mortality [32].
Hepatic encephalopathy in patients with non-cir-rhotic liver disease is observed in 32% and is a much rarer complication than in cirrhosis [33, 34].
In fact, in a series of patients with PSVD who underwent TIPS, 31% of cases develop encephalopathy after stent placement, but in most cases it is temporary and is successfully corrected by conservative treatment [35].
In contrast to cirrhosis, the risk of developing hepatocellular carcinoma in patients with non-cirrhotic portal hypertension is low [36].
In patients with non-cirrhotic liver disease, sarco-penia occurs in 36% and is a major predictor of refractory varicose vein bleeding, regardless of known predictors of portal hypertension severity, such as varicose vein size and use of beta-blockers [37]. The development of progressive liver failure together with the presence of other complications of portal hypertension in patients with porto sinusoidal vascular pathology are indications for liver transplantation [38].
After orthotopic liver transplantation, the five-year survival rate is over 70%, covering patients with chronic porto-venous thrombosis in the last 20 years [39,40,41], and the 10-year survival rate is over 56-
82% in patients with portosystemic vascular disease. [31].
Another complication of porto systemic vascular disease is extrahepatic portal vein thrombosis, which occurs in 30-40% of patients, with a frequency much higher than in patients with cirrhosis [7,8]. Currently, such patients are not recommended for prophylactic treatment with anticoagulants, but anticoagulant therapy is appropriate in the development of acute portal vein thrombosis [21, 24]. Taking into account the thrombotic potential and the spread of the thrombus to the superior mesenteric vein is important in deciding on anticoagulant therapy, but the presence of cavernoma significantly worsens the prognosis of anticoagulant therapy [39, 42]. It should be borne in mind that the severity of bleeding does not increase during anticoagulant therapy, but on the contrary has a positive effect on the survival of these patients [43].
As for the type of anticoagulant therapy, heparin (unfractionated heparin, low-molecular-weight heparin) and vitamin K antagonist are used for both patients with chronic porto-venous thrombosis and porto systemic vascular diseases. Recent reports suggest the possibility of using indirect oral anticoagulants [43,44,45,46].
Hassab in 1964 proposed a surgical method for the prevention and treatment of bleeding from varicose veins of the esophagus in liver fibrosis, and Sugiura and Futagawa in 1973 surgical treatment of idiopathic portal hypertension [47,48]. Traditionally, Sugiura procedure was performed in two stages - first thoracic, and then after 4-6 weeks abdominal access [49]. It was then performed as a single procedure with synchronous access through the abdomen and chest [50] and consisted of splenectomy, devascularization of the stomach and lower third of the esophagus, stem vagotomy, pyloro-myotomy, esophageal transection and fundoplication. Later, Sugiuri's operation was modified using thoraco-abdominal access, esophageal devascularization with selective vagotomy without pyloroplasty, and esopha-geal transestomy and reanastomosis were performed using a circular stapler followed by fundoplication [51]. There have been reports of successful esophageal devascularization without splenectomy [52].
Laparoscopic splenectomy in combination with esophageal devascularization in the treatment of patients with portal hypertension is technically possible and safe in selected patients [53]. Compared with the open method, laparoscopic showed less blood loss, shorter hospital stays and fewer postoperative complications, but such long-term results have not been sufficiently studied [54].
A number of publications on laparoscopically assisted surgery in the treatment of esophageal gastric varices in portal hypertension indicate its prevalence [55,56,57,58,59,60,61].
Thus, the treatment of patients with idiopathic portal hypertension is a complex and unresolved problem.
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