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Objective Idiopathic non-cirrhotic portal hypertension (INCPH) is a rare cause of portal hypertension, and this study aims to analyze the clinical features of patients with INCPH, and to assist in diagnosis and differential diagnosis. Methods A total of 74 patients who were hospitalized in Beijing YouAn Hospital from January 2019 to July 2022 and were diagnosed with INCPH were enrolled, and 332 patients with liver cirrhosis who were hospitalized during the same period of time were enrolled as control group. Demographic data, laboratory markers, gastroscopy, liver elasticity, pathological examination, and complications were recorded and compared between the two groups. The receiver operating characteristic (ROC) curve was used to investigate the ability of liver stiffness measurement (LSM), aspartate aminotransferase-to-platelet ratio index (APRI), and fibrosis-4 (FIB-4) in the differential diagnosis of INCPH, and the DeLong test was used to compare the area under the ROC curve (AUC). The independent-samples t test was used for comparison of normally distributed continuous data between two groups, and the Mann-Whitney U test was used for comparison of non-normally distributed continuous data between two groups; the chi-square test was used for comparison of categorical data between two groups. Results Among the patients with INCPH, 46.55% had no obvious symptoms at disease onset and 43.24% were misdiagnosed with liver cirrhosis. Compared with the patients with liver cirrhosis, the patients with INCPH had a significantly higher proportion of patients with gastrointestinal bleeding (62.16% vs 41.27%, χ 2 =10.67, P < 0.01) and a significantly lower proportion of patients with moderate-to-severe ascites (16.21% vs 29.82%, χ 2 =34.98, P < 0.01), and there were few patients with hepatic encephalopathy. As for pathology, 89.19% (66/74) of the INCPH patients manifested as typical occlusive portal vein disease. The statistical analysis showed that compared with the patients with liver cirrhosis, the patients with INCPH had significantly better liver function parameters, MELD score, and Child-Pugh score and significantly lower LSM [9.05(7.18-12.33) vs 25.32(16.21-47.23), Z =-8.41, P < 0.01], APRI score [0.70(0.41-1.28) vs 1.35(0.80-2.39), Z =-6.21, P < 0.01], and FIB-4 index [2.99(1.62-4.81) vs 6.68(4.06-10.42), Z =-8.39, P < 0.01]. LSM, FIB-4, and APRI had a good ability in differentiating INCPH from liver cirrhosis, and in particular, LSM had an AUC of up to 0.92 (95% confidence interval: 0.87-0.96), with a sensitivity of 92.68% and a specificity of 81.60%. Conclusion INCPH patients tend to have an insidious onset, a relatively high incidence rate of portal hypertension-related complications, and relatively good liver function, especially the patients with LSM < 14.5 kPa. The possibility of INCPH should be considered for such patients in clinical practice.
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Objective:To explore the medium-long term efficacy of transjugular intrahepatic portosystemic shunt (TIPS) for gastrointestinal hemorrhage in patients with idiopathic non-cirrhotic portal hypertension (INCPH).Methods:From March 2013 to July 2018, clinical data of 13 INCPH patients, including 5 males, 8 females,with gastrointestinal hemorrhage were retrospectively analyzed, who were diagnosed at the First Affiliated Hospital of Zhengzhou University, Anyang Fifth People′ s Hospital and Yuncheng Central Hospital. All patients received TIPS treatment. The general information, postoperative survival rate, the incidence of rebleeding, shunt dysfunction rate, and incidence of hepatic encephalopathy were analyzed.Results:All 13 patients with INCPH completed TIPS successfully with an average age of 45±8 (33 to 59) years. The hepatic venous pressure gradient (HVPG) decreased from 20.0-26.0 (22.6±1.9) mmHg before procedure to 8.0-14.0 (9.4±3.2) mmHg after. The median follow-up time was 44±7 (31 to 53) months. One patient died of liver failure 27 months after TIPS. Hepatic encephalopathy occurred cumulatively in 1 case (1/13), 1 case (1/13) and 1 case (1/13) in 12, 24 and 36 months after TIPS. Stent restenosis occurred cumulatively in 2 cases (2/13), 3 cases (3/13) and 3 cases (3/13) in 12, 24 and 36 months after TIPS. Portal vein thrombosis occurred cumulatively in 2 cases (2/13), and no primary liver cancer developed.Conclusions:TIPS is safe and effective in the treatment of INCPH with gastrointestinal bleeding with favorable medium-long term outcome.
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Introduction: Portal hypertension in the presence of cirrhosisof liver carries poor prognosis. The medical managementalong with endoscopic therapy helps to reduce bleeding.Surgery is reserved for patients who fail medical therapy.Patients with portal hypertension with good functioning liverbenefit from surgery. Study aimed to evaluate the resultsof surgical treatment for portal hypertension at our centerKarnataka Institute of Medical Sciences Hubli. Karnataka.Material and methods. This was a prospective observationalstudy. There were 34 patients undergoing surgical treatmentfor various presentations of portal hypertension during theperiod of 2015 to 2019.They were analyzed for demographics,etiology, presentation, various surgeries and outcome. Thedata was entered intoMicrosoft excel sheet and analyzed.Results: Of the 34 patients males were most common.Variceal bleeding was most common presentation followedby painful splenomegaly and anemia. ‘Extrahepatic portalvein obstruction’ was the leading cause of non-cirrhoticportal hypertension followed by ‘non cirrhotic portal fibrosis’and ‘left sided or sinistral portal hypertension’. Proximallinorenal shunt was the most common procedure followedby splenectomy with esophagogastric devascularization. Themorbidity and mortality were very low and yielded durablesatisfactory outcome.Conclusion: The surgery for non-cirrhotic portalhypertension has durable and satisfactory results and canbe done with minimal morbidity and mortality at trainedhands. For few selected cirrhotic patients surgery in the formof devascularization or shunt offers immediate relief frombleeding and gives time for future transplant if any.
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Antecedentes: El carcinoma hepatocelular es la neoplasia hepática más frecuente; el 90% se desarrolla sobre hígado cirrótico o con hepatopatía crónica, constituyendo así el principal factor de riesgo; la inflamación crónica, la necrosis y regeneración que estas producen condiciona la aparición de mutaciones genéticas y el desarrollo de células tumorales. Sin embargo, el 10% se desarrolla sobre hígado sano, no cirrótico y sin factores desencadenantes. Material y métodos: Se realizó un análisis descriptivo y de la supervivencia de una serie de 19 pacientes con anatomía patológica de carcinoma hepatocelular y ausencia de antecedentes de cirrosis hepática o hepatopatía crónica intervenidos en dos Unidades HPB en el período enero 2007- enero 2016. Resultados: La serie incluyó 13 varones y 6 mujeres con una edad media de 65 años. La presentación clínica más frecuente fue dolor abdominal. El 60% registraba analítica normal y solo en el 16% se elevó la AFP. El 61% presentó prueba de imagen diagnóstica. El tamaño medio fue de 110,6 mm. A todos se los trató con cirugía. Ocurrieron complicaciones en el 36,8% de los pacientes y una supervivencia a los 5 años del 62,3%. Conclusión: el carcinoma hepatocelular suele diagnosticarse cuando es de gran tamaño por hallazgos en pruebas de imagen realizadas generalmente en el estudio del dolor abdominal. La cirugía ofrece tratamiento curativo, pudiendo realizarse grandes resecciones con un alto índice de seguridad, con morbimortalidad perioperatoria baja y con bajo índice de insuficiencia hepática, ya que el remanente hepático es sano y la función hepática se mantiene.
Background: Hepatocellular carcinoma is the most common type of primary liver cancer and is the third cause of cancer related deaths; 80% of the HCC are associated with cirrhotic livers or chronic liver diseases, which constitute the main risk factor. Chronic inflammation, necrosis and regeneration due to these conditions produce genetic mutation and development of tumor cells. Yet, 10% develop in non-cirrhotic healthy livers without precipitating factors. Material and methods: We conducted a retrospective analysis of the characteristics and survival of patients with diagnosis of hepatocellular carcinoma in non-cirrhotic liver and absence of a history of liver cirrhosis or chronic liver disease undergoing surgery in two hepato-pancreato-biliary units between January 2007 and January 2016. Results: Mean age was 65 years and 13 patients were men. Abdominal pain was the most common clinical presentation. Liver panel was normal in 60% of the cases and alpha-fetoprotein was elevated in only 16%. The diagnosis was made by imaging tests in 61% of the cases. Mean tumor size was 110.6 cm. All the patients underwent surgery. Complications were observed in 36.8% of the patients and survival at 5 years was 62.3%. Conclusion: hepatocellular carcinoma is usually diagnosed as a large lesion in imaging tests ordered due to abdominal pain. Surgery provides curative treatment, and large resections can be safely performed, with low perioperative morbidity and mortality and low incidence of postoperative liver failure, since the liver remnant is healthy and liver function is maintained.
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In India, an unexplained enteropathy is present in a majority of non-cirrhotic intrahepatic portal hypertension (NCIPH) patients. Small intestinal bacterial contamination and tropical enteropathy could trigger inflammatory stimuli and activate the endothelium in the portal venous system. Groundwater contaminated with arsenic is an environmental factor of epidemic proportions in large areas of India which has similar consequences. Von Willebrand factor (a sticky protein) expressed by activated endothelium may promote formation of platelet microthrombi and occlusion of intrahepatic portal vein branches leading to NCIPH. Environmental factors linked to suboptimal hygiene and sanitation, which enter through the gastrointestinal (GI) tract, predispose to platelet plugging onto activated endothelium in portal microcirculation. Thus, NCIPH, an example of poverty linked thrombophilia, is a disease mainly affecting the lower socio-economic strata of Indian population. Public health measures to improve sanitation, provide clean drinking water and eliminate arsenic contamination of drinking water are urgently needed. Till such time as these environmental factors are addressed, NCIPH is likely to remain 'an Indian disease'.
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@#Porto-spleno-mesenteric vein thrombosis is a rare, life-threatening condition of extrahepatic portal venous system thrombosis. We report a rare case of a 49-year-old lady with late presentation of acute portal vein thrombosis in a non-cirrhotic liver with an incidental finding of left adnexal teratoma. She presented with a one-week history of severe abdominal pain associated with vomiting and diarrhea. She gave no history of prior risk for venous thromboembolism or liver diseases. Physical examination revealed a tender mass extending from suprapubic to left iliac fossa. Abdominal computed tomography scans showed a well-defined fat-containing left adnexal mass, likely a benign teratoma, with no involvement of surrounding structures or calcification. There was evidence of porto-splenic-mesenteric vein thrombosis with liver infarction, bowel and splenic ischemia. Management of the extensive thrombosis causing multi-organ failure includes resuscitation, supportive care and treatment of thrombosis. Treatment options include early anticoagulation and if feasible, thrombolysis
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Objective@#To investigate the incidence of hepatic encephalopathy (HE) in patients with non-cirrhotic portal hypertension (NCPH) and to explore its risk factors.@*Methods@#The incidence rate of HE in 150 cases with NCPH was evaluated in two hospitals, and 188 cases of compensated cirrhosis patients were taken as control. Logistic regression was used to screen for independent risk factors for HE in patients with NCPH.@*Results@#The incidence of overt hepatic encephalopathy (OHE) in patients with NCPH was not statistically significantly different from that in patients with cirrhosis (4.7% vs. 6.9%, P = 0.682). The incidence of mild hepatic encephalopathy (MHE) was significantly lower than that of cirrhosis patients (32.7% vs. 46.3%, P < 0.05). The presence of upper gastrointestinal bleeding, infection and portosystemic venous shunt were the main independent factors for HE in NCPH patients (OR > 1, P < 0.05).@*Conclusion@#HE is one of the important complications of NCP, and may be influenced by factors such as upper gastrointestinal bleeding, infection and portosystemic venous shunt.
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Although liver cirrhosis is the most common cause of portal hypertension (PH), about 20% of PH cases are caused by non-cirrhotic reasons, which are referred to as non-cirrhotic portal hypertension (NCPH), with a high incidence rate in developing countries. NCPH is a group of heterogeneous hepatic vascular diseases, including idiopathic portal hypertension (IPH) and extrahepatic portal vein obstruction (EHPVO), as well as the rare diseases in clinical practice such as Budd-Chiari syndrome, congenital hepatic fibrosis, and nodular regenerative hyperplasia. The patients with NCPH usually have the symptoms of portal hypertension, such as recurrent variceal bleeding and splenomegaly, but liver function is well preserved in these patients. At present, the diagnosis of NCPH lacks a universally accepted standard and remains a challenge. In clinical practice, the method of exclusion is usually applied for the diagnosis of HCPH, and liver biopsy is performed when necessary to make a confirmed diagnosis. This paper introduces the pathogenesis and pathological manifestations of IPH and EHPVO, as well as the selection of diagnostic methods and therapeutic strategies. If upper gastrointestinal bleeding can be effectively controlled, NCPH is considered to have a relatively good prognosis.
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Chronic infection by hepatitis C virus (HCV) is one of the main risk factors for the development of liver cirrhosis and hepatocellular carcinoma. However, the emergence of hepatocellular carcinoma (HCC) in non-cirrhotic HCV patients, especially after sustained virological response (SVR) is an unusual event. Recently, it has been suggested that HCV genotype 3 may have a particular oncogenic mechanism, but the factors involved in these cases as well as the profile of these patients are still not fully understood. Thus, we present the case of a non-cirrhotic fifty-year-old male with HCV infection, genotype 3a, who developed HCC two years after treatment with pegylated-interferon and ribavirin, with SVR, in Brazil.
A infecção crônica pelo vírus da hepatite C é um dos principais fatores de risco para o desenvolvimento de cirrose hepática e carcinoma hepatocelular. Entretanto, o surgimento do carcinoma hepatocelular em pacientes portadores de hepatite C na ausência de cirrose, especialmente após o tratamento e a obtenção de resposta virológica sustentada, é um evento incomum. Recentemente tem sido sugerido que o genótipo 3 do vírus da hepatite C possa ter um mecanismo oncogênico particular, mas todos os fatores envolvidos nestes casos, assim como o perfil destes pacientes, ainda não estão totalmente esclarecidos. Deste modo, apresentamos o caso de um paciente masculino de 50 anos de idade, com infecção pelo vírus da hepatite C genótipo 3a, não cirrótico, que desenvolveu carcinoma hepatocelular dois anos após ter atingido resposta virológica sustentada com o tratamento com interferon peguilado e ribavirina.
Subject(s)
Humans , Male , Middle Aged , Antiviral Agents/therapeutic use , Carcinoma, Hepatocellular/etiology , Hepatitis C/drug therapy , Interferon-alpha/therapeutic use , Liver Neoplasms/etiology , Polyethylene Glycols/therapeutic use , Drug Therapy, Combination , Hepacivirus/genetics , Recombinant Proteins/therapeutic use , Ribavirin/adverse effects , Treatment OutcomeABSTRACT
Antecedentes: la esclerosis hepatoportal se manifiesta como hipertensión portal no cirrótica. Su etiología parece estar relacionada con alteraciones idiopáticas en la microvasculatura hepática. Las manifestaciones de la esclerosis hepatoportal incluyen sangrado de vías digestivas altas, pancitopenia, esplenomegalia e hipertensión portal no cirrótica. Presentamos el primer caso reportado en Colombia de esclerosis hepatoportal en un paciente con serología positiva para el virus de la inmunodeficiencia humana (VIH). Métodos: paciente masculino de 60 años de edad, VIH-positivo, quien ingresa a nuestra institución por hemorragia de vías digestivas alta (várices esofágicas y fúndicas) y ascitis, cuyo manejo requirió la toma de biopsia hepática. Resultados: se realizó biopsia Trucut de hígado que evidenció la presencia de 6 a 8 espacios porta con parénquima arquitectónico conservado que demostró fibrosis perivenular y dilatación sinusoidal pericentral severa. Conclusión: la esclerosis hepatoportal es una causa de morbilidad en pacientes VIH-positivos. Debe considerarse en cada paciente que manifiesta hipertensión portal no cirrótica asociada con hemorragia de la vía digestiva alta. Sin embargo, una investigación adicional es imprescindible con el fin de describir la relación entre el desarrollo de alteraciones intrahepáticas (microtrombosis), la patogénesis del VIH y el uso de terapia antirretroviral, particularmente el uso de didanosina.
Background: Hepatoportal sclerosis manifests as non-cirrhotic portal hypertension. Its etiology appears to be related to alterations in the idiopathic micro-vasculature of the liver. Manifestations of hepatoportal sclerosis include upper gastrointestinal bleeding, pancytopenia, splenomegaly and non-cirrhotic portal hypertension. We present the first reported case of hepatoportal sclerosis in Colombia which occurred in an HIV positive patient. Methods: A 60-year-old male HIV patient positive was admitted to our institution because of ascites and upper digestive tract bleeding due to esophageal and fundal varices. Management required taking a liver biopsy. Results: A Tru-Cut biopsy needle was used to take a liver biopsy sample percutaneously. The biopsy revealed six to eight portal tracts with preserved architectural parenchyma, perivenular fibrosis and severe pericentral sinusoidal dilatation. Conclusions: Hepatoportal sclerosis is a cause of morbidity in HIV-positive patients and should be considered in each patient manifesting non-cirrhotic portal hypertension associated with upper gastrointestinal bleeding. However, further research is necessary to describe the relationship between the development of intrahepatic alterations (microthrombosis), HIV, and the use of anti-retroviral therapy, particularly the use of didanosine.
Subject(s)
Humans , Male , Middle Aged , Antiretroviral Therapy, Highly Active , Biopsy , Hypertension, Portal , Immunologic Deficiency Syndromes , Liver , SclerosisABSTRACT
El tratamiento quirúrgico ha sido tradicionalmente el primer tratamiento en mente cuando se enfrenta a un paciente con CHC; sin embargo, el advenimiento de nuevas técnicas no quirúrgicas ha replanteado su uso, y en la actualidad el éxito en el tratamiento depende básicamente de una adecuada selección del paciente para este tipo de terapia. El tratamiento quirúrgico del CHC varía cuando se trata de un tumor en un paciente con hígado cirrótico y no cirrótico, y esto debe tenerse en cuenta al momento de decidir el tipo de tratamiento.
Although surgical treatment has traditionally been the first treatment considered for patients with HCC, the advent of new non-surgical techniques has led to a rethinking of its use. Today, successful surgery basically depends on proper selection of the patient. Surgical treatment of HCC varies for tumors in patients with non-cirrhotic and cirrhotic livers which must be taken into account when deciding on the type of treatment.
Subject(s)
Humans , Carcinoma, Hepatocellular , FibrosisABSTRACT
Background & objectives: There are only a few studies on aetiology of portal hypertension among adults presenting to tertiary care centres in India; hence we conducted this study to assess the aetiological reasons for portal hypertension in adult patients attending a tertiary care centre in southern India. Methods: Causes of portal hypertension were studied in consecutive new adult patients with portal hypertension attending department of Hepatatology at a tertiary care centre in south India during July 2009 to July 2010. Results: A total of 583 adult patients (>18 yr old) were enrolled in the study. After non-invasive testing, commonest causes of portal hypertension were cryptogenic chronic liver disease (35%), chronic liver disease due to alcohol (29%), hepatitis B (17%) or hepatitis C (9%). Of the 203 patients with cryptogenic chronic liver disease, 39 had liver biopsy - amongst the latter, idiopathic non cirrhotic intrahepatic portal hypertension (NCIPH) was seen in 16 patients (41%), while five patients had cirrhosis due to non alcoholic fatty liver disease. Fifty six (10%) adult patients with portal hypertension had vascular liver disorders. Predominant causes of portal hypertension in elderly (>60 yrs; n=83) were cryptogenic chronic liver disease (54%) and alcohol related chronic liver disease (16%). Interpretation & conclusions: Cryptogenic chronic liver disease was the commonest cause of portal hypertension in adults, followed by alcohol or hepatitis B related chronic liver disease. Of patients with cryptogenic chronic liver disease who had liver biopsy, NCIPH was the commonest cause identified. Vascular liver disorders caused portal hypertension in 10 per cent of adult patients. Cryptogenic chronic liver disease was also the commonest cause in elderly patients.
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In patients with cirrhosis and portal hypertension, variceal bleeding is a severe complication, and still a major cause of death. From 1986 to 2010 (Baveno V), several consensuses related to this topic have been carried out. The main purposes of these meetings were to develop clear definitions and therapeutic recommendations aimed at the standardization and increased ease of interpretation among different studies, to be homogeneous, which is essential for meta-analysis. This applies both to the definition of events related to variceal hemorrhage and therapeutic behaviour. In Baveno V some definitions were modified such as criteria for failure to control bleeding, and failure of secondary prophylaxis, while other definitions were validated. As in Baveno IV, the level of evidence (1 being the highest, 5 being the lowest) and the grades of recommendation (A the strongest, D the weakest) were assessed according to the Oxford System. Particular emphasis was placed on management of non-cirrhotic portal hypertension, especially on the Budd-Chiari syndrome and extra-hepatic portal vein obstruction. Areas requiring further study include mechanism in the development and progression of portal hypertension; the development of non-invasive techniques to identify patients with clinically significant portal hypertension; the assessment of the impact of the management of chronic liver disease in the development of this condition; the role of regular control of portal hypertension in the prevention of the development and progression of gastroesophageal varices. Finally more information about non-cirrhotic portal hypertension is needed, especially on the frequency, primary prophylaxis of variceal bleeding, factors associated with treatment failure, progression and thrombosis recurrence.
La hipertensión portal (HP) constituye un alteración hemodinámica severa, responsable de las principales complicaciones de la cirrosis, entre las cuales está la hemorragia por várices gastroesofágicas. Desde el año 1986 y hasta el 2010 (Baveno V), se han efectuado diferentes reuniones de consensos, cuyos objetivos han sido estandarizar criterios, haciéndolos simples y reproducibles, de tal forma de homogeneizar los resultados de estudios clínicos y meta-análisis. Esto es válido tanto para la definición de eventos relacionados con hemorragia variceal, como de conductas terapéuticas. En Baveno V se han modificado algunas definiciones como los criterios de falla en el control de la hemorragia, y de falla en la profilaxis secundaria, mientra que otras se validaron. Al igual que en Baveno IV, se utilizó el Sistema Oxford, para representar el nivel de evidencia (1 el mayor; 5 el menor) y de recomendación (A la más fuerte y D la de menor peso). Especial hincapié se ha hecho en el manejo de la HP de origen no cirrótica (Síndrome de Budd-Chiari y obstrucción de la vena porta extra-hepática). Finalmente, las áreas con desafíos en investigación clínica incluyen mecanismos en el desarrollo y progresión de la HP; empleo de medidas no invasivas para identificar pacientes con HP de significación; evaluación del impacto que tiene el manejo de la enfermedad hepática de base, en el desarrollo de esta complicación; el papel de la medición de la presión portal en la prevención del desarrollo y progresión de las várices gastroesofágicas. Finalmente, se recomienda realizar estudios prospectivos sobre prevalencia y evolución clínica de la HP no cirrótica y profilaxis primaria de la hemorragia variceal; identificación de la población de riesgo y de factores asociados con falla al tratamiento, progresión de la enfermedad y recurrencia.
Subject(s)
Humans , Hypertension, Portal/complications , Hypertension, Portal/therapy , Liver Cirrhosis/complications , Gastrointestinal Hemorrhage/etiology , Gastrointestinal Hemorrhage/therapy , Esophageal and Gastric Varices/complicationsABSTRACT
Non-cirrhotic portal hypertension(NCPH)is a group of diseases that show evidences of portal hypertension but no cirrhosis is present.Common causes of NCPH include pre-sinusoidal portal lesions such as portal vein thrombosis,congenital liver fibrosis and idiopathic portal hypertension,and post-sinusoidal portal lesions.The major feature of this group of diseases is well preserved liver function in spite of prominent portal hypertensive manifestations such as esophageal varices/gastrointestinal bleeding and splenomegaly/hypersplenism.Careful differentiation from cirrhosis requires thorough clinical,radiological and pathological investigation.Preventing and control of variceal bleeding and hypersplenism through medical,endoscopic and interventional procedures yield good prognosis in most of the patients with NCPH.
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We report a case of non-cirrhotic portal hypertension in a 73 year-old woman, who had 19-year history of idiopathic myelofibrosis. There were esophageal varix, splenomegaly, and ascites. The biopsied liver showed irregular sinusoidal/ perisinusoidal fibrosis and occasional central-to-central fibrous connection. In areas with extensive fibrosis, coarse collagen fibers filled the sinusoidal spaces and compressed hepatocytes. However, nodular regeneration was absent. Double immunohistochemical stain for smooth muscle actin and proliferation cell nuclear antigen (PCNA) revealed diffusely activated stellate cells, some of which showed nuclear PCNA staining. There was also extramedullary hematopoiesis with bizarre megakaryocytes. The portal vein and its branches were patent. Idiopathic myelofibrosis is a rare cause of non-cirrhotic portal hypertension: the portal hypertension was considered to be the result of sinusoidal/perisinusoidal fibrosis in this case.