• Personal information

          

    Prof. of Hepatology & Gastroenterology, Cairo University.

    Consultant of Hepatology,Gastroenterology and Endoscopy

    Management Positions: •

    Chief of Hepatology unit El Manial University Hospital (1994-1998).

    • Chief of Gastroentero ICU in Cairo university hospital (1997-2000)

    • President of the board of AlfaScope GI Specialized center (2004-2014).

    • Head of Endoscopy Unit in Cairo University Hospitals (2005-2010).       

     

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    استاذ الكبد و الجهاز الهضمى بكلية الطب جامعة القاهرة

    استشارى الكبد و الجهاز الهضمى و المناظير

    دكتوراه امراض الكبد و الجهاز الهضمى من كلية الطب جامعة القاهرة

    الرئيس السابق لقسم الامراض الباطنية بكلية الطب جامعة ٦ اكتوبر

    الرئيس السابق لوحدة مناظير الجهاز الهضمى و مركز الكبد و الرعاية المركزة بقصر العينى

     

    إقرأ المزيد

     

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Thursday, Sep 21st

Last update10:09:06 AM

        

Liver diseases

Hepatic Hemangiomas

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Hepatic hemangiomas

Epidemiology:

Hepatic hemangiomas (cavernous hemangiomas) are the most common benign hepatic tumors, representing about 70% of HFLs diagnosed during MRI. Their prevalence from autopsy reports reaches up to 20%. They are more common in women (3:1).

Etiology:

Hepatic hemangiomas are considered to be vascular malformations or hamartomas of congenital origin that enlarge by ectasia rather than by hyperplasia or hypertrophy.

Hormonal influence over tumor growth is suggested by enlargement during pregnancy and estrogen & progesterone therapy and regression after withdrawal of therapy.

Pathology:

Hemangiomas are often solitary, but multiple lesions may be present in up to 40% of patients. They can be found in both lobes of the liver but are more common in the right lobe. They may be associated with hemangiomas in other organs, biliary hamartomas, and focal nodular hyperplasia.

They range in size from a few millimeters to over 20 cm. The majority are <5 cm. The larger lesions may be pedunculated.

Microscopically, the tumor is composed of cavernous vascular spaces of varying sizes lined by a single layer of flat endothelium and filled with blood.

Clinical picture:

 Most patients with hepatic hemangiomas are asymptomatic and are typically discovered incidentally at laparotomy, autopsy, or during imaging performed for unrelated conditions.

Symptoms are more likely with large lesions (>5 cm) in young women.

The most common symptoms are

Acute fatty liver of pregnancy

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Acute fatty liver of pregnancy (AFLP)

Definition:

A disorder which is unique to human pregnancy, characterized by microvesicular fatty infiltration of hepatocytes. 

Epidemiology:

AFLP is rare with an approximate incidence of 1 in 15,000 deliveries. It is more common with multiple gestations and possibly in women who are underweight.

Pathogenesis:

It is suggested that some affected women and their fetuses might have an inherited enzyme (LCHAD) deficiency in beta-oxidation of fatty acids in mitochondria, that predisposes the mother to this disorder.

The accumulation of long-chain 3-hydroxyacyl metabolites produced by the fetus or placenta is toxic to the liver and may be the cause of the liver disease.

Clinical Picture:

AFLP occurs typically in the third trimester. The most common symptoms are anorexia, nausea or vomiting, abdominal pain, usually epigastric, and jaundice. 50% of patients have signs of preeclampsia at presentation or at some time during the course of illness.

Extra-hepatic complications can occur, as infection, pancreatitis,  intra-abdominal bleeding & diabetes insipidus.

Investigations:

1. Laboratory tests:

Aminotransferases: elevated and may reach up to 1000 IU/L.

Serum bilirubin: usually elevated.

Platelet count: may be decreased with or without signs of DIC.

In severe cases: increased INR, hypoglycemia and increased creatinine & uric acid may occur.

2. Imaging:

 Ultrasonography & CT may be used to exclude other diagnoses.  

3. Liver biopsy:

 Liver biopsy is diagnostic, showing microvesicular fatty infiltration of the hepatocytes. Liver biopsy, being with risks, should be reserved for cases in which the diagnosis is in doubt.

Differential diagnosis:

It may be difficult to differentiate AFLP and

Budd Chiari Syndrome

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Budd-Chiari syndrome

Definition:

Occlusion (Thrombosis) of the hepatic veins and/or the intrahepatic or suprahepatic inferior vena cava.

Etiology:

An underlying disorder can be identified in over 80% of patients. Many of these disorders are characterized by a hypercoagulable state, which is important to consider when treating the patient.

1. Myeloproliferative disorders:

Up to 50% of cases of Budd-Chiari syndrome may be due to an underlying myeloproliferative disorder (as polycythemia vera, essential thrombocythemia & chronic idiopathic myelofibrosis) associated with a hypercoagulable state. Peripheral blood evidence for myeloproliferation may not be present if portal hypertension, and hypersplenism accompany Budd-Chiari syndrome (occult Myeloproliferation), but BM examination may diagnose these cases.

JAK2 mutations (present in patients with polycythemia vera,  essential thrombocythemia & chronic idiopathic myelofibrosis) have been described in more than 26% of patients with Budd-Chiari syndrome, many of whom had negative results from standard testing for myeloproliferative disorders.

2. Oral contraceptives & pregnancy:

Nearly 20% of cases of Budd-Chiari syndrome occur in women who have been on oral contraceptives, are pregnant, or have recently delivered. This is probably due to a hypercoagulable state.

3. Malignancy:

Malignancies account for nearly 10% of cases of Budd-Chiari syndrome. Compression, invasion or thrombosis, are responsible. HCC are found most often, followed by adrenal or renal tumors, and tumors of the lung, pancreas & stomach.

4. Infections & benign lesions of the liver:

Infections or benign space-occupying lesions of the liver can cause thrombosis or compression of blood vessels. They account for nearly 10% of cases of Budd-Chiari syndrome.

5. Hypercoagulable states:

  • Factor V (Leiden) mutation, was found in 25% of cases.
  • Antiphospholipid syndrome.
  • Antithrombin deficiency.
  • Protein C and Protein S deficiencies.

6. Membranous webs:

Membranous obstruction of the inferior vena cava (MOVC) and/or the hepatic veins is an unusual but potentially treatable cause of the Budd-Chiari syndrome.  

7. Other causes:

Behcet's disease, SLE, MCTD, Sjögren's syndrome, IBD and  hypereosinophilic syndrome. 

8. Idiopathic:

 Up to 20% of cases of Budd-Chiari syndrome are idiopathic.

A 2009 guideline from AASLD recommends the following approach

Intrahepatic cholestasis of pregnancy

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Intrahepatic cholestasis of pregnancy (ICP)

Incidence:

In most studies ranges from 1.5-5.5%.

Pathogenesis:

Unknown. Genetic, hormonal & environmental factors are likely involved .

1. Genetics:

There are familial cases and higher incidence in some ethnic groups.

2. Hormones:

Estrogens are known to cause cholestasis. ICP occurs mainly during the third trimester, when serum concentrations of estrogen reach their peak. ICP is also more common in twin pregnancies, which are associated with higher levels of circulating estrogens.

Administration of progesterone may be a risk factor for ICP. Progesterone treatment is recommended to be avoided in pregnant women with a previous history of ICP and immediately withdrawn when cholestasis occurs during pregnancy.

Whether in-vitro fertilization (IVF) affects

 

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  • عنوان: 98 شارع التحرير , ميدان الدقي, القاهرة , مصر
     
  • هاتف: (+202) 376 1111 8

حقوق الملكية

 المعلومات الواردة في مختلف صفحات موقع د.سامح لبيب على الإنترنت هي معلومات صادرة عنه لأغراض تعليمية-خدميه. وتلك المعلومات محمية بموجب قوانين  حماية المصنفات الأدبية والفنية واتفاقيات دولية أخرى وبمقتضى القوانين الوطنية الخاصة بحقوق التأليف والحقوق المرتبطة بها. ويجوز استعراض أجزاء من المعلومات الواردة في الموقع أو نسخها أو ترجمتها لأغراض البحث أو لإجراء دراسة شخصية ولكن ليس لبيعها أو استخدامها لأغراض تجارية.

©  د.سامح لبيب ـ2012-2107

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