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Abdominal ultrasonography of the liver, as a sagittal plane through the midclavicular line, with some standard measurements [2] Right lobe of the liver at the midclavicular line at ages 0 to 7 [16] Suspicion of hepatomegaly indicates a thorough medical history and physical examination, wherein the latter typically includes an increased liver span.
The liver is responsible for the mainstay of protein metabolism, synthesis as well as degradation. All plasma proteins except Gamma-globulins are synthesised in the liver. [50] It is also responsible for a large part of amino acid synthesis. The liver plays a role in the production of clotting factors, as well as red blood cell production.
Edema may also involve the hands, trunk, and face. Kwashiorkor is characterized by a fatty liver. This fatty liver of undernutrition phenotype is often accompanied by evidence of inflammation and fibrosis. Whereas a fatty liver of undernutrition is a consistent feature of kwashiorkor, it is only encountered sometimes in children with marasmus.
Liver damage is also a clinical feature of alpha 1-antitrypsin deficiency [11] and glycogen storage disease type II. [12] In transthyretin-related hereditary amyloidosis, the liver produces a mutated transthyretin protein which has severe neurodegenerative or cardiopathic effects. Liver transplantation can be curative.
Liver: Hepatomegaly: Medical imaging: Longitudinal axis > 15.5 cm at the hepatic midline, or > 16.0 cm at the midclavicular line [14] Autopsy: Weight over upper limit of standard reference range, of 1,860 g (4.10 lb) in men [12] and 1,770 g (3.90 lb) in women. [13] Lymph nodes: Lymphadenopathy: Generally 10 mm [15] [16
The first symptoms typically include fever, intermittent abdominal pain, and an enlarged liver.Occasionally, yellow discoloration of the skin occurs. [4] Caroli disease usually occurs in the presence of other diseases, such as autosomal recessive polycystic kidney disease, cholangitis, gallstones, biliary abscess, sepsis, liver cirrhosis, kidney failure, and cholangiocarcinoma (7% affected). [2]
Portal vein thrombosis (PVT) is a vascular disease of the liver that occurs when a blood clot occurs in the hepatic portal vein, which can lead to increased pressure in the portal vein system and reduced blood supply to the liver. The mortality rate is approximately 1 in 10. [1]
The recovery phase is characterized by resolution of the clinical symptoms of hepatitis with persistent elevations in liver lab values and potentially a persistently enlarged liver. [17] All cases of hepatitis A and E are expected to fully resolve after 1–2 months. [17] Most hepatitis B cases are also self-limiting and will resolve in 3–4 ...