It has been known that the liver organ is the main target of aflatoxins and chronic toxicity can result in immunosuppressive and carcinogenic effects. However, there is currently conflicting evidence to pinpoint a connection between kwashiorkor and aflatoxins. Studies have shown that not all children with kwashiorkor present with detectable aflatoxin levels. It has also been proposed that damage done by aflatoxins may be due to glutathione depletion (another proposed mechanism of the disease) in children with kwashiorkor. Mechanisms
Peripheral edema and hypoalbuminemia
Kwashiorkor is a form of protein deficiency, which can result in both osmotic imbalances and irregularities in the lymphatic system.Kwashiorkor is most notable for peripheral edema. The presence of edema in kwashiorkor is correlated with very low albumin concentration (hypoalbuminemia). Edema results from a loss of fluid balance between the hydrostatic and oncotic pressures across the capillary blood vessel walls due to the lack of protein which affects the bodys ability to draw fluid from the tissues into the bloodstream. Low albumin concentration influences negatively the strength of oncotic pressure. Failure leads to the fluid buildup in the abdomen, resulting in edema and belly distension.Furthermore, the release of antidiuretic hormone is stimulated by hypovolemia, also leading to the development of peripheral edema. Plasma renin is also stimulated, promoting sodium retention.It is important to distinguish the pathophysiology of marasmus and kwashiorkor when it comes to treating malnourished children who may have hypovolemic shock that is cause by an acute loss of salt and water. Children with severe albumin deficiency struggle physiologically to maintain their blood volume.
Hepatic artery thrombosis occurs when a blood clot forms in the artery that provides blood flow to the liver. Hepatic artery thrombosis may occur as a complication after liver transplantation, and represents the most common complication of liver transplantation. Smoking tobacco increases the risk of hepatic artery thrombosis in people who have undergone liver transplantation.Hepatic artery thrombosis may cause severe elevations in serum aminotransferases, alanine transaminase (ALT) and aspartate transaminase (AST). Often the AST is greater than the ALT. Hepatic artery thrombosis is usually diagnosed with ultrasound with doppler, although it may be diagnosed using computed tomography (CT) or magnetic resonance imaging (MRI). The treatment for recently developed or acute hepatic artery thrombosis include anticoagulant medications, fibrinolytic therapy to break up the blood clot, or surgical revascularization. If acute hepatic artery thrombosis occurs after liver transplantation, then retransplantation with a new liver may be necessary. Signs and symptoms
Hepatic artery thrombosis can cause severe elevations in serum liver enzymes, AST and ALT. Often the AST is greater than the ALT. When it occurs after liver transplantation, it usually develops within 4 months after surgery. Diagnosis
Hepatic artery thrombosis is diagnosed with ultrasound with doppler, which shows a lack of blood flow through the hepatic artery. Hepatic artery thrombosis may also be diagnosed using CT or MR imaging, which would show evidence of a blood clot within the hepatic artery. Treatment
Treatment for acute hepatic artery thrombosis include anticoagulant medications, fibrinolysis therapies to break up the blood clot, or surgical revascularization.