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Liver disease congenital malformation

Although we have discussed briefly the implications of biochemical individuality for alcoholism, for gout, and for arthritis, these are merely examples. A host of other diseases need to be attacked with the same point of view and hold the same promise of success. These include multiple sclerosis, muscular dystrophy, myasthenia gravis, atherosclerosis, essential hypertension, ulcers, diabetes, epilepsy, rheumatic heart disease, nephrosis, liver cirrhosis, congenital heart disease (as well as a host of other malformations which probably involve nutritional deficiencies during fetal life) and even infective diseases such as tuberculosis or poliomyelitis. [Pg.242]

First- and second-trimester abortion Cervical reopening Induction of labor Augmentation of labor Postpartum hemorrhage Ectopic pregnancy Lactation suppression In gastrointestinal disease Peptic ulceration Liver transplantation Chemotherapy-induced mucosal lesions In cardiovascular disease Congenital cardiac malformations Raynaud s syndrome Chronic obstructive pulmonary disease Adult respiratory distress syndrome Pulmonary hypertension Arterial occlusive disease Extracorporeal circulation In urology Erectile dysfunction... [Pg.103]

Caroli s disease is, instead, a congenital malformation consisting of multifocal dilatation of segmental bile ducts. It is a diffuse liver disease, but should be considered in the differential diagnosis of cystic lesions of the hver, since it may resemble this condition. [Pg.81]

Hyperammonemia may also result from congenital or acquired causes that are not related to inherited metabolic diseases. Examples of congenital causes include malformations such as portosystemic shunts, extrahepatic portal vein obstructions, and cirrhosis with portal hypertension. Transient hyperammonemia of the newborn (THAN) is typically identified in premature infants and does not appear to have a neurologic effect on those asymptomatic preterm infants [11]. Liver failure may also result in fulminant hyperammonemia. In severe liver failure, all of the enzymes expressed in the liver are deficient, resulting in complete impairment of the urea cycle as well as a deficiency of other important liver-specific enzymes snch as the glycine cleavage enzyme. [Pg.78]


See other pages where Liver disease congenital malformation is mentioned: [Pg.68]    [Pg.194]    [Pg.362]   


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