Hepatitis clinical presentation

In a South African study 20 children were identified as suffering from hepatic veno-occlusive disease thought to be caused by the administration of traditional remedies (3). The predominant clinical presentation was ascites and hepatomegaly. Nine children died. The surviving patients progressed to cirrhosis and portal hypertension. In four cases early urine specimens were available, and in all of these the presence of pyrrolizidine alkaloids was confirmed. 

The clinical presentation of these 7 cases was that of a spectrum involving the kidneys with GIT manifestations in all, as well as hepatic failure in two. Sepsis and hemorrhage were secondary manifestation of mucosal damage and in one case, rectal perforation (probably traumatic enema) was an additional finding. 

Watson described 50 black children who had died following the administration of this toxin [16]. Post-mortem examination was conducted in all cases confirming the diagnosis of impila poisoning. No common trend was noted in the clinical presentation of these children. It was concluded that hypoglycemia and evidence of hepatic and renal dysfunction, were strong indicators of impila poisoning. 

Symptoms in patients with Wilson s disease usually begin in the second or third decade of life, but may be earlier or later. However, mutations that completely destroy gene function may be associated with onset of liver disease as early as 3 years of age. The initial clinical presentation may be hepatic, with presentation similar to acute hepatitis or to chronic active hepatitis neurological (e.g., clumsiness, dysarthria, ataxia, and tremors) renal (renal tubular acidosis with aminoaciduria) or, less commonly, hematological, with hemolysis secondary to acute release of free copper from tissue and subsequent oxidation of erythrocyte membranes. The hepatic, and possibly CNS, damage may also be secondary to copper-induced oxidative damage to mitochondrial membranes. Hepatic levels of Cp messenger ribonucleic acid (mRNA) are reduced in patients with Wilson s disease, probably secondary to inhibition of transcription by increased intracellular levels of apoCp. ... 

Wilson s disease is an autosomal recessive disease of copper metabolism. It has a prevalence of 1 in 30,000 live births in most populations. The disease has a highly variable clinical presentation. It is characterized by impairment of biliary copper excretion, decreased incorporation of copper into ceruloplasmin, and accumulation of copper in the liver and, eventually, in the brain and other tissues. The biochemical findings include low serum ceruloplasmin, high urinary copper excretion, and high hepatic copper content. Some patients have normal serum cerulo-plasmia levels, and heterozygous individuals do not consistently show reduced levels of this protein. 

Drug-induced liver disease occurs as several different clinical presentations idiosyncratic reactions, allergic hepatitis, toxic hepatitis, chronic active toxic hepatitis, toxic cirrhosis, and liver vascular disorders. 

In this chapter, we reviewed the present situation, epidemiology, clinical presentation and importance of Hepatitis B. 

IV. Diagnosis is based on a history of exposure and the clinical presentation of mucous membrane irritation, CNS depression, arrhythmias, and hepatic necrosis. Carbon tetrachloride is radiopaque and may be visible on abdominal x-ray after acute ingestion. 

III. Clinical presentation. The onset of symptoms is characteristically delayed 6-12 hours or even up to 24 hours after ingestion. Death occurring within the first 1-2 days is uncommon but may result from massive fluid loss due to gastroenteritis, while death occurring later is usually caused by hepatic failure. 

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