Liver opportunistic infections

Pneumocystis carini pneumonia (PCP), the most common of the opportunistic infections, occurs in more than 80% of AIDS patients (13). Toxoplasmosis, a protozoan infection of the central nervous system, is activated in AIDS patients when the CD4+ count drops and severe impairment of cell-mediated immunity occurs. Typically, patients have a mass lesion(s) in the brain. These mass lesions usually respond well to therapy and can disappear completely. Fungal infections, such as Cyptococcalmeningitis, are extremely common in AIDS patients, and Histoplasma capsulatum appears when cell-mediated immunity has been destroyed by the HIV virus, leading to widespread infection of the lungs, liver, spleen, lymph nodes, and bone marrow. AIDS patients are particularly susceptible to bacteremia caused by nontyphoidal strains of Salmonella. Bacteremia may be cleared by using antibiotic therapy. 

Dose-related toxicities of azathioprine or 6-mercaptopurine include nausea, vomiting, bone marrow depression (leading to leukopenia, macrocytosis, anemia, or thrombocytopenia), and hepatic toxicity. Routine laboratory monitoring with complete blood count and liver function tests is required. Leukopenia or elevations in liver chemistries usually respond to medication dose reduction. Severe leukopenia may predispose to opportunistic infections leukopenia may respond to therapy with granulocyte stimulating factor. Hypersensitivity reactions to azathioprine or 6-mercaptopurine occur in 5% of patients. These include fever, rash, pancreatitis, diarrhea, and hepatitis. 

Adverse reactions. Erythromycin is remarkably nontoxic, but the estolate can cause cholestatic hepatitis with abdominal pain and fever which may be confused with viral hepatitis, acute cholecystitis or acute pancreatitis. This is probably an allergy, and recovery is usual but the estolate should not be given to a patient with liver disease. Other allergies are rare. Gastrointestinal disturbances occur frequently (up to 28%), particularly diarrhoea and nausea, but, with the antibacterial spectrum being narrower than with tetracycline, opportunistic infection is less troublesome. 

In practice, treatment of amoebiasis can be divided into treatment of bowel lumen amoebiasis, and tissue-invading amoebiasis. The bowel lumen infection, which is usually asymptomatic, may be in trophozoites form (non-infective) or in cysts form (infective) and treatment is directed at eradicating cysts with a luminal amoebicide (e.g. diloxanide). The tissue-invading amoebiasis (giving rise to dysentery, hepatic amoebiasis and liver abscess) must be treated with systemically active drugs (systemic amoebicides) active against trophozoites (e.g. metronidazole, tinidazole also, in dangerously ill patients dehydroemetine may be used, which is less toxic than the parent emetine (derived from ipecacuanha). Sometimes antibiotics (e.g. tetracycline) are used concurrently to stop opportunist infections. 

Toxic manifestations include myelosuppression, GI symptoms, rashes, and abnormal liver function studies at standard (4 mg/rri ) doses. Depletion of normal T cells occurs at these doses, and neutropenic fever and opportunistic infections can occur. Immunosuppression may persist for several years after discontinuation of pentostatin therapy. At higher doses (10 mg/m ), major renal and neurological complications are encountered. The use of pentostatin in combination with fludarabine phosphate may result in severe or even fatal pulmonary toxicity. 

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