Peliosis hepatitis

Oral testosterone-replacement regimens can cause hepatotoxicity, ranging from mildly elevated hepatic transaminases to serious liver diseases (e.g., peliosis hepatitis, hepatocellular and intrahepatic cholestasis, and benign or malignant tumors). 

Liver was not examined histologically in the subchronic study used to set concentrations for the NCI chronic gavage bioassay of 1,2-dibromoethane (NC11978). In the NCI (1978) gavage bioassay (discussed in detail in Section 2.2.2.8), a nonneoplastic hepatic lesion, peliosis hepatis, occurred in a small number of treated male and female Osborne-Mendel rats and had an equivocal relationship to... 

Hepatotoxicity Prolonged use of high doses of androgens has been associated with the development of potentially life-threatening peliosis hepatis, hepatic neoplasms, and hepatocellular carcinoma. Cholestatic hepatitis and jaundice occur with fluoxymesterone and methyltestosterone at relatively low doses. Drug-induced jaundice is reversible when the medication is discontinued. 

Experience with long-term therapy with danazol is limited. Peliosis hepatis and benign hepatic adenoma have been observed with long-term use. Peliosis hepatis and hepatic adenoma may be silent until complicated by acute, potentially life-threatening intra-abdominal hemorrhage. Therefore, alert the physician to this possibility. Attempts should be made to determine the lowest dose that will provide... 

Hepatic events Experience with long-term therapy with danazol is limited. Peliosis hepatis and benign hepatic adenoma have been observed with long-term use (see Black..Box.WamlDfl). 

Long-term experience Long-term experience with danazol is limited. Long-term therapy with other steroids alkylated at the 17 position has been associated with serious toxicity (cholestatic jaundice, peliosis hepatitis). Similar toxicity may develop after long-term danazol. 

Peliosis hepatitis (liver, spleen replaced with blood-filled cysts), hepatic neoplasms, and hepatocellular carcinoma have been associated with prolonged high dosage. 

Oral contraceptives, estrogens, and benign liver tumors The effects of oral contraceptives on the liver include not only benign liver tumors (focal nodular hyperplasia, hepatic adenoma, and hemangioma) (74) and hepatocellular carcinoma, but also peliosis hepatis (75), sinusoid dilatation (76), and such probably unrelated shorter-term complications as jaundice and gallstones. 

Peliosis hepatis has been described in association with contraceptive-induced hepatic tumors and has sometimes developed in isolation, perhaps as a herald of more serious changes to follow, for example cirrhosis and portal hypertension one such case ultimately required an orthotopic liver transplant (219). 

Adverse hepatic effects have been linked to the use of oral contraceptives, including hepatic dysfunction, cholestatic jaundice, benign hepatic tumours and peliosis hepatis. In addition, oral contraceptives have a number of less common but important effects on the liver. A correlation between the development of the Budd-Chiari syndrome and COCs has been described, and progestational derivatives have been linked to exacerbations of hepatic porphyria [12]. 

Peliosis hepatis consists of a focal dilatation of the portal tract sinusoids. The condition is associated with contraceptive-induced hepatic tumours and can occasionally develop in isolation [13]. 

Focal liver diseases Biopsy material cannot be guaranteed as being representative. A higher degree of diagnostic accuracy can be achieved by a 2 to 3 fold liver biopsy in the course of a laparoscopic-bioptic examination of both lobes of liver. The same is true for peliosis hepatis (236, 305), granulomas and chronic hepatitis C, for example. (120)... 

A particular hepatotropicity causing severe herpes hepatitis is ascribed to herpesvirus 6 (HHV-6). There have even been reports of a fulminant course with this virus infection. (18, 23, 35) HHV-8 causes Kaposi s sarcoma. The liver is the most common site, with dark reddish-violet tumour nodes. Histological analysis reveals endothelial cell proliferations and growths of spindle-shaped fibroblast-like cells. The bile ducts may be altered. Transaminase levels are elevated, and jaundice occurs. There may be a causal relationship between HHV-8 infection and multicentric Castlemans disease. The latter usually implies the presence of peliosis hepatis, perisi-nusoidal fibrosis and nodular regenerative hyperplasia. 

Non-specific toxic liver damage may be evident in this connection, possible tuberculostatic toxic effects must also be considered. With severe courses of tuberculosis, peliosis hepatis is often observed. Frequently, retothelial nodules are detectable, as demonstrated for the first time in tuberculosis patients by H. Hamperl in 1953. (50) In the course of chronic pulmonary tuberculosis,infiltration of liver cells was noted, as reported in several publications. (50) It was attributed to toxic effects and/or undernourishment or malnutrition. Secondary hepatic amyloidosis, developing in the course of chronic lung tuberculosis, has also been postulated. (50) A restriction of hepatic function in chronic tuberculosis, which was first observed by E. Leuret et al. in 1922, has been described in a number of publications. (51, 60, 63) Depending on the severity and duration of the disease as well as the tuberculostatic pretreatment, we found pathological laboratory parameters in 15-20% and 25-40% of cases respectively. (50)... 

Medicinal agents (such as contraceptives) may result in proliferations of the intima in the hepatic artery and its branches. In some cases, these arterial alterations were associated with thrombosis in the hepatic veins. Phar-macons can trigger three different forms of damage to the sinusoids (7.) dilation of the sinusoids (e.g. by contraceptives), (2.) perisinusoidal fibrosis (e.g. by azathio-prine, vitamin A and cytostatic agents), and (i.) peliosis hepatis (e. g. by contraceptives, anabolic and androgenic steroids, azathioprine, chenodesoxycholic acid). (13, 28, 130) (s. p. 398) (s. fig. 21.8)... 

The principal side effects of the 17a-alkylated androgens are hepatic, including cholestasis, and uncommonly, peliosis hepatis (blood-filled hepatic cysts). Hepatocellular cancer has rarely been reported. When administered at high doses, these androgens are more likely than others to affect serum lipid concentrations, specifically to decrease high-density lipoprotein cholesterol and increase low-density lipoprotein cholesterol. 

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