Primary pericardial mesothelioma is an extremely rare and lethal cardiac tumor. We report an autopsy case of a primary pericardial mesothelioma in a 52-year-old man. He developed dyspnea, cough, low-grade fever and night sweats approximately 3 months before last admission. Initially, he was evaluated at a hospital in another city, without a firm diagnosis. Due to progressive symptoms and the development of lower-extremity edema, he presented at our hospital in September 2005. The physical examination at admission demonstrated signs of pericardial tamponade. Chest radiography revealed marked enlargement of the cardiac silhouette. Specimens of bloody pericardial fluid were positive for pericardial mesothelioma by cytologic examination. The general condition of the patient worsened very rapidly and he was transferred to the intensive care unit where he later died. Postmortem examination confirmed primary pericardial mesothelioma of the mixed/biphasic type with lymphatic metastasis in the right lung. By using immunohistochemical analysis for specific markers of mesothelioma and for differentiation of the mesothelioma from the lung adenocarcinoma, definitive diagnosis was established: primary pericardial mesothelioma

The ultrastructural research has a decisive role in gathering the knowledge on the liver's response to the influence of some drugs. The aim of the study was to perform an ultrastructural analysis of the liver in chronic intravenous heroin addicts.The study involved the autopsy conducted on 40 bodies of intravenous heroin addicts and 10 control autopsies. The liver tissue was fixed in glutaraldehyde and moulded with epon for investigation purposes of ultrastructural changes. The analysis was performed using the method of transmission electron microscopy.In the group of intravenous heroin addicts, the liver autopsy samples showed degenerative vesicular and fat changes, chronic active and persistent hepatitis, cirrhosis, reduction in the amount of glycogen in hepatocytes, as well as the Kupffer cell's dominant hypertrophy. Various changes occur in organelles, plasma membrane of hepatocytes and biliary channels as well as in the nucleus. The most important ultrastructural findings include: hyperplasia and hypertrophy of the smooth endoplasmic reticulum, which is histologically proven vesicular degeneration of hepatocyte occurring as a result of the increased synthesis of enzymes of smooth endoplasmic reticulum due to chronic intravenous heroin intake, and the presence of continuous basal membrane followed by transformation of the sinusoids into capillaries (in the cases of chronic active hepatitis and cirrhosis) which leads to a disorder of microcirculation and further progress of cirrhosis.

Intravenous heroin intake leads to significant morphological changes in the liver tissue (vesicular changes, fatty changes, chronic hepatitis and cirrhosis). The intensity of these changes increases with the duration of heroin use. Direct hepatotoxic effects of heroin are vesicular changes in hepatocytes, fatty changes are the result of chronic influence of alcohol, whereas the rest of the morphological liver lesions are the result of the interaction of heroin, viral infection and alcohol. In the present study, we analyzed a total of 50 autopsies, 40 from the group of intravenous heroin users and 10 from the control group (dead bodies of young and healthy people with mechanical injuries that did not affect the liver). For ease of analysis, all autopsy cases of intravenous heroin abuse were divided into 4 groups according to the duration of intravenous heroin intake: up to 2 years, between 2 and 5 years, between 5 and 10 years, and longer than 10 years.

Apart from the usual morphological changes in the liver of intravenous heroin users such as vesicular and fatty changes, various forms of viral hepatitis and development of cirrhosis, the onset of amyloidosis, the change in the number of hepatic sinusoidal macrophages, and dysplastic changes are of particular significance from the forensic point of view since they can indicate heroin abuse, probably associated with alcohol effects, and they can also be a factor for the occurrence of severe morphological liver damage with a possible lethal outcome. A histopathologic and morphometric study of changes in the liver of heroin users aimed to show the presence of rarer morphologic changes in the liver as the indicators of heroin abuse, additional alcohol effects and viral infections. The present study included 40 autopsies of intravenous heroin users and 10 control autopsies. In order to facilitate the investigation, all autopsies of intravenous heroin users were grouped according to the duration of intravenous heroin intake into 4 groups: up to 2 years, 2-5 years; 5-10 years; over 10 years. Paraffin sections 5 µm thick, were stained by hematoxylin method (HE), van Gieson and Congo red. Morphometric investigation of sinusoidal macrophages in the liver was done using the M42 test system. Liver tissue samples taken to be tested for ultrastructural changes were fixed in glutaraldehyde and epon-embedded, and the analysis was done using transmission electron microscopy JEM 100 CX JEOL. Amyloidosis localized in portal tracts, mostly underneath the endothelium of the smaller branches of the hepatic artery was established in 9 cases (22,5%), out of which in 78% (in 7 of 9) the duration of intravenous intake lasted longer than 5 years. In 55,5% of cases (in 5 of 9), amyloidosis was associated with fatty alcohol changes. There was a statistically significant change in the number of sinusoidal macrophages in relation to the controls only in cases with chronic active hepatitis regardless of coexisting cirrhosis, whereas the other cases with established fatty alcohol changes showed no significantly higher number of these cells in relation to controls. Severe dysplastic changes were established in three cases with vesicular and fatty changes complicated with viral hepatitis, two of which were with coexisting cirrhosis; in all three cases (100%), the duration of intravenous heroin abuse lasted longer than 5 years. Long duration of heroin abuse is a condition for the occurrence of liver amyloidosis and dysplastic changes in the liver. The high percentage of association of amyloidosis with fatty alcohol changes in the liver points to the conclusion that the inactivation of hepatic sinusoid macrophages and the reduction of their enzymatic capacities occur due to additive, immunosuppressive effect of alcohol which may enable the onset of liver amyloidosis.

Introduction. The liver plays a key role in the removal of lipophyllic substances from the plasma, including both morphine and its derivative heroin. Intravenous heroin abuse leads to liver damages, so that the effects of heroin intake are the most marked and characteristic in the liver. Objective. A histochemical and ultrastructural study of the liver, particularly hepatocyte glycogen content, should provide a precise insight into the type and degree of liver damage induced by intravenous heroin abuse. Methods. The study included the analysis of 50 autopsies, 40 from the group of intravenous heroin abusers and 10 control autopsies. Paraffin sections, 5 µm thick, were stained by PAS method for deposited glycogen staining. The ultrastructural investigation was performed on transmission electron microscope. Results. Glycogen amount was reduced proportionally to the severity and distribution of degenerative and necrotic hepatocytic lesions. Regarding deposited glycogen depletion in particular acinar zones, glycogen was most preserved in zone 1 (30% of studied cases), then in zone 3 (preserved in 25%), while the depletion was most significant in intermediary zone (preserved in 5%). In the intravenous heroin abusers group of up to 2 years glycogen was preserved in the acinar zones 1, 2 and 3 in 43%, 30% and 57%, respectively; in the group of over 10 years glycogen preservation in zone 1 was 25% and in other zones 0%. Conclusion. Intravenously administered heroin directly influences glycogen reduction in the hepatocytes, and the effect is potentiated by morphologic changes in the liver due to intravenous heroin abuse. Glycogen depletion in the hepatocytes reduces energy reserves in these cells and causes cell death, which is an important segment of general liver injury in intravenous heroin abusers. The degree of reduction of glycogen depositions is proportional to the duration of intravenous heroin abuse