Making residential treatment available to methadone clients.

This article addresses challenges to integrating clients on methadone into residential treatment, with the goal of promoting greater access for this population. It describes the basic administrative conditions needed for success, and discusses barriers and problems within the methadone program and the residential program. Staff communication, procedures for coordination, client and staff attitudes and understanding, and ongoing education are seen as the key to creating an environment conducive to success for the client.

[Budd-Chiari syndrome, pulmonary thromboembolism, and deep venous thrombosis associated with "lupus anticoagulant" and recent use of oral contraceptives]. / Síndrome de Budd-Chiari, tromboembolismo pulmonar y trombosis venosa profunda, asociado con "anticoagulante lúpico" y uso reciente de anticonceptivos orales.

The Budd-Chiari syndrome is the clinical manifestation of the total or partial obstruction of the hepatic veins and/or inferior vena cava. It is an infrequent cause of portal hypertension. The chronic presentation is the most frequent and is characterized by right upper quadrant pain, hepatomegaly, and ascites of slow onset. We report a case of a 26 year old woman affected by this disorder associated to a recent use of oral contraceptive and a "Lupus Anticoagulant". She subsequently developed deep venous thrombosis and pulmonary embolism. She died almost 6 years after the onset of symptoms.

PIP: A 26-year-old woman sought medical care in April 1983 because she had been experiencing pain in the right upper quadrant for 2 months, as well as an enlarged abdomen and postprandial fullness accompanied by nausea and vomiting. She had used oral contraceptives (OCs) for a period of 11 months up to 4 months before the inception of the symptoms. Examination showed normal vital functions but painful hepatomegaly. Hepatic biopsy showed dilatation of the central vein of the lobe; ultrasound of the liver showed hepatomegaly, the dilatation of hepatic veins, and suprahepatic veins; and echos of the inside were suggestive of thrombosis. The Doppler instrument revealed inversion of the hepatic flow towards the spleen and the presence of multiple collateral veins. Venocavography confirmed almost total obstruction of the inferior vena cava in its retrohepatic trajectory. Percutaneous transhepatic splenoportography demonstrated evidence of slow suprahepatic drainage with obstruction of the contrast medium in the area of the cava. The pressure in the suprahepatic vein was 43 cm of H2O. As the illness progressed, profound venous thrombosis of the left lower extremity developed, which was treated with heparin and managed with fenindione for 4 years. 5 years later, multiple pulmonary thromboembolism was confirmed by pulmonary gammagram of perfusion and digital arteriography. She received medical treatment based on low sodium and diuretic diet. Her hepatic function progressively deteriorated with increased ascites and collateral venous network. She died in December 1988.

Lymphocyte subsets and HLA-DR expression in normal pancreas and chronic pancreatitis.

In an attempt to study the mechanisms leading to fibrosis in chronic pancreatitis, an in situ immunohistochemical investigation of lymphocytes and of class II major histocompatibility complex expression (HLA-DR) by epithelial cells has been designed. Samples of normal pancreas (n = 8), chronic calcifying pancreatitis (n = 4), chronic obstructive pancreatitis (n = 6), and diffuse fibrosing pancreatitis (n = 6) have been studied. In normal pancreas, T-lymphocytes were rare and were located in the epithelial layer of pancreatic ducts and in the periductal connective tissue. Duct cells were constantly HLA-DR negative. In chronic calcifying pancreatitis and chronic obstructive pancreatitis, T cells were numerous and were located around ducts and in the spreading areas of fibrous septa. In chronic obstructive pancreatitis, the duct cells strongly expressed the HLA-DR antigen. In diffuse fibrosing pancreatitis, fibrous tissue was devoid of lymphocytes and duct cells never expressed the HLA class II antigen. These results suggest that lymphocytes are involved in the fibrosing process occurring in chronic calcifying pancreatitis and chronic obstructive pancreatitis but not in diffuse fibrosing pancreatitis. The significance of de novo expression of HLA-DR antigen by duct cells is discussed.

Expression of histocompatibility antigens and characterization of the lymphocyte infiltrate in hyperplastic polyps of the large bowel.

HLA-DR expression, lymphocyte subsets, and the distribution of proliferating cells were studied in hyperplastic polyps from the colorectum. The density of T-cells (CD5+) (mean of cells/mm2 of tissue +/- SEM) was higher in the lamina propria of hyperplastic polyps (64.2 +/- 4.2) than in normal colonic mucosa (36.7 +/- 2.6, P less than .001). The CD4/CD8 ratio was higher in hyperplastic polyps (6.3 +/- 0.9, P less than .0001) and in colonic adenomas (5.9 +/- 0.9, P less than .001) compared with normal mucosa (2.3 +/- 0.2). Lymphocytes of the lamina propria were never Ki-67 positive either in normal mucosa or in hyperplastic polyps or adenomas. The epithelial layer of hyperplastic polyps and of normal mucosa did not express the HLA-DR antigen, whereas pericryptal fibroblasts and most of the leukocytes of the lamina propria were strongly positive for this antigen. In the epithelial layer proliferating cells were localized exclusively in the lower part of epithelial crypts, as was the case in normal mucosa, whereas in adenomas Ki-67-positive cells were present throughout the entire height of the mucosa. Thus, in hyperplastic polyps lymphocytes are increased in the lamina propria, with a predominance of the CD4 subset in close contact with HLA-DR positive pericryptal fibroblasts.

Quantitative estimation of the collagen content in normal and pathologic pancreas tissue.

The aims of the study were to measure the collagen content in pancreas using a colorimetric method and to compare the amount of collagen in normal pancreas (11 cases), diffuse fibrosing pancreatitis (17 cases), and chronic calcifying pancreatitis (11 cases). The procedure of fibrosis measurement was based on the selective capacity of two dyes, Sirius red and fast green, to set on collagen and noncollagenous proteins, respectively. After staining of sections, colors were eluted from the sections and the specific absorbance of each eluted dye was read on a spectrophotometer. The collagen content in normal pancreata was 26.5 +/- 7.2 micrograms collagen/mg protein. The amount of collagen increased with the age of patients: the mean value of the patients under the age of 50 was 18.2 +/- 4 micrograms collagen/mg protein whereas the mean value in older patients was 31.9 +/- 8 micrograms collagen/mg protein (p less than 0.01). The value of collagen in pancreas with a diffuse fibrosing pancreatitis was 44.7 +/- 7.5 micrograms collagen/mg protein. This value was significantly different from the collagen content in normal pancreas (p less than 0.001) and in pancreas with a chronic calcifying pancreatitis (77.9 +/- 8 micrograms collagen/mg protein, p less than 0.001). This method permits discrimination between different chronic diseases that can also be differentiated on a histopathologic basis.

A longitudinal study of histologic and immunohistologic changes in an experimental model of sclerosing cholangitis.

A longitudinal study of intra and extrahepatic bile duct injuries was performed in an animal model of secondary sclerosing cholangitis induced by formalin injection into the common bile duct. Lymphocytic infiltration inside and around the bile ducts occurred seven days after injection. The disease later evolved to a fibrous cholangitis of the small bile ducts. Septal intrahepatic and extrahepatic bile duct involvement became evident three months after formalin injection. The ductular proliferation led to a progressive biliary cirrhosis with portal to portal fibrous septa. After formalin injection, bile duct cells expressed the Ia antigen in the cytoplasm and/or on the membrane of bile duct cells. The intensity of staining did not correlate with the duration or severity of the disease. Lymphocytes infiltrating into and around the bile duct were mainly T-cells. This study suggests that a local cell-mediated immune response to the injection of a toxic agent induces pathological features similar to those of sclerosing cholangitis in man.

Effects of fixation and processing on the immunohistochemical visualization of type-I, -III and -IV collagen in paraffin-embedded liver tissue.

We compared the effects of different fixatives and enzymatic-digestion procedures on the immunohistochemical visualization of type-I, -III and -IV collagen in paraffin-embedded normal human liver sections. None of the fixatives tested allowed the staining of these antigens without prior enzymatic digestion. The best results i.e. strong staining intensity and well-defined localization, were obtained when liver tissue was fixed in Bouin's fluid or in other solutions containing picric acid. Several other fixatives, including Carnoy's fluid, Lillie's AAF, 10% neutral formalin and 96% ethanol, gave unsatisfactory results. Pepsin was ineffective for unmasking type-I and -III collagen antigens, and was only partially effective for visualizing the type-IV collagen antigen. The best results were obtained when material fixed in Bouin's fluid was embedded in paraffin and digested with trypsin. Using this procedure, the results were comparable to those obtained in unfixed frozen sections with respect to the staining intensity, specificity and non-specific staining.