Search

The dendritic cells in skin biopsies from 36 fetuses (from 16 weeks' gestational age on) and neonatal infants of different ages were investigated using a number of markers for various cells of the immune system and immunohistochemistry. Epidermal Langerhans' cells were found in all cases in a predominantly basal localization. The number of OKT6-positive Langerhans' cells and the development of their dendritic processes gradually increased with age. Dermal dendritic cells were present as well. Both HLA-DR-positive and Leu-10-positive dermal dendritic cells were found in the superficial and deep dermis, often in a perivascular distribution. The OKT6-positive dermal dendritic cells were few in number and occurred only in the upper dermis.

Gallbladders of 12 cases with chronic cholecystitis showing pseudopyloric glands (PPG) and of 18 cases with acute cholecystitis or chronic cholecystitis but without PPG were examined by the peroxidase - antiperoxidase (PAP) method using rabbit antibody against human lysozyme (LM). LM-immunoreactivity was detected in the cytoplasm of PPG and, to a lesser extent, in the pits of epithelial crypts that gave rise to PPG. No LM was found in normal gallbladders; in cases of cholecystitis without PPG, LM-immunoreactivity was restricted to infiltrating inflammatory cells. The presence of LM in PPG suggests that PPG represent functional metaplastic areas, involved in the non-specific defence mechanisms through participation of LM. [ABSTRACT FROM AUTHOR]

By use of the indirect immunoperoxidase method, lysozyme was localized in the serous glands and serous parts of mixed mucous-serous glands of the nasal respiratory area. Histochemically, lysozyme was absent from acini containing acid mucosubstances. These findings are in agreement with localizations of lysozyme in glands at other sites. [ABSTRACT FROM AUTHOR]

ABSTRACT- Twenty specimens of focal nodular hyperplasia were studied with special attention to the histological features of chronic cholestasis (grouped under the headings of cholestasis, cholate-stasis and signs of ductular reabsorption). In all specimens, evidence was found for one or more features of cholestasis and cholate-stasis. Signs of ductular reabsorption were less constant, and apparently varied according to the developmental stage of the lesion. The cholestatic features emphasize the bile secretory capacity of the lesional parenchyma, and are apparently due to the lack of real bile ducts in the portal tract equivalents of the lesional tissue. Evidence is presented that the 'ductular component' in FNH is not due to proliferation of pre-existing ductules, but rather derives from ductular metaplasia of liver cell plates in zone 1 equivalents. This metaplastic development of a ductular network may serve the function of reabsorbing the biliary constituents produced by the lesional parenchyma, leading to periductular inflammation and progressive fibrosis, thus producing an equivalent of biliary fibrosis and biliary cirrhosis. [ABSTRACT FROM AUTHOR]

ABSTRACT- Ten liver biopsy specimens from nine patients with PBC stages II to IV were studied immunohistochemically with a broad panel of monoclonal antibodies. In areas of bile-duct proliferation, many BA1+ B-lymphocytes and OKT4+/Leu3a+ helper/inducer T-cells were observed, admixed with some C3b-receptor positive, mono-and polymorphonuclear OKM1+ cells. Numerous IgM-containing plasma cells were seen in portal tracts showing bile-duct proliferation. In contrast, areas of piecemeal necrosis and intralobular spotty necrosis consisted mainly of OKT4+/Leu3a+ helper/inducer, and OKT8+ suppressor/cytotoxic T-cells, admixed with some OKM1+ polymorphonuclear granulocytes. Almost no BA1+ B-lymphocytes or Ig-containing plasma cells were observed in areas of piecemeal necrosis and spotty necrosis. Major histocompatibility complex (MHC)-class I antigens (i.e. HLA-A,B,C) were demonstrated either on the liver cell membrane, or on sinusoidal lining cells. The latter also expressed MHC-class II antigens (i.e. HLA-DR). In two liver biopsies, an increased expression of HLA antigens was observed near areas of piecemeal and spotty necrosis. Our results indicate that several immune mechanisms each with a particular topographical distribution, are operative in PBC. Inflammatory cells, involved in humoral immunity, are present mainly in areas of bile duct proliferation. In contrast, the effector cells of antigen-specific cellular cytotoxicity are present in areas of piecemeal necrosis and spotty necrosis. In the latter areas, a pronounced expression of MHC products representing the afferent limb of the cell-mediated immune response, may permit an optimal T-cell-mediated immune effect or, eventually, result in adverse effects. [ABSTRACT FROM AUTHOR]

ABSTRACT- Deparaffinized sections of hepatitis B surface antigen (HBsAg) positive liver biopsies, when incubated in a human fibrinogen solution, reveal a strong labelling of ground-glass hepatocytes with fibrinogen. This implies an interaction between HBsAg and fibrinogen. The binding of fibrinogen to HBsAg is thought to be mediated by the protein moiety of HBsAg, since its binding capacity is destroyed by trypsin digestion, and to occur through formation of disulphide bridges because the binding can be disrupted by the reducing effect of 2-mercapto-ethanol. Not all ground-glass hepatocytes exhibit fibrinogen binding. The reason for this is at present unclear. No relationship between serum HBeAg positivity and binding of HBsAg to fibrinogen was observed. Preincubation in a fibrinogen solution did not alter the immunoreactivity of HBsAg. We conclude that there is a striking analogy between the interaction of HBsAg with polymerized human serum albumin and its interaction with fibrinogen. [ABSTRACT FROM AUTHOR]

ABSTRACT- The predictive value of piecemeal necrosis (PMN) in acute hepatitis was investigated in 62 patients (39 hepatitis B virus infection, 9 hepatitis A virus infection and 14 possible hepatitis NANB virus infection). The 62 initial biopsies were blindly recoded and classified into three groups: 1. Acute hepatitis with signs of possible transition to chronicity (AHTC) (n = 35)(i.e. a picture of acute hepatitis associated with PMN). 2. AHTC-borderline group (BL) (n = 15) (i.e. a picture of acute hepatitis with minimal PMN). 3. Uncomplicated acute hepatitis (AH) (n = 12) (i.e. a picture of acute hepatitis without PMN). Follow-up of the patients revealed an evolution to chronicity in a very high percentage of the AHTC-cases of hepatitis B (95%) and NANB (89%) etiology. Also 67% of the BL-cases of hepatitis B etiology developed chronic liver disease. In hepatitis B the immunohistochemical pattern of HBsAg is of additional help. In hepatitis A, PMN is often present (5/9) but no evolution to chronicity was observed. This study shows that PMN in acute hepatitis appears to be a useful prognostic feature for chronicity in hepatitis B and NANB. [ABSTRACT FROM AUTHOR]

ABSTRACT- A syndrome resembling human Primary Biliary Cirrhosis (PBC) and occurring spontaneously in a strain of domesticated rabbits from the Faenza region in Italy, is reported. The syndrome is characterized by histological liver changes consisting of chronic non-suppurative destructive cholangitis and copper accumulation, biochemical and immunological abnormalities mainly represented by an elevation of serum alkaline phosphatase and a positive antimitochondrial antibody test. The abnormalities were not observed in newborn rabbits from the same area nor in control rabbits from the island of Sardinia. A toxic effect related to some environmental factor may be responsible for the disease. Alternatively, a continuous process of partial inbreeding among consanguineous animals may have resulted in a selection of a strain genetically predisposed to the development of PBC. Whatever the etiology, the domesticated Faenza rabbit proves to be an interesting animal model for a chronic non-suppurative destructive cholangitis, very similar to the human disease known as PBC. [ABSTRACT FROM AUTHOR]

ABSTRACT- A new ultrastructural cytoplasmic marker designated as type 2, and distinct from type 1 previously associated with NA-NB hepatitis in chimpanzees, was found in hepatocytes of two patients and of one experimentally infected chimpanzee. These cases represent a minority of all cases we studied as presumed NA-NB viral hepatitis. Type 2 marker consists of tubular structures composed of an assembly of ring-like units coated with smaller uniform fragments, accumulated in different patterns in dilated cisternae of the endoplasmic reticulum. Preliminary data using immunofluorescence with NA-NB hepatitis convalescent serum and antiserum against fibrinogen are reported. Type 2 marker may represent a different agent or a different reaction pattern to one agent of NA-NB viral hepatitis. Its features are compared with those of hepatitis B. [ABSTRACT FROM AUTHOR]

ABSTRACT- Ultrastructural investigation of liver biopsies from two patients with non-A, non-B hepatitis revealed cytoplasmic and nuclear alterations in the hepatocytes. The lesions in both patients, one with acute and one with chronic hepatitis, were similar and distinct from those previously described in other forms of hepatitis. These findings are compared with the reported findings in chimpanzee liver after inoculation with non-A, non-B infective material. The intranuclear findings are similar to the aggregations of 20-27 nm particles described in some infected chimpanzees, and the cytoplasmic alterations seem to be similar to the cytoplasmic structures and tubular arrangements reported in other inoculated chimpanzees. A striking finding of this study is the presence of both alterations together in the same biopsy in two different patients, suggesting that they represent a different stage of viral infection or different parts of the viral agent. It still remains to be proved that the ultrastructural particles indeed contain antigen(s) of the non-A, non-B hepatitis virus. The nuclear and cytoplasmic alterations are, however, characteristic for non-A, non-B hepatitis and are useful as ultrastructural hallmarks of this form of hepatitis. [ABSTRACT FROM AUTHOR]

The expression of transferrin receptors (TfR's) has been investigated in eight liver biopsy specimens (four from patients without demonstrable iron and four from patients with iron storage due to primary hemochromatosis (HC)) using immunoelectron microscopy to demonstrate TfR's by the simultaneous application of two specific monoclonal antibodies (OKT9 and B3/25) to tissue chopper sections. In the four specimens without iron overload, hepatocytes, but not sinusoidal lining cells, stained positively and immunoreactivity was mainly localized in the cytoplasm. Positively stained cisternae of the endoplasmic reticulum indicated synthesis of the TfR. The presence of TfR's on segments and coated invaginations of the sinusoidal membrane and in small, but otherwise unidentified vesicles in the cytoplasm is compatible with endo-/exocytotic transport and recycling of TfR's as demonstrated by biochemical studies. Ocassional positively stained material in canalicular lumina together with positively stained canalicular microvilli and pericanalicular vesicles suggest that transcellular transport may be an additional pathway for TfR's. In three biopsies showing severe iron overload due to HC, TfR immunoreactivity was completely absent. The remaining specimen showing HC, exhibited relatively mild iron overload and showed only a few positively stained hepatocytes. This supports the previously reported disappearance of hepatic TfR expression in HC when iron overload is severe. [ABSTRACT FROM AUTHOR]

The enzyme and immunohistochemical features of lymphnodes showing sinus histiocytosis have been studied. Sinus histiocytes with phenotype OKM1 0KT4 Leu3a To5 OKIal showed strong acid phosphatase and non-specific esterase, weak endogenous peroxidase and no ATPase activities. In nine out of ten lymph nodes, paracortical collections of dendritic OKT6 OKIal cells were observed. In two of the four cases studied these dendritic cells showed strong ATPase activity. We suggest that the dendritic OKT6 OKIal ATPase interfollicular cells represent newly arrived veiled cells (VC) which have entered the lymph node by the afferent lymph, settled in the interfollicular area and are probably involved in the induction of a cellular immune response. OKT6 OKIal ATPase VC may subsequently transform into mature, OKT6 OKIal ATPase interdigitating reticulum cells which are involved in the negative feedback of the cellular immune response. The association with sinus histiocytosis is probably related to the fact that an increase in mononuclear phagocytes in the afferent lymph is accompanied by a relative increase in VC. Our results demonstrate that in lymph nodes showing sinus histiocytosis, two cell types increase in number, i.e. an Ia sinusoidal cell, engaged in phagocytosis of foreign material, and an Ia dendritic cell in the interfollicular area, probably involved in the induction of a cellular immune response. [ABSTRACT FROM AUTHOR]

We compared the paracortical area in 4 cases of dermato-pathic lymphadenitis (DL) with the same area in 11 cases of various other reactive conditions of the lymph node by immuno- and enzymehis-tochemical techniques. In addition, electron microscopy was performed on threee cases of DL. The paracortical nodules in DL proved to be composed of a variable number of dendritic, OKT6+ OKIa+ ATP-ase+ cells, admixed with helper T-lymphocytes. All other lymph nodes studied lacked dendritic OKT6+ cells, whereas OKIa positivity was found in the cortical (follicular centers and mantle zones) and paracortical area (lymphocytes and scattered dendritic cells). Short incubation for ATPase revealed a paracortical, pericellular staining pattern in cases of DL, whereas in all other cases this staining pattern was observed only after long incubation times. On electron microscopy, three types of dendritic cells were found in DL, namely interdigitating reticulum cells (IDRC), Langerhans cells (LC) and macrophages. Intermediate forms between IDRC and LC, containing a few Birbeck granules and a well developed rough endoplasmic reticulum, were found. It is suggested that immunoreactivity for the monoclonal antibody 0KT6 is restricted to cases of DL, and is due to the appearance of dendritic cells that have LC-characteristics. These cells either arrive from the skin along afferent lymph vessels, or are the result of a local transformation process of IDRC that acquire LC-characteristics, i.e. OKT6 immunoreactivity and Birbeck granules. [ABSTRACT FROM AUTHOR]

The effect of interferon-gamma on the expression in situ of major histocompatibility complex (MHC) products in human corneas was studied in vitro. Incubation for four days with 5 or 50 mg/l of Escherichia coli-derived recombinant human interferon-gamma resulted in the appearance de novo of MHC class II or HLA-DR antigens on variable numbers of corneal epithelial cells as well as on corneal endothelium, whereas it had no effect on the expression of MHC class I or HLA-ABC antigens. These results may help to explain the mechanism underlying the expression of HLA-DR antigens on corneal and limbal epithelium in various inflammatory eye diseases. [ABSTRACT FROM PUBLISHER]

Upper palpebral conjunctival biopsy specimens obtained from eight patients with active trachoma were examined by routine histological and immunohistochemical methods. The epithelium expressed class I major histocompatibility complex (MHC) products throughout and class II MHC products in the superficial layers. The epithelial inflammatory infiltrate consisted of polymorphonuclear leucocytes, macrophages, T lymphocytes, and dendritic cells. In the underlying stroma the inflammatory infiltrate was organised as B lymphoid follicles, and there was also a diffuse infiltrate consisting of plasma cells and scattered B lymphoid cells, dendritic cells, T cells, macrophages, and polymorphonuclear leucocytes. Each type of cell has its special location in the tissue. Plasma cells were located on a subepithelial band and as a dense infiltrate round the acini of accessory lacrimal glands. IgA+ plasma cells outnumbered IgG+ cells, whereas IgM+ and IgE+ cells were few. Our data provide good evidence for the presence of both humoral and cell mediated immune responses and a possible role for autoimmune mechanisms in the conjunctival tissues of trachoma patients. [ABSTRACT FROM PUBLISHER]

The cellular composition of the inflammatory infiltrate present in 13 patients with the limbal form of vernal keratoconjunctivitis was examined in the conjunctival scrapings and the limbic replicas by means of Giemsa stain and immunohistochemistry. Conjunctival scrapings showed the presence of mast cells, lymphocytes, plasma cells, polymorphonuclear leucocytes, and very few basophils in all the specimens. Eosinophils were present in only four scrapings. The superficial epithelium of the limbic lesion and the adjacent cornea and conjunctiva was studied by the replica technique. The limbic lesion area showed the presence of necrotic epithelial cells mixed with inflammatory cells, including eosinophils, mast cells, lymphocytes, plasma cells, and polymorphonuclear leucocytes and very few basophils. Most of the inflammatory cells were HLA-DR+. Many OKT6+ cells were present, indicating the presence of Langerhans cells. T-lymphocytes including a few helper/inducer cells and many suppressor/cytotoxic cells, were detected in the infiltrate. In addition many B-lymphocytes were observed. These findings suggest that other immune mechanisms in addition to type 1 reaction are involved in the pathogenesis of the disease. [ABSTRACT FROM PUBLISHER]

Eighteen liver biopsy specimens from patients with hepatitis B surface antigen (HBsAg) positive chronic aggressive hepatitis were studied by electron microscopy. All cases were selected on the basis of positive liver cell membrane fluorescence for HBsAg on immunohistochemical investigation. Striking changes in the morphology of the liver cell membrane were observed in nearly all cases. Furthermore, a dual aspect of hepatitis B core antigen (HBcAg) is described. HBcAg particles may occur as either 'naked' or 'cloudy' particles surrounded by semi electron dense material. The nature of the 'cloud' remains to be identified. [ABSTRACT FROM PUBLISHER]

This study reports the incidence of HBsAg in a series of chronic lymphoproliferative disorders in which a high incidence of cirrhoses had been previously observed. Twenty-three cases were collected from the necropsy records. The type of lymphoma was reviewed in the light of the new functional classifications of non-Hodgkin malignant lymphomas introduced by Lennert and Lukes. The presence of HBsAg in the liver was investigated by the indirect immunofluorescence technique. Eleven cases showed plasmocytoid features and were considered as immunocytomas. Seven cases showed cirrhosis of the liver; six of them belonged to the immunocytoma group. Four cases were positive for HBsAg. Three of them were found among the group combining cirrhosis and immunocytoma. They presented the abundant nodular distribution of HBsAg typical of inactive cirrhosis. A parallel is drawn between the often reported association of Waldenström's syndrome and cirrhosis and the association of immunocytoma and cirrhosis observed in this study. The analogy is all the more justified since most of the lymphomas associated with Waldenström's syndrome happen to be immunocytomas. Therefore the association between HB virus infection and cirrhosis on the one hand and chronic lymphoproliferative disorders on the other may not be purely coincidental. A chronic antigenic stimulus such as persisting HBsAg could trigger the proliferation of a malignant lymphoid clone. [ABSTRACT FROM PUBLISHER]

One hundred liver biopsies from 100 hepatitis patients were examined by the indirect immunofluorescent technique for the detection of HBsAg. Of the 60 positive specimens 52 were diagnosed as various types of chronic hepatitis and 8 were acute hepatitis. Four main distribution patterns of HBsAg were obtained: full cytoplasmic fluorescence with diffuse lobular distribution; cytoplasmic fluorescence with spotty distribution; peripheral fluorescence in the cell membrane and/or cell peripheries; and focal cytoplasmic positivity. There was an inverse relationship between the number of positive hepatocytes and the extent of liver cell necrosis. The distribution patterns of HBsAg were distinctive in each type of chronic hepatitis and in acute hepatitis. Homogeneous full cytoplasmic fluorescence, distributed diffusely in the whole liver lobule, was observed in chronic persistent hepatitis and in cirrhosis with little activity whereas peripheral liver cell membrane and/or peripheral cytoplasmic fluorescence associated with cytoplasmic positivity in a smaller number of hepatocytes was a characteristic finding in chronic aggressive hepatitis, active cirrhosis, and acute hepatitis with possible transition to chronicity. Focal cytoplasmic fluorescence was observed in acute hepatitis and a group of biopsies in chronic hepatitis in which HBsAg was detected in the liver but no antigen was detectable in the serum. The results show that the different patterns of distribution of HBsAg in the liver biopsy are helpful for the histological diagnosis of different types of HBAg positive viral hepatitis and are consistent with the hypothesis of the role of specific immune response in the pathogenesis of type B viral hepatitis. [ABSTRACT FROM PUBLISHER]

Chronic hepatitis was diagnosed on liver biopsy of 76 patients; 52 (68%)had HBsAg. Of the 52 patients with HBsAg, 23% had HBsAg shown by immunofluorescence on the liver, while it could not be detected with radioimmunoassay on the serum; 77% had HBsAg detectable in liver and in serum, and none had HBsAg in serum only. HBsAg was detected more frequently in chronic aggressive hepatitis and active cirrhosis than in chronic persistent hepatitis and cirrhosis with little activity. No correlation was found in the different forms of chronic hepatitis between the HBsAg status on the one hand, and levels of transaminases, gammaglobulins, and auto-antibodies on the other. Acute hepatitis was diagnosed on liver biopsy of 24 patients; 50% had HBsAg. Liver tissue positivity was very low in the fully developed stage compared to serum positivity. In 146 patients with other liver ailments, both liver and serum were negative for HBsAg. [ABSTRACT FROM PUBLISHER]

Alpha1-antitrypsin was detected by indirect immunofluorescence in frozen sections of liver biopsies from patients with clinically and biochemically proven alpha1-antitrypsin deficiency. The antigen could also be demonstrated in those liver specimens of the same patients which were fixed in Bouin's fluid and embedded in paraffin. The cellular localization and the brightness of the fluorescence were the same in both frozen and paraffin sections. Four additional biopsies from three other patients were selected on the basis of PAS-positive diastase-resistant inclusions reported in the hepatocytes. All these biopsies showed bright fluorescence in the cytoplasm of the liver cells although one of the biopsies was stored for as long as eight years. Specific fluorescence was constantly found in the periportal hepatocytes with varying degrees of positivity. No fluorescence was observed in the six control biopsies from patients with various other liver diseases. These findings prove that paraffin embedded specimens are suitable for immunofluorescence detection of alpha1-antitrypsin and that a retrospective study on old paraffin blocks is possible. [ABSTRACT FROM PUBLISHER]

A solitary hepatic metastasis is amenable to surgery. However, if surgery is contraindicated or if multiple lesions are present in both liver lobes, other treatment modalities have to be considered. We compared the effect of interstitial laser hyperthermia with damage caused by alcoholization. Six anaesthetized beagle dogs were studied. Three animals were treated with laser hyperthermia. A bare laser fibre (400 μm diameter) was introduced through a 17-gauge needle, length 170 mm, positioned into the liver under real time ultrasonographic guidance. Lesions were produced by continuous 500-s exposure of 1W YAG laser (Medilas MBB 40N) power. Three dogs were subjected to an injection of 4 ml of 98% pure ethanol into the liver through the same needle system. Two days after the procedure the animals were killed and the livers examined. The surface of the livers treated with the YAG laser were entirely normal; superficial lesions were, however, clearly visible. Laserinduced lesions were well reproducible, clearly demarcated, roughly spherical with a mean diameter of 1.01±0.23 cm (n=16). In contrast, the dogs treated with alcohol had free intraperitoneal serohaemorrhagic fluid and the surface of the liver was diffusely abnormal. The lesions had a more or less cylindrical shape, 1.22±0.43 cm on 0.40±0.10 cm (n=12) although exact measurement was often difficult. The border of the lesions was irregular and there was a clear necrotic zone along the puncture track. On microscopic examination the laser-induced lesions consisted of a central evaporation area, a zone of carbonized material and an outer zone of coagulation necrosis. The alcohol-induced lesions were characterized by both 'fixation' necrosis and coagulative necrosis but surprisingly, there was also necrosis present at a distance of the lesions extending along the centrilobular and even portal veins. These data show that laser-induced interstitial necrosis in the liver is better controlled and more reproducible than necrosis induced by injection of pure ethanol. Moreover, pure ethanol may cause damage to the liver surface and even at a distance of the injection site. [ABSTRACT FROM AUTHOR]

The expression of the selectin receptor LAM-1/Leu 8 was analysed in normal and in inflamed liver tissue and its expression on mononuclear inflammatory cells was correlated with their topographical distribution in various compartments of the inflamed liver, in order to obtain new insights on possible molecular mechanisms involved in the traffic of mononuclear inflammatory cells throughout the diseased hepatic parenchyma. In normal liver tissue, few scattered mononuclear cells in portal and lobular parenchyma corresponded lo both CD4+ and CD8+, as well as to CD45RA+ (2H4+) naive and CD45RO+ (UCHLI+) memory T cells, and were LAM-1/Leu 8+. In acute and chronic inflamed liver biopsies. CD45RO+ (UCHLI+)CD4+ and CD8+ memory T cells largely predominated in both portal and lobular parenchyma. The expression of LAM- 1/Leu 8 antigen on these memory T cells varied according to their localization in the liver parenchyma, and it was not correlated with specific aetiological causes. In acute hepatitis, the vast majority of T lymphocytes were LAM-1/Leu 8 . In chronic active hepatitis, memory T cells in portal tracts expressed LAM-1/Leu8, whereas virtually all intralobular T cells accumulating in areas of periporial and intralobular inflammation were LAM-1/Leu8+. In chronic persistent hepatitis, the LAM-1/Leu8+ T cells largely predominated among the numerous mononuclear inflammatory cells within enlarged portal tracts, whereas LAM-1/Leu 8 T cells were restricted to areas of intralobular "spotty" inflammation. Therefore, two phenotypical populations can be recognized among the memory T cells in inflamed liver tissue, according to their topographical localization: LAM-1/Leu8+ T cells predominating in portal tracts, and LAM-1/Leu 8- T cells predominating in the lobular parenchyma. These data show that during their migration through the inflamed liver parenchyma, memory T lymphocytes undergo phenotyical changes (LAM-1/Leu8 shedding) according to their localization indifferent liver compartments (portal tracts vs. lobular parenchyma), suggesting multiple cellular and molecular mechanisms involved in the regulation of the leucocyte traffic through inflamed liver tissue. [ABSTRACT FROM AUTHOR]

The present study reports a rare case of systemic M. serofulaceum infection in an AIDS patient and analyses the inflammatory infiltrate in a lymph node by immunohistochemistry. Special emphasis is put on the histiocytes. The diffuse infiltrate consists mainly of large histiocytes that contain numerous bacilli. These cells display the phenotype of mature histiocytes and in addition coexpress the antigens recognized by RFD7 and RFD9, both markers of different subsets of histiocytes which have been reported to be co-expressed by the infected histiocytes in the infiltrate of lepromatous lepra. Interdigitating reticulum cells are rare as well as T cells which are mainly of the suppressor/cytotoxic type. These findings are similar to those reported for lepromatous lepra and might indicate common deficiencies in T cell macrophage interactions in both conditions. Superimposed on the diffuse infiltrate of large histiocytes we observed 'monocytic granulomas', the presence of which might he related to a reactional state comparable to crythema nodosum leprosum, a reactional state of lepromatous lepra. [ABSTRACT FROM AUTHOR]

Although there is increasing evidence that the majority of cases of hairy cell leukemia represent B-lymphoproliferative disorders, the exact subset of B-cells from which hairy cells are derived, is still unclear. On the basis of results obtained in previous studies, and data collected from the literature, it is suggested that B-lymphocytes normally residing in the marginal zone of the splenic white pulp (so called 'marginal zone lymphocytes') represent the cell type from which B-lineage derived hairy cells originate. [ABSTRACT FROM AUTHOR]

Recent observations on a correlation between fetal serum ferritin and gestational age, consistent with an increase in fetal iron stores during pregnancy, led us to study liver iron content in 22 human stillborns, newborns and infants of different gestational and postnatal age. At autopsy, a longitudinal liver slice was subdivided into ten blocks. Each sample was analyzed for iron content by atomic absorption spectroscopy. The mean iron concentration in the studied livers was 21.6 μM/g dry tissue (d.t.). A striking interindividual variability in iron content was observed: the hepatic concentration of the metal ranged from 3.3 to 64.4μM/g d.t. No correlation was found between the hepatic iron concentration and gestational age or other clinical parameters of the patients studied. Moreover, the total storage iron of the liver did not appear to be correlated with the gestational age. The analysis of iron concentration in ten blocks in each liver revealed an irregular distribution of the metal. Lobar differences were observed, with a tendency of the left lobe to accumulate more iron than the right one. Furthermore, striking differences in iron content were found between adjacent liver samples, ranging in one instance from 4.5 up to 109.0 μM/g of dry tissue. Perls' stain for iron was positive in 7 out of the 22 livers examined, showing an irregular acinar distribution, with preferential periportal localization. Our data show that the newborn liver can be considered an interesting model for the study of iron storage. The observed uneven distribution of the metal, even in the absence of fibrosis normally associated with iron storage in adults, casts doubt on the interpretation of iron concentration of a small liver sample as representative of the mean hepatic iron concentration. [ABSTRACT FROM AUTHOR]

Eleven cases of hepatic injury attributed to the intake of flucloxacillin were reported to the Netherlands Center for Monitoring of Adverse Reactions to Drugs between 1982 and 1992. They concerned four men and seven women, with a mean age of 57 years, treated for 2-28 days with an oral dose varying from 1500-4000 mg per day. Symptoms mostly appeared 10 to 30 days after starting treatment with flucloxacillin. Biochemically, the pattern was compatible with cholestatic hepatitis in seven cases, with a mixed cholestatic-hepatocellular type of injury in one case, a hepatocellular pattern in two cases, and mild liver enzyme elevations in one patient. Two patients died, one due to fatal bleeding from the liver after biopsy, and the second patient to a combination of hepatic and cardiac failure. The other patients recovered, on average 72 days after peaking of serum aminotransferase values. Histology in seven cases showed cholestatic hepatitis in five, with cholangitis or cholangiolitis in four of these patients. In the other two patients, there was centrilobular cholestasis with extensive bridging fibrosis and portal-central bridging necrosis, respectively. [ABSTRACT FROM AUTHOR]

ABSTRACT- Seven patients with decompensated posthepatitis B cirrhosis were treated with low doses of interferon alpha. The initial plasma level of HBV-DNA ranged from 3.0 to 189.3 pg/ml, and that of ALT from 37 to 156 IU/1. Liver biopsies demonstrated ongoing piecemeal necrosis. In sera of all but one patient, HBV-DNA became undetectable by hybridisation techniques within 10 to 28 weeks. Plasma HBeAg became negative in four and HBe-antibodies positive in three patients. Serum transaminase levels showed a marked initial rise 3 to 13 weeks after onset of therapy; they dropped to normal values later in all except one patient. Therapy was initiated at 1 MU (million units) three times a week for 2 weeks and was increased to 2.5 MU for 16 weeks. Later, this dosage was raised to 5 MU three times a week in some patients. Complications included variceal haemorrhage, aggravation of ascites or of encephalopathy, development of pneumonia, recurrence of spontaneous bacterial peritonitis or of gastric ulcer bleeding. One year after stopping the therapy, three patients are well and without any feature of liver decompensation. Three patients died before they could undergo a liver transplantation. In one patient treatment was interrupted because of marked exacerbation of liver cell necrosis. It thus seems possible to suppress HBeAg and HBV-DNA in patients with decompensated cirrhosis. This is important to prepare them for possible liver transplantation. Interferon should be initiated at low doses and the patients be very carefully monitored. Prophylactic therapy for bacterial peritonitis and for variceal haemorrhage is warranted. [ABSTRACT FROM AUTHOR]