Renal cell carcinoma (RCC) commonly metastasizes to areas such as the lungs, liver, bone, brain, adrenals, and lymph nodes. We present a rare case of a 59-year-old female patient with RCC metastasis to the gallbladder. The patient had undergone right nephrectomy for RCC more than 6 years prior to the metastasis. During routine follow-up, a polypoid lesion of the gallbladder was identified. Laparoscopic cholecystectomy was performed, and pathologic examination of the specimen revealed metastatic RCC. The patient was completely asymptomatic, which reinforces the importance of postoperative follow-up. Renal cell carcinoma is one of the few common malignancies for which there is good evidence of survival benefit from surgical resection of the metastatic tumours.
We read with interest the paper by Granito et al 1 reporting on the clinical and diagnostic significance of anti-filamentous actin antibodies (A-FAA) in autoimmune hepatitis type 1 (AIH-1). The authors found that A-FAA, measured by a new commercially available ELISA based on a modified cut-off of 30 instead of the manufacturer’s 20 arbitary units (AU), strictly correlates with the smooth muscle antibody glomerular/tubular (SMA-G/T) pattern,2 also known as the microfilament pattern, mostly seen in patients with AIH-1.1 Their findings further indicate F-actin as the predominant, if not the sole, target of AIH-1-specific SMA reactivity, a notion that has been questioned in the past because of the inconsistent results obtained by several actin-based assays.3,4
We agree with Granito et al 1 …
Abstract Background/Aims: Primary biliary cirrhosis (PBC) is characterised by the presence of immunoglobulin (Ig) G antimitochondrial antibodies (AMA), which are routinely detected by indirect immunofluorescence (IFL) using composite rodent tissue substrate. The IgG subclass distribution and clinical significance of IFL‐detected AMA in patients with PBC have not been previously studied in detail. Methods: We have examined IgG subclass‐specific AMA detected by IFL on rodent liver, kidney and stomach tissue substrate using affinity‐purified IgG subclass monospecific antisera as revealing reagents in 95 AMA‐positive PBC patients from Greece. Results: AMA of any of the IgG1, IgG2 or IgG3 subclasses were present in 89/95 (93.7%) patients. Among those 89, 55 (61.8%) had IgG1, 2, 3 AMA positivity; eight (9%) had IgG1, 2; seven (7.9%) had IgG2, 3; eight (9%) had IgG1, 3; nine (10.1%) had IgG1 subclass and two (2.2%) single IgG3 AMA reactivity. IgG4 AMA was absent. IgG3 titres were higher than IgG2 and IgG1 ( P <0.001) and IgG1 higher than IgG2 ( P <0.001). IgG3 AMA‐positive patients had a histologically more advanced disease ( P <0.01) and were more frequently cirrhotic compared with those who were negative ( P <0.01). There was a positive correlation between AMA IgG3 titre and Mayo risk score ( r =0.55, P =0.009, Spearman's correlation). Conclusions: Our findings suggest that AMA are not restricted to a specific IgG subclass. AMA of the IgG3 subclass are associated with a more severe disease course, possibly reflecting the peculiar ability of this isotype to engage mediators of damage.
To investigate whether complement pathway activation contributes to the clinical and histological features of acute alcoholic hepatitis, we studied the activation of the classical and alternative pathways in patients with alcoholic hepatitis (n = 20), inactive alcoholic cirrhosis (n = 8), heavy drinkers without alcoholic liver disease (n = 10), patients with liver disease of nonalcoholic etiology (n = 11), and healthy control subjects (n = 18). Complement activation was evaluated in the alcoholic hepatitis patients by its correlation with a number of clinical and laboratory features indicative of the severity of liver injury, as well as by comparison of the patient groups. There was no significant difference in circulating C3 [1.02 g/liter, confidence interval (CI) = 0.76-1.28] or C4 (0.25 g/liter, CI = 0.17-0.33) in patients with alcoholic hepatitis when compared with the four control groups. Factor B levels (0.24 g/liter, CI = 0.21-0.27) were higher in the alcoholic hepatitis patients than the control groups (p < 0.01). However, activation of complement (given by the ratios C3d/C3, C4d/C4, and Ba/factor B) was not different in alcoholic hepatitis patients when compared with the control groups. Univariate analysis of a wide range of clinical and laboratory features in the alcoholic hepatitis subjects showed a positive correlation between plasma C3 and serum alkaline phosphatase (r = 0.68, p = 0.0014), AST (r = 0.55, p = 0.015), and gamma-glutamyltranspeptidase (r = 0.47, p = 0.035), but no correlation with clinical or laboratory features associated with high morbidity or mortality. There is no relationship between clinical or laboratory indicators of disease severity and complement activation, and it is unlikely that complement activation contributes to the clinical and histological features of alcoholic liver disease.
SUMMARY In vitro studies have indicated that T lymphocyte activation may be of importance in the pathogenesis of HIV infection. In order to define the role of immune activation in vivo, we assessed the expression of the T cell activation markers HLA-DR and CD25 by flow cytometry in peripheral blood in relation to disease severity and the surrogate markers CD4 and β2-microglobulin in 157 patients with HIV infection and 53 healthy seronegative blood donors. Percentage levels of CD3+HLA-DR+ T lymphocytes were significantly higher (P<0·0001) and percentage levels of CD3+CD25+ T lymphocytes significantly lower (P<0·0001) in all HIV+ patients compared with controls. A significant correlation was observed between increasing percentage levels of CD3+HLA-DR+ T lymphocytes and both declining CD4 counts (r = 0·52; P<0·001) and increasing β-microglobulin levels (r = 0·56; P<0·001). Percentage levels of CD4+HLA-DR+ and CD4+CD25+ lymphocytes were significantly higher in all HIV+ patients compared with controls (P< 0·001). Levels of activated (HLA-DR+ and CD25+) CD4+ lymphocytes showed a significant step-wise linear increase with increasing disease severity (P < 0·001). High levels of CD3+ HLA-DR+ T lymphocytes were found in a greater proportion (81·8%) of asymptomatic HIV+ patients (Centres for Disease Control (CDC) group II) than low CD4 counts (51·5%) (P<0·001). Compared with controls, HIV+ patients had higher percentage levels of CD8+HLA-DR+ lymphocytes (P<0·001), but similar levels of CD8+CD25+ lymphocytes. These results indicate that T cell activation is not only a consistent but also an early feature in HIV infection. Monitoring levels of activated T cells and their subsets is of value in assessing progression of HIV-related disease.
Two children developed acute liver failure while taking carbamazepine. Clinical and laboratory findings suggested an immunoallergic reaction, but only one child improved on steroids. Determination of liver function during the first few weeks of treatment and early detection of signs of idiosyncrasy may prevent this rare but severe complication.
In vitro studies implicate classical and alternative complement pathway activation in the pathogenesis of human immunodeficiency virus (HIV) infection. To ascertain their importance in vivo, activation fragments of the classical (C4d), alternative (Ba), and common (C3d) pathways were measured and fragment to parent molecule ratios derived in 74 HIV-infected individuals and related to circulating immune complex (CIC) levels, Centers for Disease Control (CDC) stage, and beta 2-microglobulin, neopterin, and CD4-positive (CD4+) lymphocyte levels. All fragments and ratios were significantly higher in patients (P less than .01) than controls. C4 conversion indices (C4d and C4d to C4) increased linearly with increasing CDC stage (P less than .001), while CD4+ lymphocytes decreased linearly (P less than .001). C4d, C3d, C4d to C4, and C3d to C3 correlated with increasing CIC and beta 2-microglobulin, and C4d and C4d to C4 correlated with decreasing CD4+ lymphocytes (P less than .05). The relationship of classical complement pathway activation to disease progression and CD4+ lymphocytes suggests its involvement in the pathogenesis of HIV infection.
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