Assessment of central nervous system involvement in gambiense trypanosomiasis: value of the cerebro-spinal white cell count

objective  To assess, in a clinical setting, the comparative values of conventional criteria used in the diagnosis of central nervous system (CNS) involvement in Trypanosoma brucei gambiense sleeping sickness: white cell count (WCC) in cerebrospinal fluid (CSF) > 5 × 10⁶ cells/l; total protein concentration in CSF > 40 mg/100 ml); evidence of trypanosomes in CSF following double centrifugation (DC).
method   In vitro culture of CSF was used as the gold standard.
results  The study showed that WCC is, by itself, as sensitive for the diagnosis of the CNS involvement as the usually recommended combination of three conventional criteria. The specificity of WCC is improved while the sensitivity is reduced when the cut-off point is set at a higher value (WCC > 10 × 10⁶/l).
conclusion  In poorly equiped laboratories, the diagnosis of CNS involvement in patients with confirmed systemic infection should be based only on the WCC. However, a pilot study is needed to assess the feasibility and reliability of the WCC handled by 'front line' personnel, for different cut-off values.     

Kinetics of IgM and IgG responses to Japanese encephalitis virus in human serum and cerebrospinal fluid

We measured levels of antibodies to Japanese encephalitis virus (JEV) in serum and in cerebrospinal fluid (CSF) specimens obtained from 32 patients with acute encephalitis by using "antibody-capture" solid-phase enzyme-linked immunoassays specific for IgM or IgG to JEV. The proportions of confirmed cases with IgM to JEV detectable in CSF were 68% (obtained on day 1), 100% (day 7), 96% (day 30), and 72% (day 180). For IgG in CSF the proportions were 47% (day 1), 89% (day 7), 100% (day 30), and 100% (day 180). Twenty-five CSF samples were obtained from control patients with other diseases with possible nervous system involvement (but none with a clinical diagnosis of viral encephalitis); none had detectable IgM to JEV. Five JEV-infected but asymptomatic siblings of patients with encephalitis were also examined; all had high levels of IgM to JEV in serum, but none had detectable IgM to JEV in CSF.     

Cerebrospinal fluid IgM, IgA, and IgG indexes in systemic lupus erythematosus. Their use as estimates of central nervous system disease activity

Paired serum and cerebrospinal fluid (CSF) specimens from 13 patients with systemic lupus erythematosus (SLE) and central nervous system involvement (CNS-SLE) were studied for CSF IgM, IgA, and IgG indexes (indicators of intrathecal immunoglobulin synthesis) and CSF-serum albumin quotient (Q albumin) (an indicator of blood-brain-barrier function). We also studied 20 patients with noninflammatory neurologic diseases and seven patients with SLE without CNS involvement for comparison. In addition to an increase in the CSF IgG index, IgM and IgA indexes also were elevated in patients with CNS-SLE. All three indexes decreased significantly when CNS manifestations subsided by successful treatment. The Q albumin was normal in most patients. The elevation of CSF immunoglobulin indexes may be a result of polyclonal B-lymphocyte activation within the CNS, rather than the leak of immunoglobulins from the systemic circulation into the CNS. Since these indexes reflect CNS disease activity in SLE, they may be a successful tool for the management of SLE.     

Increased CXCL-13 levels in human African trypanosomiasis meningo-encephalitis

Objectives  To determine the role of the B-cell attracting chemokine CXCL-13, which may initiate B-cell trafficking and IgM production in diagnosing HAT meningo-encephalitis.
Methods  We determined CXCL-13 levels by ELISA on paired sera and CSF of 26 patients from Angola and of 16 controls (six endemic and ten non-endemic). Results were compared to standard stage determination markers and IgM intrathecal synthesis.
Results  CXCL-13 levels in patients' sera had a median value of 386.6 pg/ml and increased levels were associated with presence of trypanosomes in the CSF but not with other stage markers. CXCL-13 levels in patients' CSF had a median value of 80.9 pg/ml and increased levels were associated with all standard stage determination markers and IgM intrathecal synthesis.
Conclusion  CXCL-13 levels in CSF increased significantly during the course of HAT. Hence the value of CXCL-13 for diagnosis, follow-up or as a marker of disease severity should be tested in a well-defined cohort study.     

De novo autoimmune hepatitis after living donor liver transplantation is unlikely to be related to immunoglobulin subtype 4-related immune disease

Background and Aim:  Recently, we reported that immunoglobulin subtype 4 (IgG4) is involved in autoimmune hepatobiliary diseases, such as autoimmune hepatitis, sclerosing cholangitis, and pancreatitis. However, the association of IgG4 with autoimmune hepatic disease after living donor liver transplantation (LDLT) has not been investigated.
Methods:  Of the 72 LDLT recipients, four patients (5.6%) were suspected of having autoimmune-related hepatic disease after LDLT. The diagnosis was made based on a histological diagnosis following an examination of a biopsy liver specimen in three cases, while in one case a pemphigoid appeared in the flank with liver fibrosis of unknown cause. Human leukocyte antigen (HLA) mismatches were 3, 2, 2, and 2, respectively. The serum level of IgG4 in the patients was measured, and IgG4 immunohistochemical staining in the liver biopsy specimens was also performed.
Results:  In all cases, steroid pulse therapy or recycle treatment and subsequent increased steroid dose as well as additional azathioprine or mycophenolate mofetil were effective. While a few positive-stained cells for IgG4 were observed in the liver of one case, negative staining for IgG4 was observed in the other cases. All serum subclasses of IgG4 were within normal limits.
Conclusion:  In our series of LDLT, IgG4-related immune disorder is unlikely to be involved in post-transplant, autoimmune-related liver disease.     

Antibodies to Schistosoma mansoni in human cerebrospinal fluid

Cerebrospinal fluid (CSF) and serum samples from patients suspected of having neuroschistosomiasis (NS) were evaluated by an enzyme-linked immunosorbent assay. Monoclonal antibodies of various immunoglobulin isotypes (IgM, IgA, IgE, total IgG, IgG1, IgG2, IgG3, and IgG4) were used to detect antibodies against Schistosoma mansoni soluble egg antigen (SEA) and soluble worm adult preparation (SWAP). Of the 83 CSF samples tested, 55% were reactive to SEA (26% were reactive only to SEA and 29% to both SEA and SWAP), 34% were reactive to SWAP (5% only to SWAP and 29% to both SEA and SWAP), and 40% were not reactive with any antigen. Cases that tested positive for SWAP in CSF and negative in serum were not found. Samples with high specific IgG antibody titers were selected for immunoglobulin isotype profiling. In the CSF samples, the antibodies against SEA and SWAP were mainly IgM, IgG1, and IgG4, although other immunoglobulins were also detected. Interestingly, nine patients had high levels of IgG1 only in the CSF. These results suggest that there is local synthesis of IgG1, and that this isotype could be an important immunologic marker in the diagnosis of NS.     

Detection of hepatitis E virus RNA and genotype in Bangladesh

Background/Aims:  Hepatitis E virus (HEV) in Bangladesh has not been adequately documented. We report HEV RNA and genotype detection in Bangladesh.
Methods:  In total, 82 samples were used; 36 sporadic acute hepatitis (AH), 12 fulminant hepatitis (FH), 14 chronic liver disease (CLD) and 20 from an apparently healthy population (HP) positive for both immunoglobulin (Ig) M and IgG specific anti-HEV antibodies (anti-HEV). The male/female ratio was 61/21, ages 12–67 (mean 30.4) years. RNA was extracted, transcribed to cDNA and amplified in nt 6345–6490 (ORF2) of HEV. Nucleic and amino acid sequences were determined. Homology comparison between Bangladesh clones and other representative HEV clones and phylogenetic tree analyses were done. Relations between HEV RNA-positivity and clinical factors were analyzed.
Results:  HEV RNA was positive in 9/36 (25.0%) of AH cases, 4/12 (33.3%) FH, 3/14 (21.4%) CLD and 0/20 (0%) HP samples; total 16/82 (19.5%). Four factors correlated significantly with HEV RNA-positivity (Mann-Whitney U test); alanine aminotransferase (ALT) ( P  = 0.0229), aspartate aminotransferase (AST) ( P  = 0.0448), and titers of IgG ( P  = 0.0208) and IgM ( P  = 0.0095) specific anti-HEV. The 16 HEV clones were divided mainly into two groups, A and B, including six different cDNA sub-groups.
Conclusion:  HEV RNA was found in sporadic AH and FH and sub-clinical CLD cases, but not in HP. HEV RNA-positivity was significantly related to values of ALT and AST and titers of IgG and IgM specific anti-HEV, with IgM specific anti-HEV showing the most significant relationship. All clones were genotype I, which is prevalent in South Asia.     

Elevated cerebrospinal fluid (CSF) leptin in idiopathic intracranial hypertension (IIH): evidence for hypothalamic leptin resistance?

Objective  The aetiology of idiopathic intracranial hypertension (IIH) is not known, but its association with obesity is well-recognized. Recent studies have linked obesity with abnormalities in circulating inflammatory and adiposity related cytokines. The aim of this study was to characterize adipokine and inflammatory cytokine profiles in IIH.
Design  Paired serum and cerebrospinal fluid (CSF) specimens were collected from 26 patients with IIH and compared to 62 control subjects. Samples were analysed for leptin, resistin, adiponectin, insulin, IL-1β, IL-6, IL-8 (CXCL8), TNFα, MCP-1 (CCL2), hepatocyte growth factor, nerve growth factor and PAI-1 using multiplex bead immunoassays.
Results  CSF leptin was significantly higher in patients with IIH ( P  = 0·001) compared to controls after correction for age, gender and body mass index (BMI). In the control population, BMI correlated with serum leptin ( r  = 0·34; P  = 0·007) and CSF leptin ( r  = 0·51; P  < 0·0001), but this was not the case for the IIH population. Profiles of other inflammatory cytokines and adipokines did not differ between IIH patients and controls once anthropometric factors had been accounted for.
Conclusions  IIH was characterized by significantly elevated CSF leptin levels which did not correlate with BMI. We suggest that CSF leptin may be important in the pathophysiology of IIH and that obesity in IIH may occur as a result of hypothalamic leptin resistance.     

Systemic inflammation in chronic obstructive pulmonary disease and asthma: Similarities and differences

Background and objective:   While recent studies have shown that patients with COPD and patients with asthma exhibit evidence of airway and systemic inflammation, markers of systemic inflammation have not been compared between the two diseases.
Methods:   To evaluate circulating inflammatory markers, blood was sampled from 111 patients with COPD, 75 control subjects and 46 asthmatic patients (some of whom were smokers). Measurements of WCC, serum levels of fibrinogen, high-sensitivity (hs)-CRP, IL-8, IL-6, tumour necrosis factor-α (TNF-α), transforming growth factor (TGF)-β1, tissue inhibitors of metalloproteinase (TIMP)-1, neutrophil elastase and alpha1-antitrypsin (α1-AT) were performed.
Results:   Serum TNF-α, IL-6 and TIMP-1 concentrations were significantly higher in patients with stable COPD and patients with asthma than in control patients. Serum α1-AT levels were significantly higher in COPD patients than in asthmatic patients and control subjects, and serum TGF-β1 levels were higher in asthma patients than in COPD patients. Smoking status had no effect on markers in COPD and asthmatic patients.
Conclusions:   Although COPD and asthma share common markers of systemic inflammation, serum levels of TGF-β1 and α1-AT may reflect differences between the diseases.     

Pulmonary and serum isotypic antibody responses of mice to live and inactivated influenza virus

Primary and secondary immunoglobulin class-specific antibody responses in serum and pulmonary lavage fluids of mice were studied after respiratory infection and intramuscular vaccination with influenza virus. Infection and vaccination with inactivated virus vaccine induced primary IgM and IgG antibody responses in the serum and pulmonary lavage fluids (PLF). Neither immunizing method induced detectable serum IgA antibodies, and only infection generated IgA antibodies in PLF. The major portion of antibodies in PLF was derived from serum, but local synthesis of IgG and IgA antibodies was detected after virus infection. Vaccination of infection-primed mice boosted the IgM and IgG antibody concentrations in serum and PLF but had no effect on IgA antibody concentrations. Nonlethal infection of vaccine-primed mice generated secondary IgM and IgG antibody responses in serum and PLF and an IgA antibody response in PLF. Again, most of the antibody detected in PLF was derived from serum, but low concentrations of IgA and IgG were synthesized locally after infection. Although mice immunized with inactivated vaccine lacked the capacity to synthesize IgA antibody, they were protected from severe pulmonary disease when challenged with lethal influenza virus. These data support the concept that serum IgG antibodies are sufficient for prevention of severe pulmonary disease.     

Cerebrospinal fluid in benign and malignant monoclonal dysglobulinemias

The authors compared 9 cases of myeloma and 2 cases of Waldenstr?m's disease with 10 cases of benign monoclonal gammapathies. None of the patients (except one) had neurological involvement; one patient hab diabetes. The study was focused on the immunoglobulins and proteins in the CSF. The following observations were made: - The CSF protein was raised in 8 out of the 11 malignant gammopathies and in 5 out of the 10 benign gammopathies; - An identical monoclonal protein was found in the CSF and serum in all the cases of malignant gammopathies. In the cases considered to be benign, the results were less concordant: one IgM lymphoma had normal CSF; three IgG dysglobulinemias had different immunoglobulins proteins in their CSF: - The mean CSF immunoglobulin level was much higher in the myeloma patients than in the benign gammopathies; - A number of findings suggest intrathecal secretion (at least in the malignant gammopathies). This is also true in a good number of the benign gammopathy cases. Direct tumoural invasion of the CSF may be more common than generally supposed. However, the study of CSF immunoglobulins alone does not establish the diagnosis of malignant dysglobulinemia. Nevertheless, the authors consider that the finding of intrathecal secretion of immunoglobulin, especially in patients with a discordance in FAB and FC fractions, should lead to a closer follow-up of these patients.     

Diagnostic utility of estimation of mycobacterial antigen A60 specific immunoglobulins in serum and CSF in adult neurotuberculosis

An ELISA assay based on mycobacterial antigen A60 (Anda, Biologicals France) was used to detect specific immunoglobulins (IgM, IgA and IgG) in 48 cases of adult neurotuberculosis (24 TBM; 24 Tuberculoma) and in 48 controls (24 diseased controls; 24 healthy controls). Serum was analysed in all the subjects whereas CSF was assayed only in TBM cases and diseased controls. The cut off values used for IgM, IgG and IgA in this study were 1.500 ODI (optical density index) at 1:100 dil, 250 units/ml and 150units/ml respectively in serum; and 1.500 ODI at 1:10 dil, 10 units/ml and 10 units/ml respectively in CSF. The mean titres of all three antibodies were found to be significantly higher in cases as compared to controls. In cases of TBM, in serum, the percentage positivity for IgM, IgG, IgA and combination of IgG or IgA were 41.67, 87.50 87.50 and 95.83 respectively. The corresponding figures in CSF were 62.50, 75.0, 66.67 and 79.16 for IgM, IgG, IgA and 'IgA or IgM' respectively. In tuberculoma cases, in serum, the figures were 37.50, 75.0, 75.0 and 83.33 respectively. Overall, a high sensitivity and specificity were obtained in cases of TBM (Serum: ST = 95.83%: SP = 87.50%; CSF ST = 79.16%. SP = 100%) and Tuberculoma cases (serum: ST = 83.33% SP = 87.50%) employing the combined antibody estimations.     

Serum immunoglobulin levels in systemic lupus erythematosus: the effects of age, sex, race and disease duration

To determine whether factors other than disease activity influence immunoglobulin levels in patients with systemic lupus erythematosus (SLE), the effect of age, sex, race, and duration of disease on serum IgG and IgM levels in 170 patients with SLE were investigated. Serum IgM and IgG levels did not differ between men and women, while IgM levels were higher in whites. Serum IgG levels did not vary with age or duration of SLE. In contrast, serum IgM levels were negatively correlated with both age (r = -0.236; p = 0.002) and duration of SLE (r = 0.248; p = 0.001), and demonstrated a U-shaped age relationship, being higher in children and older patients. These patterns of immunoglobulin expression in patients with SLE contrast with those exhibited in populations of healthy individuals, suggesting that the immunoregulatory disturbances of SLE predominate over the normal mechanisms regulating levels of IgM and IgG.     

Influence of trypanocidal therapy on the haematology of vervet monkeys experimentally infected with Trypanosoma brucei rhodesiense

The aim of this study was to characterise the sequential haematological changes in vervet monkeys infected with Trypanosoma brucei rhodesiense and subsequently treated with sub-curative diminazene aceturate (DA) and curative melarsoprol (MelB) trypanocidal drugs. Fourteen vervet monkeys, on a serial timed-kill pathogenesis study, were infected intravenously with 10⁴ trypanosomes of a stabilate T. b. rhodesiense KETRI 2537. They were treated with DA at 28 days post infection (dpi) and with MelB following relapse of infection at 140 dpi. Blood samples were obtained from the monkeys weekly, and haematology conducted using a haematological analyser. All the monkeys developed a disease associated with macrocytic hypochromic anaemia characterised by a reduction in erythrocytes (RBC), haemoglobin (HB), haematocrit (HCT), mean cell volume (MCV), platelet count (PLT), and an increase in the red cell distribution width (RDW) and mean platelet volume (MPV). The clinical disease was characteristic of human African trypanosomiasis (HAT) with a pre-patent period of 3 days. Treatment with DA cleared trypanosomes from both the blood and cerebrospinal fluid (CSF). The parasites relapsed first in the CSF and later in the blood. This treatment normalised the RBC, HCT, HB, PLT, MCV, and MPV achieving the pre-infection values within two weeks while RDW took up to 6 weeks to attain pre-infection levels after treatment. Most of the parameters were later characterised by fluctuations, and declined at one to two weeks before relapse of trypanosomes in the haemolymphatic circulation. Following MelB treatment at 140 dpi, most values recovered within two weeks and stabilised at pre-infection levels, during the 223 days post treatment monitoring period. It is concluded that DA and MelB treatments cause similar normalising changes in the haematological profiles of monkeys infected with T. b. rhodesiense, indicating the efficacy of the drugs. The infection related changes in haematology parameters, further characterise the vervet monkey as an optimal induced animal model of HAT. Serial monitoring of these parameters can be used as an adjunct in the diagnosis and prognosis of the disease outcome in the vervet monkey model.     

Anti-IL-8 autoantibodies and complexes in rheumatoid arthritis: polyclonal activation in chronic synovial tissue inflammation

The chemokine interleukin-8 (IL-8) is frequently associated with inflammatory diseases, and autoantibodies against IL-8 are present in the periphery at elevated levels in such conditions as rheumatoid arthritis (RA). Circulating free anti-IL-8 IgG autoantibodies correlate with inflammatory parameters and disease severity in RA. In this study, correlations were sought between these disease parameters and other antibody subclasses. We assayed IgM, IgA and IgG anti-IL-8 antibodies and IL-8 immunoglobulin immune complexes in the serum of 29 healthy controls and 56 patients with defined RA, and compared the results with clinical and humoral disease parameters. IgG and IgM antibodies directed against IL-8 were present in all samples. In the disease groups, all isotypes of free anti-IL-8 antibodies correlated with increasing humoral disease parameters like CRP and CIC and their related anti-IL-8 immune complexes. Samples which contained high titers of anti-IL-8 antibody subclasses and complexes were RF subclass-positive, while IgM RF-negative sera showed low levels of anti-IL-8 and complexes. Detectable levels of IgG and IgA RF were found in all sera. Patients with extra-articular organ manifestation showed significantly increased free IgA and IgA/IL-8 complexes, with no correlation to the IgA RF titer or IgA hypergamma-globulinemia. The highest titers were seen in two RA cases with vasculitis and in one patient with colitis. Polyclonal activation of the humoral antibody system, which normally precedes the resolution of an inflammatory response, can itself lead to secondary stimulation of inflammatory processes via immune complex formation. In the immune pathology of RA, it degenerates into a persistent chronic inflammation accompanied by progressive joint destruction. The presence of elevated IgA subclass anti-IL-8 autoantibodies in RA patients with extra-articular manifestations suggests these autoantibodies as a clinically useful marker of disease severity and extra-articular manifestations. Received: 10 June 1998 / Accepted: 5 October 1998     

Experimental Transfusion Reactions in Monkeys: Haemolytic, Coagulant and Renal Effects of Transfused Isoimmune IgG and IgM

S ummary . IgG and IgM fractions were purified from plasmas of six pairs of monkeys cross-immunized with each others' red cells. Essentially all haemolytic activity was found in IgG fractions. Immune IgG or IgM was transfused into incompatible recipients. A dose of immunoglobulin equivalent to that present in 10 ml of plasma per kg of recipient body weight was used. Red cell mass decreased in direct proportion to quantitative haemolysin content of IgG during the first 4 hr after transfusion. A small decrease was also noted after one IgM transfusion. Parallel increases in plasma and urinary haemoglobin were observed. Disseminated intravascular coagulation (DIC) and anuria or oliguria were seen after every immune IgG infusion. DIC, characterized by falls in platelet count, fibrinogen content, levels of factors V and VIII, and fibrin clots at autopsy varied in severity with the extent of the haemolysis. The amount of haemolysis in vivo was accurately predictable by the QH₅₀, a sensitive in vitro assay of antibody haemolytic activity. No coagulation changes or decreases in urinary volume were noted after immune IgM or control immunoglobulin infusions. These immune IgG infusions in monkeys provide a model for the study of the pathophysiology and therapy of human transfusion reactions.     

Combining MYD88 L265P mutation detection and clonality determination on CSF cellular and cell-free DNA improves diagnosis of primary CNS lymphoma

Diagnosis of primary central nervous system lymphoma (PCNSL) is challenging, and although brain biopsy remains the gold standard, cerebrospinal fluid (CSF) constitutes a less invasive source of lymphomatous biomarkers. In a retrospective cohort of 54 PCNSL cases tested at diagnosis or relapse, we evaluated the contribution of immunoglobulin heavy chain (IGH) gene clonality and MYD88 L265P detection on both CSF cell pellets and supernatants, in comparison with cytology, flow cytometry, interleukin (IL)-10 and IL-6 quantification. Clonality assessment included a new assay to detect partial IGH-DJ rearrangements. Clonal IGH rearrangements and/or MYD88 L265P mutation were detected in 27 (50%) cell pellets and 24 (44%) supernatant cell-free (cf) DNA. Combining analyses on both compartments, 36 (66%) cases had at least one detectable molecular marker, present only in cfDNA for 9 (16%) of them. While cytology and flow cytometry were positive in only 7 (13.0%) and 9 (17.3%) cases respectively, high IL-10 levels were observed in 36 (66.7%) cases. Overall, taking into account molecular and cytokine results, 46/54 (85%) cases had at least one lymphomatous biomarker detectable in the CSF. These results show that this combination of biomarkers evaluated on both cell pellet and supernatant CSF fractions improves significantly the biological diagnosis of PCNSL.     

Serologic responses to Mycobacterium leprae-specific phenolic glycolipid-I antigen in sooty mangabey monkeys with experimental leprosy

Four pairs of sooty mangabey monkeys (Cercocebus atys) were inoculated with serial, 10-fold dilutions of Mycobacterium leprae. The highest-dose pair received 4.8 X 10(10) M. leprae. Serum samples were obtained and clinical signs of leprosy were recorded at intervals of 35 months. Longitudinal serum samples were assayed by an ELISA method for the presence of IgG and IgM antibodies to the M. Leprae-specific phenolic glycolipid-I (PGL-I) antigen. In general, the onset of disease symptoms paralleled the number of M. leprae inoculated, but the ultimate course of disease depended upon individual animal susceptibility. Both IgG and IgM anti-PGL-I isotypes were observed in variable levels and patterns, related to the disease stage, among the eight mangabeys. The data suggest that high IgG and low IgM anti-PGL-I levels correlated with less severe disease; whereas initial high IgM titers and/or rising or sustained high IgM titers, especially together with low IgG anti-PGL-I titers, preceded or corresponded to periods of progressive leprosy. The results show that IgG and IgM anti-PGL-I antibodies can be present in significant titers among mangabeys early after infection with M. leprae. It appears likely that the relative levels of these anti-PGL-I isotypes may be correlated with the susceptibility of individual animals to the development of lepromatous leprosy.     

Identification and characterization of a Fc Receptor activity on the Toxoplasma gondii tachyzoite

The Immunoglobulin (Ig) binding capacity of Toxoplasma gondii tachyzoites was investigated using fluorescence flow-cytometry analysis. Polyclonal mouse, human and rat immunoglobulins without specific anti- Toxoplasma activity bound to parasites in a concentration-dependent manner, saturating them at circulating serum concentrations. The immunoglobulin class and subclass specificity of binding was investigated using irrelevant monoclonal antibodies. IgM, IgA and IgG reacted with the parasite membrane. The attachment of mouse IgM to the parasite surface was hampered by mouse IgG1, IgG2a, IgG2b and IgG3. The binding of mouse IgG was proportionally reduced with increasing concentrations of mouse monoclonal IgM. The binding of murine immunoglobulin was diminished when in presence of human IgG. Purified Fc- but not Fab portions of immunoglobulins, fixed to parasites. Using labelled calibrated beads, the Ig binding capacity of parasites was estimated to be 6900 ± 500 sites per tachyzoite. The Kd of the T. gondii Fc Receptor (FcR) activity was determined at 1.4 ± 0.1 μM (mean ± SEM). Such FcR activity was reduced by phospholipase C, trypsin and pronase treatment of the parasites. These data show a low affinity FcR activity on T. gondii tachyzoites which recognizes Ig of different species and isotypes and is likely supported by a glycosyl-phosphatidylinositol (GPI)-anchored surface protein of the parasite .     

Is portal hypertension associated with protein-losing enteropathy?

Background and Aim:  Hypoalbuminemia in patients with decompensated cirrhosis has traditionally been assumed to be a result of to impaired liver synthesis; however, protein-losing enteropathy (PLE) may also contribute. The aim of this study was to assess whether hypoalbuminemic cirrhotic patients with portal hypertension had evidence of PLE.
Methods:  Sixteen patients with alcoholic cirrhosis, hypoalbuminemia and portal hypertension underwent whole gut lavage with polyethylene glycol solution. The effluent obtained was analyzed for albumin, immunoglobulin (Ig)G and α1-antitrypsin (α1-AT). Serum C-reactive protein (CRP) was also measured to assess the systemic inflammatory response.
Results:  Twelve of the 16 enrolled patients had a persistently low albumin concentration at the time of lavage. Only one patient (who was subsequently found to have celiac disease) had elevated concentrations of lavage albumin, α1-AT and IgG levels. There was a significant correlation between lavage albumin and α1-AT ( r  = 0.671, P  = 0.024), and between lavage albumin and IgG ( r  = 0.614, P  = 0.045). There was no correlation between serum albumin and lavage proteins. Six patients had elevated serum CRP levels, but serum albumin or lavage protein concentrations did not correlate with serum CRP.
Conclusion:  There is no evidence of a significant PLE in patients with alcoholic cirrhosis, hypoalbuminemia and portal hypertension.