Ureteropelvic junction obstruction and renal calculi: Simultaneous treatment by robot-assisted laparoscopic pyeloplasty and transcutaneous retrograde flexible ureteroscopy. Technique description and early outcomes.

BACKGROUND: Ureteropelvic junction obstruction (UPJO) and renal calculi are associated in 20 to 30% of cases and treatment is mandatory. The simultaneous surgical management is a therapeutic challenge that is still a source of controversy. We describe our technique combining robot-assisted laparoscopic pyeloplasty and transcutaneous retrograde flexible ureteroscopy (fURS), assessing the feasibility of simultaneous treatment through an original technique. METHODS: This single centre series reports our initial experience with 12 patients. From January 2014 to September 2018, 12 patients underwent robot-assisted laparoscopic pyeloplasty with simultaneous fURS for UPJO and renal calculi. Mean age was 46 years (24-68). 92% had multiple renal stones and the mean cumulative stone diameter was 31,3mm. Robot-assisted pyeloplasty was performed with peroperative transcutaneous retrograde fURS through a ureteral access sheath introduced in an incision on the bassinet through a subcostal trocar. Stone extraction was performed using a basket. RESULTS: All patients underwent surgery successfully, achieving UPJ repair and complete stone extraction. Mean operating time was 92,5min (85-110). All reported Clavien-Dindo complications were grade 1. Non-contrast enhanced abdominal CT performed 1 month after surgery confirmed the absence of residual stones in all patients. Mean follow-up time was 10 months with no recurrence of UPJO. CONCLUSION: This small series confirms the feasibility with good surgical results of concomitant robot-assisted laparoscopic pyeloplasty and transcutaneous retrograde fURS stone extraction. No major complications were observed. This technique is easily reproducible but requires 2 experienced urologists to be achieved in a contained operative time.

Triphenylsulfonium topophotochemistry.

The products from the 193 nm irradiation of triphenylsulfonium nonaflate (TPS) embedded in a poly(methyl methacrylate) (PMMA) film have been characterized. The analysis of the photoproduct formation was performed using chromatographic techniques including HPLC, GPC and GC-MS as well as UV-vis and NMR spectroscopic methods. Two previously unreported TPS photoproducts, triphenylene and dibenzothiophene, were detected; additionally, GPC and DOSY-NMR spectroscopic analyses after irradiation suggested that TPS fragments had been incorporated into the polymer film. The irradiation of acetonitrile solutions containing 10% w/v PMMA and 1% w/v TPS in a 1 cm-path-length cuvette showed only a trace amount of triphenylene or dibenzothiophene, indicating that topochemical factors were important for the formation of these molecules. The accumulated evidence indicates that both products were formed by in-cage, secondary photochemical reactions: 2-(phenylthio)biphenyl to triphenylene, and diphenylsulfide to dibenzothiophene.

[Patterns of prescription of opioid analgesics in Hôtel-Dieu de France of Beyrouth]. / Les modalités de prescription d'analgésiques opiacés par les médecins de l'Hôtel-Dieu de France de Beyrouth.

OBJECTIVES: Use of chronic opioid therapy has increased substantially over the past few years, even though opioid therapy is associated with potentially serious harms, including opioid-related adverse effects and outcomes. Prescription of opioids for chronic pain, particularly nonmalignant chronic pain, remains controversial. In the midst of this controversy, patterns of actual prescription and influences on these patterns are not well understood. This study aims to describe the frequency of prescription of opioid analgesics in a university hospital, the attitudes of doctors towards this category of drugs, and the follow-up modalities of patients taking these drugs. The study also explores the association between the practitioners' characteristics and the modalities of prescription. DESIGN AND METHODS: A survey was delivered to 112 doctors and surgeons in the hospital during the four months between August and December 2013 and it was returned by 55 (49.0%). The survey consists of three parts. The first part addresses the frequency and reluctance of doctors' prescription of opioids and other analgesics for acute and chronic pain. The second part studies the doctors' attitudes and concerns towards opioids. It explores the belief of the doctors in the efficacy of this category of drugs, their confidence in prescribing such medications and the eventual side effects they might worry about. The third part of the survey studies the modalities of evaluation prior to the prescription and the modalities of follow-up of the patients receiving a long-term opioid treatment. RESULTS: Overall, 76.4% of doctors reported they sometimes, frequently, or always, prescribe opioids, which, using the Wilcoxon test, proved to be a significantly lower frequency than for prescribing of minor analgesics or nonsteroidal anti-inflammatory drugs (NSAIDS). Similarly, 60.1% reported a reluctance to prescribe opioids for chronic nonmalignant pain, which was a significantly greater reluctance than for cancer pain. The age and sex of the participants were unrelated to prescribing, but those with specialty training and use of practice guidelines were more likely to prescribe opioids and were less reluctant to do so. A majority of practitioners felt that opioids are effective for the treatment of chronic nonmalignant pain and that they have the sufficient training to prescribe them adequately; however, they still worry about the long-term prescription of opioids, particularly fearing the psychological dependence this treatment might cause. Using a series of Spearman correlation tests, we found that practitioners who thought they were adequately trained and who believed in the efficacy of long-term opioid treatment were more likely to prescribe them but that the worries about side effects decreased the frequency of prescription. A significant proportion of practitioners do not evaluate addiction risk factors of patients before prescribing opioids. The results concerning the modalities of follow-up of prescription were very heterogeneous with 87% of practitioners not explaining and 65% not screening for adverse effects. We similarly found that the frequency of follow-up and the management of patients who were exhibiting signs of dependence were very diverse. CONCLUSION: The results of this study were compatible with those of other recent studies about opioid prescription. The doctors practicing in the university hospital Hôtel-Dieu de France de Beyrouth present comparable prescription patterns, independent of their personal or professional characteristics, and they are more confident in their prescription when professionally trained for it. However, they exhibit a notable heterogeneity in their attitudes towards opioids and in their modalities of evaluating patients receiving long-term treatment. These results suggest a need for additional training in the management of this category of drugs.

Risk factors for the environmental spread of different multidrug-resistant organisms: a prospective cohort study.

BACKGROUND: Substantial scientific evidence shows that contamination of environmental surfaces in hospitals plays an important role in the transmission of multidrug-resistant organisms (MDROs). To date, studies have failed to identify the risk factors associated with environmental contamination. AIM: To evaluate, compare, and identify factors associated with environmental contamination around carriers of different MDROs. METHODS: This was a prospective cohort study from May 2018 to February 2020. A total of 125 patients were included, having been admitted to Avicenne Hospital and Hotel Dieu de France de Beyrouth Hospital who were faecal carriers of MDROs (extended-spectrum ß-lactamase-producing Enterobacterales (ESBL-PE), carbapenemase-producing Enterobacterales (CPE), vancomycin-resistant enterococci (VRE)). For each patient, quantification of MDRO in stool was undertaken, plus a qualitative evaluation of the presence of MDRO in six different environmental sites; and clinical data were collected. FINDINGS: MDROs comprised ESBL-PE (34%), CPE (45%), and VRE (21%). The most frequent MDRO species was Escherichia coli. Contamination of at least one environmental site was observed for 22 (18%) patients. Only carriage of VanA was associated with a significantly higher risk of dissemination. Having a urinary catheter, carriage of OXA48 and E. coli were protective factors against environmental contamination. There were no significant differences in environmental contamination between E. coli and other Enterobacterales or between ESBL-PE and CPE. CONCLUSIONS: Hospital environmental contamination rates are substantially higher for patients with VRE, compared to the low environment dissemination rates around ESBL-PE and CPE. Further studies on a larger scale are needed to confirm the validity of our findings.

Intraphagocytic beta-N-acetylglucosaminidase. Properties of the enzyme and its activity on group A streptococcal carbohydrate in comparison with a soil bacillus enzyme.

The beta-N-acetylglucosaminidases of rabbit and human polymorphonuclear leukocytes and of rabbit alveolar macrophages have been studied in comparison with the beta-N-acetylglucosaminidase derived from a soil bacillus which had previously been shown to hydrolyze the group-specific polysaccharide of Group A streptococci. The phagocytic enzymes are lysosome associated and have an acid pH optimum. In contrast, the soil bacillus enzyme is an extracellular product, has a higher pH optimum, and is probaby of smaller molecular size. When tested on p-nitrophenyl-betaN-acetylglucosaminide as substrate, the K(m) of the phagocytic enzymes is slightly higher than that of the soil bacillus. However, there were extreme differences in their effect on the Group A streptococcal polysaccharide. Thus, 5 x 10(6) units of the alveolar macrophage enzyme were required to hydrolyze the available N-acetylglucosamine of 1 mg of polysaccharide in 18 hr, while 100 units of the soil bacillus enzyme were sufficient to achieve this hydrolysis. In both cases, the serological reactivity of the polysaccharide is altered with loss of Group A specificity and acquisition of a new specificity characteristic of A-variant streptococci. Possible explanations for differences in the activity of the enzymes are considered, and the role of the phagocytic enzymes in intracellular degradation of Group A streptococci is discussed.

Persistence of streptococcal group A antibody in patients with rheumatic valvular disease.

Antibody levels to streptococcal Group A and A-variant carbohydrates were determined using a radioactive immune precipitation technique on patients with rheumatic fever, with and without valvular disease, on patients with post-streptococcal acute glomerulonephritis, and on age-matched controls. During the acute phase of the above illness, the means of the antibody levels to both carbohydrate antigens were equally elevated and were significantly higher than the normal controls. When Group A antibody levels were determined on sera obtained at intervals of 5-12 months and 1-5 yr after the acute illness) it was found that the antibody levels declined within the normal range at the 5-12 month interval in patients with glomerulonephritis as well as in patients with rheumatic fever in whom no valvular involvement had complicated the disease, i.e., patients with pure Sydenham's chorea. However, in patients with rheumatic valvulitis, who had been on penicillin prophylaxis after the last acute episode, the A antibody level showed little decline from the level obtained during the acute illness. The elevated antibody level in patients with rheumatic valvulitis, including patients with Sydenham's chorea with valvulitis, persisted for periods of at least 1 yr and up to 20 yr after the last acute attack. The pattern of the decline of the antibody levels to the A-variant carbohydrate as well as of the antibody titers to the other streptococcal antigens tested, ASO and anti-DNase B, was similar in all patients studied regardless of the presence of valvular disease. These findings suggest that prolonged persistence of the Group A antibody is a phenomenon peculiar to patients with rheumatic valvular disease. Whether this persistence is involved in the pathogenesis or is an outcome of the valvular disease remains to be determined.

Temperature-dependent variation in the synthesis of group-specific carbohydrate by streptococcal variant strains. I. Immunochemical studies.

A temperature-dependent alteration in the synthesis of the group-specific polysaccharide was found to occur in two "variant" streptococcal strains, A-486-Var and C 121/46/4. These strains synthesize a polysaccharide with variant immunochemical characteristics when grown at 37 degrees C. However, when these organisms are grown at lower temperatures, 22 degrees C, an enhanced synthesis of Group A carbohydrate occurs. Other variant strains show no appreciable alteration of the cell wall carbohydrate composition when grown at lower temperatures. Studies on an intermediate strain show that this organism has a propensity for the synthesis of a polysaccharide with higher glucosamine content and enhanced Group A serological reactivity when grown at 22 degrees C. Immunochemical studies performed on the carbohydrates produced by the A-486-Var at various temperatures revealed that the appearance of Group A serological reactivity at lower temperatures is due to the additional synthesis of a polysaccharide with Group A specificity along with the continued synthesis of a variant carbohydrate. This finding contrasts with data obtained on the carbohydrate produced by the intermediate organisms that appears to consist predominently of one molecule bearing dual A and variant antigenic determinants.

Experimental IgA nephropathy.

An animal model for IgA immune complex nephritis was developed. IgA immune complexes formed in vitro with an IgA anti-dinitrophenyl (DNP) derived from MOPC-315 plasmacytoma, and dinitrophenylated bovine serum albumin (DNP-BSA) produced mild focal glomerulonephritis in mice. Similar, but more severe pathological changes were produced with complexes formed in vivo either in normal mice or MOPC-315 tumor-bearing mice. In contrast to the focal nature of the PAS-positive glomerular lesions observed by light microscopy, immunofluorescent examination revealed IgA deposits in all glomeruli. This discrepancy between immunofluorescent and histopathologic findings as well as the distribution of the immune complexes within the affected glomeruli, are some of the features which bear resemblance between this experimental model and human IgA nephropathy. Fixation of complements by DNP-BSA-IgA immune complexes, formed in vitro or in vivo, was shown to occur in the glomeruli of mice with IgA immune complex nephropathy. The pattern of C3 glomerular deposits was similar to that of IgA. However, complement proved to be nonessential for complex deposition. This conclusion is based on the observation that decomplemented mice, although showing no deposition of C3 in their glomerulus, developed glomerular immunohistological changes similar to those observed in experimental mice that were not decomplemented. Polymeric IgA was observed to be critical for renal deposition of complexes and induction of nephritic histological changes. In contrast, monomeric IgA immune complexes failed to produce glomerular deposits. This finding raises the possibility that secretory IgA, which is predominantly polymeric, may play a role in human IgA-associated glomerulonephritis.

A single center experience of combined liver kidney transplantation.

With advancements in the operative techniques, patient survival following liver transplantation (LTx) has increased substantially. This has led to the acceleration of pre-existing kidney disease because of immunosuppressive nephrotoxicity making additional kidney transplantation (KTx) inevitable. On the other hand, in a growing number of patients on the waiting list to receive liver, long waiting time has resulted in adverse effect of decompensated liver on the kidney function. During the last two decades, the transplant community has considered combined liver kidney transplantation (CLKTx) to overcome this problem. The aim of our study is to present an overview of our experience as well as a review of the literature in CLKTx and to discuss the controversy in this regard. All performed CLKTx (n = 22) at our institution as well as all available reported case series focusing on CLKTx are extracted. The references of the manuscripts were cross-checked to implement further articles into the review. The analyzed parameters include demographic data, indication for LTx and KTx, duration on the waiting list, Model for End-Stage Liver Disease (MELD) score, Child-Turcotte-Pugh (CTP) score, immunosuppressive regimen, post-transplant complications, graft and patient survival, and cause of death. From 1988 to 2009, a total of 22 CLKTx were performed at our institution. The median age of the patients at the time of CLKTx was 44.8 (range: 4.5-58.3 yr). The indications for LTx were liver cirrhosis, hyperoxaluria type 1, polycystic liver disease, primary or secondary sclerosing cholangitis, malignant hepatic epithelioid hemangioendothelioma, cystinosis, and congenital biliary fibrosis. The KTx indications were end-stage renal disease of various causes, hyperoxaluria type 1, polycystic kidney disease, and cystinosis. The mean follow-up duration for CLKTx patients were 4.6 +/- 3.5 yr (range: 0.5-12 yr). Overall, the most important encountered complications were sepsis (n = 8), liver failure leading to retransplantation (n = 4), liver rejection (n = 3), and kidney rejection (n = 1). The overall patient survival rate was 80%. Review of the literature showed that from 1984 to 2008, 3536 CLKTx cases were reported. The main indications for CLKTx were oxalosis of both organs, liver cirrhosis and chronic renal failure, polycystic liver and kidney disease, and liver cirrhosis along with hepatorenal syndrome (HRS). The most common encountered complications following CLKTx were infection, bleeding, biliary complications, retransplantation of the liver, acute hepatic artery thrombosis, and retransplantation of the kidney. From the available data regarding the need for post-operative dialysis (n = 673), a total of 175 recipients (26%) required hemodialysis. During the follow-up period, 154 episodes of liver rejection (4.3%) and 113 episodes of kidney rejection (3.2%) occurred. The cumulative 1, 2, 3, and 5 yr survival of both organs were 78.2%, 74.4%, 62.4%, and 60.9%, respectively. Additionally, the cumulative 1, 2, 3, and 5 yr patient survival were 84.9%, 52.8%, 45.4%, and 42.6%, respectively. The total number of reported deaths was 181 of 2808 cases (6.4%), from them the cause of death in 99 (55%) cases was sepsis. It can be concluded that there is still no definitive evidence of better graft and patient survival in CLKTx recipients when compared with LTx alone because of the complexity of the exact definition of irreversible kidney function in LTx candidates. Additionally, CLKTx is better to be performed earlier than isolated LTx and KTx leading to the avoidance of deterioration of clinical status, high rate of graft loss, and mortality. Shorter graft ischemia time and more effective immunosuppressive regimens can reduce the incidence of graft malfunctioning in CLKTx patients. Providing a model to reliably determine the need for CLKTx seems necessary. Such a model can be shaped based upon new and precise markers of renal function, and modification of MELD system.

What's next after the clot? Residual pulmonary vascular obstruction after pulmonary embolism: From imaging finding to clinical consequences.

Surviving an embolism exposes patients to potential long-term complications, such as altered quality of life, persistent dyspnea, impaired exercise capacity or pulmonary hypertension. The common objective factor in most of these situations is the presence of residual pulmonary vascular obstruction (RPVO). Planar ventilation/perfusion scintigraphy (V/Q lung scan) is the gold standard for assessing RPVO, which occurs in 46 to 66% of patients at 3 months and persists in 25 to 29% of patients a year after acute PE. Assessed early (i.e. before discharge), RPVO could predict acute PE development with a high negative predictive value. Evaluated after anticoagulation therapy, RPVO could help to manage anticoagulation treatment and predict the risk of PE recurrence and patients identified at risk of developing chronic thromboembolic pulmonary hypertension. In this comprehensive review, we provide an overview of the current knowledge of RPVO after PE from imaging diagnosis to clinical consequences. In the first part, we mainly focus on the imaging modalities capable of detecting and quantifying RPVO. We then focus on the symptoms and syndromes linked with this residual obstruction after PE. Although the occurrence of RPVO and long-term complications varies greatly from one patient to another, we finally aim to identify the patients and diseases at risk of developing residual obstruction.

Qualitative and quantitative aspects of the human antibody response to streptococcal group A carbohydrate.

The lack of impressive quantitative differences in antibody to various streptococcal extracellular and cellular antigens among patients with acute rheumatic fever, acute glomerulonephritis, and following uncomplicated streptococcal infection has prompted investigation of qualitative aspects of the antibody response among these patients. By using a radiolabeled antigenically univalent hapten derived from streptococcal A carbohydrate, affinity of serum antibody to A-carbohydrate (A-antibody) was studied by an ammonium sulfate precipitation technique. The data obtained demonstrate average association constants (K0S) of acute rheumatic fever patient sera to be significantly lower than those of acute glomerulonephritis or streptococcal infection patients (P<0.02 and P<0.001, respectively). Further analysis of the data from hapten binding studies documents the fact that the radioimmune precipitin assay for the determination of A-antibody level is little influenced by K0 but directly correlates with the concentration of antibody binding sites. These data suggest that qualitative differences in A-antibody are present between rheumatic and non-rheumatic individuals. It is unclear whether the finding of low-affinity A-antibody among acute rheumatic fever patients reflects a generalized phenomenon or one restricted to the A-antibody-A-carbohydrate system.

Association of class II human histocompatibility leukocyte antigens with rheumatic fever.

The association of class I and II HLA antigens with rheumatic fever and its manifestations was examined in 72 patients, including 48 blacks and 24 Caucasians. No significant association was found between class I antigens and rheumatic fever. In contrast, HLA-DR2 and HLA-DR4 phenotypes were encountered in a significantly higher frequency in black and Caucasian patients with rheumatic fever, respectively, compared with the control populations (P less than 0.005). The most significant association (P less than 0.005) of these DR antigens with a major manifestation of rheumatic fever was found for mitral insufficiency. In addition, a significant association was encountered between persistent elevation of antibody to the group A streptococcal carbohydrate and HLA-DR4 in Caucasian patients (P less than 0.04) or HLA-DR2 in the black patients (P less than 0.001). The frequency of HLA-DR2/4 heterozygotes among patients with rheumatic fever did not differ significantly from controls. These findings support the concept of a genetically determined susceptibility to rheumatic fever and, particularly, to rheumatic heart disease. The association of the clinical manifestations of rheumatic fever and the immune hyperresponsiveness to a streptococcal antigen could be ascribed to a disease-associated immune-response gene which is in linkage disequilibrium with the DR2 and DR4 alleles of HLA-DR locus on chromosome six.

Cellular immune responses to extracellular streptococcal products in rheumatic heart disease.

The lymphocyte transformation responses to purified preparations of two extracellular products of group A streptococci (blastogen A and nuclease B), to phytohemagglutinin, and to Candida albicans antigen were measured in tonsillar and peripheral blood lymphocytes from patients with rheumatic heart disease (RHD) and suitably matched nonrheumatic (control) subjects. The mean phytohemagglutinin dose responses of tonsillar and peripheral lymphocytes from RHD patients were essentially indistinguishable from those of controls. In contrast, the responses of tonsillar and peripheral blood lymphocytes to the two extracellular products of group A streptococci were significantly lower in RHD patients than in nonrheumatic control subjects. Candida antigen produced very little stimulation of lymphocytes in any of the subjects. The geometric means of antibody levels against streptolysin O, nuclease B, and nicotinamide adenine dinucleotidase showed no consistent differences between the control group and the group of RHD subjects. Group A streptococci were isolated from the tonsils of approximately 25% of both groups of subjects. The RHD patients clearly had a depressed cellular immune response to the two purified streptococcal extracellular antigens. The equal frequency in recovery of group A streptococci from tonsils and the absence of consistent difference in titers of humoral antibodies to streptococcal extracellular antigens, particularly nuclease B, suggest that this differential response is not due to a lower level of stimulation by repeated exposure to group A streptococcal products.

The influence of the site of infection on the immune response to group A streptococci.

The immune response after streptococcal infection of the skin and of the upper respiratory tract (URT) was studied prospectively in a group of normal children, ages 3-6 yr. The children were examined and cultures for group A streptococci were obtained weekly from the throat, nose, and skin lesions (when present). Paired sera were collected at the beginning and end of the study, and the changes in antibody titers were measured for three different streptococcal antigens: streptolysin O, deoxyribonuclease B (DNAse B), and nicotinamide adenine dinucleotidase (NADase). The findings suggest that in contrast to infection of the URT antibody response to streptolysin O is relatively feeble after streptococcal infection which is limited to the skin. The response to NADase is also poor after cutaneous infection. Antibody responses to DNAse B are generally good regardless of the site of the infection. These and other studies indicate that anti-DNAse B is the antibody of choice in studying streptococcal infection of the skin and its complications.

On defining Sydenham's chorea: where do we draw the line?

Sydenham's chorea (SC) is a major manifestation of rheumatic fever characterized by an array of neuropsychiatric symptoms that vary in severity, timing, and character. Some of the same symptoms are seen in Tourette's syndrome and childhood-onset obsessive-compulsive disorder. Genetic vulnerability appears to play a role in all three conditions. The term PANDAS (pediatric autoimmune neuropsychiatric disorder associated with streptococcus) has been introduced to describe a putative subset of obsessive-compulsive disorder and Tourette's syndrome that bears some resemblance to Sydenham's chorea. This article discusses whether PANDAS should be subsumed under Sydenham's chorea, thus expanding the diagnostic boundaries of Sydenham's chorea to include primarily neuropsychiatric presentations now classified as cases of obsessive-compulsive disorder or Tourette's syndrome. We conclude that PANDAS is a useful construct, but that it would be premature to view it as a subset of Sydenham's chorea-whether defined narrowly or broadly.

High prevalence of obsessive-compulsive symptoms in patients with Sydenham's chorea.

The 20-item Leyton Obsessional Inventory--Child Version was completed by children and adolescents who had had Sydenham's chorea (N = 23) or rheumatic fever without chorea (N = 14). The Sydenham's chorea subjects had significantly more obsessive thoughts and compulsive behaviors and significantly greater interference from these behaviors. Three Sydenham's chorea patients but no rheumatic fever patients had substantial obsessional interference and met criteria for obsessive-compulsive disorder when interviewed by telephone. This suggests that obsessive-compulsive disorder, at least in some patients, may be due to basal ganglia dysfunction.

B lymphocyte antigen D8/17: a peripheral marker for childhood-onset obsessive-compulsive disorder and Tourette's syndrome?

OBJECTIVE: It has been hypothesized that Sydenham's chorea, a major manifestation of rheumatic fever, may provide a medical model for obsessive-compulsive disorder and associated conditions, such as Tourette's syndrome. Monoclonal antibody D8/17 identifies a B lymphocyte antigen with expanded expression in nearly all patients with rheumatic fever and is thought to be a trait marker for susceptibility to this complication of group A streptococcal infection. The authors investigated whether D8/17 expression is greater than normal in some forms of obsessive-compulsive disorder and Tourette's syndrome. METHOD: By immunofluorescence techniques, 31 patients with childhood-onset obsessive-compulsive disorder and/or Tourette's syndrome or chronic tic disorder and 21 healthy comparison subjects were evaluated for percentage of D8/17-positive B cells. None had rheumatic fever or Sydenham's chorea. Levels of antineuronal antibodies and streptococcal antibodies were also determined. RESULTS: The average percentage of B cells expressing the D8/17 antigen was significantly higher in the patients (mean = 22%, SD = 5%) than in the comparison subjects (mean = 9%, SD = 2%). When classified categorically, all patients but only one comparison subject were D8/17 positive. No difference between groups in the presence of antineuronal antibodies or high streptococcal titers was found. CONCLUSIONS: Patients with childhood-onset obsessive-compulsive disorder or Tourette's syndrome had significantly greater B cell D8/17 expression than comparison subjects despite the absence of documented Sydenham's chorea or rheumatic fever. These findings suggest that D8/17 may serve as a marker for susceptibility among some forms of childhood-onset obsessive-compulsive disorder and Tourette's syndrome, as well as rheumatic fever or Sydenham's chorea.

Detection of receptors for the Fc region of IgG on streptococci.

A semi-quantitative absorption test to measure Fc-reactive proteins on the surface of streptococci is described. The ability of bacteria to remove intact IgG in the presence of an equimolar amount of F(ab')2 fragments was used to identify streptococci with Fc-reactive proteins on their surface. This method was found to be more objective, reproducible and quantitative than the hemagglutination and 125I-labeled IgG binding methods currently in use. Methods for detection of secreted Fc-reactive materials with protein A-like reactivity are also described.

Progress toward analysis of D8/17 binding to B cells in children with obsessive compulsive disorder and/or chronic tic disorder.

BACKGROUND: Previous research has suggested that a subgroup of children with obsessive compulsive disorder (OCD) have neuropsychiatric sequelae of streptococcal pharyngitis, similar to that seen in the neurological manifestation of rheumatic fever (RF). Monoclonal antibody D8/17 demonstrates increased binding to B cells in patients with RF and in patients with neuropsychiatric disorders using immunofluorescent microscopy. OBJECTIVE: The aim of this study was to determine if an earlier immunofluorescent microscopy study of monoclonal antibody D8/17 in childhood-onset OCD and/or chronic tic disorder (CTD) could be replicated using the more objective method of flow cytometric analysis. METHOD: D8/17 binding to B cells was determined in patients with OCD and or CTD (N=32), and healthy controls (N=12) by flow cytometric analysis. RESULTS: Subjects with OCD/CTD showed increased mean cell binding (26.0%) of monoclonal antibody compared with healthy controls (9.1%) (p<0.001). When using the threshold of greater than 19% binding (95% upper confidence interval) as a measure of positivity, 65.6% of patients compared with 8.3% of controls showed increased antibody binding to B cells (p=0.01). CONCLUSIONS: Although this study reports positive results, many methodological issues will need to be addressed before generalized use of assay for diagnostic purposes.