[Introduction to debriefing for internists: how to transform real or simulated clinical situations into learning moments]. / Initiation au débriefing pour les internistes : état des connaissances et mise en pratique pour transformer des situations cliniques réelles ou simulées en moments d'apprentissage.

Debriefing is a phase of synthesis and reflection that immediately follows a real-life or simulated situation. It is an essential educational step that forces the learners to reflect upon the thought processes that underlie their actions. Debriefing encourages a personal and collective reflection in order to remodel erroneous mental schemas and rectify actions done in context. Debriefing cannot be improvised; it requires a sound structure and regular practice in order to be truly effective. The debriefer must be considerate, choose appropriate learning objectives and dedicate ample time to the learners. Debriefing is focused on learning acquired in context-in other words, on the actions that were performed within a real-life or simulated clinical practice situation-and immediately follows the situation. After an initial phase of emotional release, the debriefer will help learners analyse their actions to identify their underlying rationale (contextualization), extract the overarching principles related to the lived situation in order to modify the rationale if needed (decontextualization) and assist the transfer of learning to real life (in the case of simulation) and to similar situations (recontextualization). A final summary of learning achieved during the training session concludes the debriefing. Debriefing is useful in any learning situation, including in internal medicine. Even if simulation is still underused in internal medicine, post-event debriefing can be implanted in our clinical services. Indeed, training our students and shaping them into healthcare professionals rest in no small part on hospital rotations where the intern is confronted with real-patient situations that are suitable to learning. Some in-hospital clinical encounters can be actively transformed into learning opportunities thanks to post-event debriefing, but can also passively morph into bad daily practice if no supporting action is implemented. Debriefing can thus provide an opportunity to develop non-technical skills in critical situations, or doctor-patient communication skills, within a team or between colleagues. These competencies are the hallmark of well-trained interns and are indispensable for the proper functioning of a care team. We will not develop the emotional and psychological management of debriefing in this article. We hope we will helpfully introduce as many of our colleagues as possible to the art of debriefing in most circumstances.

[Knowledge and beliefs of 4th-year medical students concerning professional practices in general medicine. Results of a survey conducted at the School of Medicine of Brest]. / Connaissances et croyances des étudiants en 4e année des études de médecine à l'égard des pratiques professionnelles en médecine générale. Résultats d'une enquête conduite à la Faculté de médecine de Brest.

As part of preparations for the first seminar in general practice, organized for medical students in their forth year at the Brest faculty of medicine, students were asked to fill in a questionnaire concerning their beliefs and knowledge concerning general-practice medicine. Fifty-two students, or 89.6% of the class, completed the questionnaires. The results showed that despite the lack of formal contacts with this type of practice during their studies, the students had a good idea of what general-practice medicine is and of the role of the general practitioner in our health-care system. However, this study has illustrated the difficulties students experience in defining their future professional direction, since they receive no information during their training on the different options in medical practice.

Interaction between certain major histocompatibility complex class II and T-cell receptor V beta alleles promotes the antibody production to extractable nuclear antigen-related peptides.

Our objective was to study the interaction between major histocompatibility complex (MHC) class II and T-cell receptor (TCR) alleles in the recognition of extractable nuclear antigen-derived peptides in 32 patients with systemic lupus erythematosus and 173 of their family members. MHC genes were analyzed using sequence specific oligonucleotides, and TCR beta-chain gene polymorphism using restriction fragment-length polymorphism. One dominant peptide (as defined by enzyme-linked immunosorbent assay autoantibody reactivity) was identified in each antigen studied: peptide 1-20 in Sm-D, peptide 35-58 in U1-RNP-A, and peptide 304-324 in the Ro/SSA 60 Kd protein. None of the MHC class II and TCR beta haplotypes was directly associated with any of the autoantibodies. Twenty-six subjects had antibodies to the peptide Sm-D1-20; nine of them were DRB1*0101/DQB1*0501. Among subjects with this haplotype, the number of responders was higher (p < 0.028, p corrected, pc = 0.336) in those with the 2-25-9 TCR beta haplotype than in the remainder. Conversely, the number of DRB1*04/DQB1*0302 responders was lower (p < 0.030, pc = 0.360) among subjects with the 23-20-9 TCR beta haplotype than in those without. The odds ratios (OR) were 4.23 and 0.21, respectively. Of the 54 subjects positive for anti-U1-RNP-A 35-38, 13 were DRB1*0101/DQB1*0501 and eight DRB1*04/DQB1*0302. The percentage of responders was higher (p < 0.041, pc = 0.492, OR = 3.48) in the former group of subjects with the 2-25-9 TCR beta haplotype, and lower (p < 0.02, pc = 0.024, OR = 0.09) in the latter with the 23-20-9 TCR beta haplotype. Three of the 12 anti Ro/SSA 60Kd 304-324-positive subjects were DRB1*0101/DQB1*0501. All had the 2-25-9 TCR beta haplotype (p < 0.046, pc = 0.552, OR = 6.29) and none the 23-20-9 (p < 0.031, pc = 0.372, OR = 0.10). The same combinations of genes were associated with high/low response toward the three peptides. These data provide evidence for an interplay of the MHC class II and TCR beta alleles in the control of specific autoantibody response to well-defined nuclear Ag peptides.

Interplay of four idiotypes and interaction with autoantibodies in lupus patients, their relatives and their spouses.

Our aim was to investigate links between systemic lupus erythematosus (SLE)-associated autoantibodies, idiotypes (Id) and genetic predisposition to their development. We studied four public Ids (16/6, WRI 176 beta, RT72 and RT84), identified the Km and Gm phenotypes and sought six selected autoantibodies in 32 SLE patients, 174 of their relatives and 15 spouses. Though anti-double-stranded DNA antibody was uncommon in the relatives (9%), the range of antinuclear reactivities was as broad in the relatives as in the probands. Antibodies to the synthetic peptide U1-RNP-A 35-38 were found in 56% of the patients, 28% of their relatives and 20% of the spouses, whereas antibodies to the Golgi apparatus was present in 7% of the patients, 26% of their relatives and 33% of the spouses. However, most of these family members were unaffected. RT84 Id was positively associated with antibodies to Sm-D peptide 1-20 and to Ro/SSA 60 kD peptide 304-324, but negatively associated with anti-dsDNA activity. The median of age was significantly lower in the RT84 Id-positive than in the RT84 Id-negative individuals. These data suggest that genetic as well as environmental factors are involved in the aetiology of SLE. In addition, RT84-carrying immunoglobulins (Ab2) might be directed to one of many cross-reactive Ids of dsDNA-binding antibodies (Ab1), perhaps down-regulating their production.

Some nutritional parameters in patients with rheumatoid arthritis.

Its was our aim to appreciate the respective influence of age, sex, duration of disease, inflammatory status and treatment on protein markers in patients with rheumatoid arthritis (RA). Serum albumin (SA), thyroxin-binding prealbumin (TBPA), transferrin and retinol-binding protein (RBP) were determined in 155 RA patients. Since the cut off, levels of these proteins are highly dependent on sex and age, several groups of sex- and age-matched normal controls were evaluated. The levels of SA (p < 0.03) and RBP (p < 0.002) were reduced in the women under 45 years of age. SA and RBP reached a nadir following one year of evolution. There were inverse correlations between SA and Lee's index (p < 0.01) and TBPA and Lee's (p < 0.05) and Ritchie's index (p < 0.01). Sa correlated inversely with the inflammatory status. The complex challenge of nutritional evaluation in RA patients is thus impossible to adequately portray and results should be interpreted with caution.

The relationship of anti-endothelial cell antibodies to anti-phospholipid antibodies in patients with giant cell arteritis and/or polymyalgia rheumatica.

Sera from patients with giant cell arteritis and/or polymyalgia rheumatica were tested for the presence of IgG, IgM and IgA antibody to endothelial cells (AEC), cardiolipin (ACL) and phosphatidylethanolamine (APE) using enzyme-linked immunosorbent assays. There were strong correlations between ACL and APE, but also between AEC and ACL IgM (p < 0.02) and between AEC and APE IgA (p < 0.003). Inhibition of AEC binding was achieved by absorption onto EC, but ACL and APE binding was also significantly reduced. In contrast, the binding of AEC antibody could not be inhibited by incubation with CL. Our data suggest that AEC constitute a heterogeneous population of autoantibodies.

Dopamine B hydroxylase deficiency responsible for severe dysautonomic orthostatic hypotension in an elderly patient.

We report the case of an elderly woman with severe dysautonomic orthostatic hypotension in whom a deficit in dopamine B hydroxylase has been established. In the literature, such a deficit has been described in six young adults with long standing symptoms of postural hypotension. This enzyme catalyses the conversion of dopamine to noradrenaline. In our elderly patient, noradrenaline and adrenaline were undetectable in the plasma, but plasma dopamine was detectable. Treatment with the synthetic amino acid, DL-threo-dihydroxyphenylserine, which is converted to noradrenaline by dopa-decarboxylase, resulted in a significant increase in blood pressure. The mechanism of this acquired deficit is not elucidated.

[Immunogenetics of systemic lupus: adequacy between HLA molecules class II and the germinal genes of antigen receptor of T-lymphocytes favours the production of various antibodies]. / Immunogénétique du lupus systémique: l'adéquation entre molécules HLA de classe II et gènes germinaux du récepteur d'antigènes des lymphocytes T favorise la production de certains anticorps.

The study of 30 patients with systemic lupus and of 153 relatives failed to show any differences in HLA and TCR beta haplotype frequencies between patients and relatives. A significant interaction between TCR V beta and HLA-DR/DQ genes in the response to the peptide U1-RNP A 35-58 was demonstrated.

Anti-neutrophil cytoplasm antibodies in patients with giant cell arteritis and/or polymyalgia rheumatica.

Anti-neutrophil cytoplasm antibodies (ANCA) were detected at low titers by indirect immunofluorescence in 1 out of 13 patients with giant cell arteritis (GCA) alone, 7 out of 30 with polymyalgia rheumatica (PMR) alone and 4 out of 15 with GCA plus PMR (8, 23 and 27%, respectively). Anti-myeloperoxidase antibodies were also demonstrated by an enzyme-linked immunosorbent assay in 4 patients with GCA alone (31%), 13 with PRM alone (42%) and 5 with GCA plus PRM (33%). The C-reactive protein response was significantly higher (p < 0.05) in ANCA-positive than in ANCA-negative patients.

Sjögren's syndrome in patients with the CREST variant of progressive systemic scleroderma.

Twenty-three patients with the CREST (calcinosis, Raynaud's phenomenon, esophageal dysmotility, sclerodactyly, telangiectasia) variant of progressive systemic sclerosis, were clinically, histopathologically and serologically examined for the presence of Sjögren's syndrome (SS). Fourteen were found to be positive. No significant difference could be demonstrated between them and the remaining 9. Characteristics of patients with CREST were compared with those of 29 randomly chosen patients with primary SS. Parotid gland enlargement was more frequently present (p less than 0.01) in the latter than in the former. Virtually no patients with CREST with SS had antibodies to Ro(SSA)/La(SSB).

Nonorgan-specific autoantibodies in individuals infected with type 1 human immunodeficiency virus.

Fifty-six human immunodeficiency virus-1-positive asymptomatic carriers were tested for the presence of a variety of nonorgan-specific autoantibodies. Antinuclear antibodies were detected in 34 sera, of which 27 were directed to the mitotic spindle apparatus and all were of the IgG isotype. Anti-Golgi complex, anti-centriole, and anti-vimentin antibodies were also present in 20.4, and 4 sera, respectively. Ten patients had less than 500 CD4-carrying T lymphocytes per cubic millimeter. Nine of them had more than one autoantibody. No correlation could be demonstrated between the number of autoantibodies and the level of serum immunoglobulins.

Serial measurements of anticardiolipin antibodies in primary Sjögren's syndrome.

Twenty-four out of 54 patients with primary Sjögren's syndrome (SS) were shown to be positive for IgG and/or IgM anticardiolipin antibodies (aCL). Extraglandular manifestations were related to the IgG-, but not to the IgM-aCL. Twenty SS patients were examined over a 3 year period. Of these, 6 displayed a marked increase in IgG- and IgM-aCL and, among them, 4 developed extraglandular manifestations of SS throughout the follow-up.

IgA-containing immune complexes in the circulation of patients with primary Sjögren's syndrome.

IgA-, IgM- and IgG-containing immune complexes (CIC) were detected in 48, 19 and 12% of 52 patients with primary Sjögren's syndrome (SS), in 36, 38 and 56% of 45 patients with rheumatoid arthritis, and in 8, 5 and 3% of 40 normal controls. A high proportion of primary SS patients also had considerable amounts of serum IgA and elevated levels of IgA with rheumatoid factor (RF) activity. IgA-CIC and IgA-RF were more frequent (P less than 0.03 and less than 0.001) in the 27 primary SS patients with, than in the 25 without extraglandular manifestations. IgA-CIC could play a role in mediating the tissue injury associated with primary SS.

Serological arguments for classifying Raynaud's phenomenon as idiopathic.

Twenty-five patients with idiopathic Raynaud's phenomenon were followed prospectively for a mean period of 48 months. Clinical and laboratory assessments were performed on admission and on followup. The sera were analyzed for the presence of autoantibodies (antinuclear, antiskeleton and antiorganelle antibodies). Sixteen patients were antinuclear antibody positive and 2 anticentromere antibody positive. Eight patients produced antivimentin, 5 antimitochondrial, 4 anti-Golgi complex, and 3 anticentriol antibodies. Eleven patients produced antidesmosome antibodies. Only one patient (anti-RNP and antidesmosome antibody positive) developed a systemic disease (mixed connective tissue disease) during followup. The initial screening of sera may help to classify Raynaud's phenomenon as idiopathic more accurately.