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Sandrine Guis

Publications and source records attributed to Sandrine Guis.

12 recordsLinked to original sources
PubMed2006

Calcaneal osteomyelitis due to fistulization of an ulcerated rheumatoid nodule.

UNLABELLED: Calcaneal osteomyelitis is uncommon and difficult to treat. Cases due to fistulization of an infected rheumatoid nodule are exceedingly rare. PATIENT: A 65-year-old patient with nodular rheumatoid arthritis (RA) experienced osteomyelitis of the left calcaneus due to inoculation from a fistula draining an ulcerated rheumatoid nodule. Pseudomonas aeruginosa and Enterobacter cloacae were recovered. The conventional treatment of calcaneal osteomyelitis relies on antibiotics and calcanectomy or foot amputation. We used two appropriate antibiotics and monthly intravenous injections of 90 mg of pamidronate. RESULT: One year into treatment, the patient was free of pain and the skin wound was fully healed. On a follow-up computed tomography (CT) scan, the fistulous tract was seen to be closed and the large calcaneal defect almost completely filled with new bone. CONCLUSION: Combining two antibiotics and pamidronate may be a viable alternative to excision surgery or amputation in some patients with bone infection carrying a risk of fracture.

Aged↗
PubMed2006

Platelet-endothelial cell adhesion molecule-1 and CD146: soluble levels and in situ expression of cellular adhesion molecules implicated in the cohesion of endothelial cells in idiopathic inflammatory myopathies.

OBJECTIVE: Idiopathic inflammatory myopathies (IIM) are a heterogeneous group of diseases characterized by chronic inflammation of muscles. We investigated the role of cellular adhesion molecules implicated in the cohesion of endothelial cells in IIM. METHODS: In 22 patients with IIM we investigated plasma concentrations of soluble junctional adhesion molecules [platelet-endothelial cell adhesion molecule (sPECAM-1) and sCD146] and cellular adhesion molecules [sP-selectin, sE-selectin, intercellular adhesion molecule (sICAM-1), and vascular cell adhesion molecule (sVCAM-1)] implicated in leukocyte/endothelial cell interactions. Results were compared to a control group. Muscle biopsy samples from 8 out of 22 IIM patients were studied by immunohistochemistry for tissue expression of these molecules and compared to normal muscle samples. PECAM-1 and CD146 expression was also studied using immunoblots from muscle biopsies from 5 patients and 2 controls. RESULTS: We observed distinct patterns of soluble levels and in situ expression between dermatomyositis (DM), polymyositis (PM), and sporadic inclusion body myositis (s-IBM). PM samples showed significantly increased levels of sCD146, sPECAM-1, and s-ICAM1 and increased expression of CD146, CD31, and ICAM-1 in endothelial cells, whereas CD146 and ICAM-1 were also recorded in some muscle fibers. In DM, sE-selectin, sP-selectin, and sPECAM-1 were significantly increased, with abnormal expression of ICAM-1 in endothelial cells and perifascicular muscle fibers. In the small group of s-IBM samples, results were similar to PM, but the only significant increase was the level of sPECAM-1. Immunoblots confirmed increased expression of PECAM-1 and CD146 in all IIM muscles in comparison to controls, with the highest expression in PM and IBM samples. CONCLUSION: We observed abnormal increases of soluble levels of adhesion molecules implicated in endothelial cell junctions in PM (sCD146, sPECAM-1) and to a lesser extent in DM and s-IBM (sPECAM-1). We conclude that the distinctly different profiles between PM/s-IBM and DM reflect differences in the pathophysiological background of these diseases.

CD146 Antigen↗
PubMed2005

Influence of HLA-DR genes on the production of rheumatoid arthritis-specific autoantibodies to citrullinated fibrinogen.

OBJECTIVE: Antibodies directed against citrullinated fibrinogen are highly specific for rheumatoid arthritis (RA). This study was undertaken to test whether RA-associated HLA-DR alleles are associated with anti-citrullinated fibrinogen in RA patient sera and whether replacement of arginyl by citrullyl residues on fibrinogen peptides modifies their binding to HLA-DR molecules and their recognition by T cells. METHODS: Antikeratin, antifilaggrin, and anti-citrullinated fibrinogen antibodies were assayed in RA patients who had undergone HLA-DR typing. Direct assays were performed to investigate binding of citrullinated or native fibrinogen peptides (encompassing the entire alpha- and beta-chains of fibrinogen) to purified HLA-DR molecules. T cell proliferative responses to citrullinated or native fibrinogen peptides were measured in RA patients and controls. RESULTS: HLA-DRB1*0404 was associated with anti-citrullinated fibrinogen in RA sera (P = 0.002). For the RA-associated alleles HLA-DRB1*0401 and HLA-DR1, there was a nonsignificant trend toward association (P = 0.07). Multiple peptides from the alpha- and beta-chains of fibrinogen bound many HLA-DR alleles; DRB1*0404 was the best fibrinogen peptide binder. Citrullination did not influence fibrinogen peptide binding to HLA-DR or fibrinogen peptide recognition by T cells. Peripheral blood T cells that recognized native or citrullinated fibrinogen peptides were common in RA patients but not in healthy controls. CONCLUSION: The RA-associated HLA-DRB1*0404 allele is also associated with production of antibodies to citrullinated fibrinogen. DRB1*0401 and DRB1*01 tend to be associated with anti-citrullinated fibrinogen, but this is not statistically significant. Citrullination of fibrinogen peptide does not influence peptide-DR-T cell interaction. Finally, T cell proliferation in response to citrullinated or uncitrullinated fibrinogen peptides is frequent in RA patients and very infrequent in controls.

Alleles↗
PubMed2005

Pathophysiology and clinical presentations of rhabdomyolysis.

Rhabdomyolysis has sparked new interest in recent years. The causes of rhabdomyolysis include drugs and other toxic agents, infections, physical exertion, crush injury, and muscle diseases (dystrophinopathies and metabolic myopathies). Prompt identification of the pathophysiological mechanism is the key to rapid control of the acute episode and to prevention of recurrences. In this update, we discuss the pathophysiological mechanisms and nosology of rhabdomyolysis, as well as diagnostic investigations, with special emphasis on noninvasive methods.

Humans↗
PubMed2004

Multiminicore disease in a family susceptible to malignant hyperthermia: histology, in vitro contracture tests, and genetic characterization.

BACKGROUND: Histological anomalies associated with malignant hyperthermia (MH) have been scarcely reported. In some patients susceptible to MH (MHS), central cores have been identified and a genetic association has been proposed, but multiminicore lesions have not been systematically reported. OBJECTIVE: To analyze the association between multiminicores and MHS in a large family with MH with an approach combining histology, in vitro contracture tests, and genetic analysis. PATIENTS AND METHODS: Twenty-nine members of an MH family (147 members) were investigated. MAIN OUTCOME MEASURES: Muscle biopsy specimens were analyzed histologically and with in vitro contracture tests. Genetic analyses were performed to determine the presence of mutations in the ryanodine receptor (RYR1) gene. RESULTS: According to the gold standard in vitro contracture tests, 17 patients were diagnosed as having MHS and 10 as not being susceptible. Multiminicores were found in 16 of the 17 MHS patients and in a single nonsusceptible participant. A linkage between the MH trait and the RYR1 locus in chromosome 19 was demonstrated, whereas no already known mutations were found. Two missense heterozygous mutations (R2676W and T2787S) were identified from sequencing of the entire coding complementary DNA. Overall, we found a significant association between MHS and the presence of multiminicores (chi(2) = 26.5, P<.001) on the one hand and the presence of new mutations in the RYR1 gene (chi(2) = 19.0, P<.001) on the other hand. This remarkably high occurrence of multiminicores in an MHS family is uncommon, and genetic analyses indicate that the association between multiminicores and MHS is linked to a novel R2656W and T2787S substitution present on the same allele of the RYR1 gene. CONCLUSIONS: These results indicate that multiminicore lesions are observed in MHS patients with neither clinical signs related to multiminicore disease nor histological features of congenital myopathies. These multiminicore lesions may be secondary to mutations in the RYR1 gene. As a consequence, these patients must be distinguished from patients with multiminicore disease and from other MHS patients for whom multiminicores are not observed.

DNA Mutational Analysis↗
PubMed2004

Multifocal discitis caused by Staphylococcus warneri.

Staphylococcus warneri is a coagulase-negative staphylococcus that is a normal inhabitant of the skin but occasionally causes septicemia and endocarditis. We report a case of multifocal discitis caused by S. warneri in an immunocompetent patient. Only three cases of spinal S. warneri infections have been reported in the literature. They illustrate the atypical clinical presentation, with chronic pain of increasing severity in the thoracic or lumbar spine instead of the abrupt onset that characterizes S. aureus discitis. In our patient, despite the multifocal distribution of the lesions, heretofore unreported, clinical presentation suggested common low back pain. This presentation may be ascribable to the unique bacteriological characteristics of S. warneri. The case reported here illustrates the diagnostic challenges sometime raised by discitis due to coagulase-negative staphylococci.

Aged↗
PubMed2003

Drug-induced and toxic myopathies.

Drug-induced myopathies and, more rarely, rhabdomyolysis, are a common biological and clinical setting for clinical rheumatologists. The focus of this chapter is to review (i) the clinical presentation and management of these adverse drug reactions (ADR) according to pain and associated neurological symptoms, (ii) the common drugs prescribed by rheumatologists which may induce reactions such as ADR, with special reference to new drugs, (iii) the pathological classification associated with specific patterns, and (iv) the risk factors leading to myotoxicity (including genetic predisposition). Specific features to be reviewed include macrophage myofasciitis and biological agents of major importance when considering terrorist attacks with biological weapons. When diagnosis is suspected, discontinuation of the putative drug(s) is mandatory and should be carefully monitored.

Humans↗
PubMed2002

Three-year outcome in a patient with Staphylococcus lugdunensis discitis.

The few reported cases of bone and joint infection by Staphylococcus lugdunensis indicate that the clinical manifestations are severe, the diagnosis elusive, and the treatment difficult. We report a case of lumbar discitis caused by Staphylococcus lugdunensis in a 67-year-old man receiving chemotherapy for stage III IgA lambda multiple myeloma. Treatment was with ofloxacin and pristinamycin for 1 year. Although he started to improve only 5 months after treatment initiation, the outcome was favorable. Follow-up at the time of this writing is 3 years.

Aged↗