Evaluation de l'antibiothérapie des pneumopathies aigües communautaires dans un service de médecine interne

BESANCON-BU Médecine pharmacie (250562102) / SudocSudocFranceF

Localisations artérielles extra-crâniennes de la maladie de Horton (à propos de 10 cas)

BESANCON-BU Médecine pharmacie (250562102) / SudocSudocFranceF

Dysphagia and hypervitaminosis A: cervical hyperostosis.

International audienceVertebral hyperostosis typically predominates at the thoracic spine and causes only minor symptoms. Involvement of the cervical spine may cause dysphagia due to pressure on the esophagus. We report three cases of dysphagia revealing cervical hyperostosis. CASE REPORTS: The patients were 3 men aged 54-73 years. Dysphagia was moderate in 2 patients and severe in 1 patient who had lost 4 kg over 6 months. Stiffness of the neck with mild pain was present. One patient reported a neck injury in childhood and another had a brother and father with similar symptoms. Radiographs showed exuberant anterior cervical hyperostosis. Two patients also had hyperostotic changes at the thoracic spine and pelvis. The skin and neurological evaluation were normal. Findings were normal from standard blood tests (C-reactive protein, calcium, and vitamin D). Tests were negative for the HLA-B27 antigen in all 3 patients. Serum vitamin A levels were high, ranging from 894 to 1123 microg/L (normal, 489-720). None of the patients reported taking retinoids or having unusual eating habits. DISCUSSION: Dysphagia can result from anterior cervical hyperostosis. A role for hypervitaminosis A in the genesis of hyperostosis has long been suspected. In our patients, the absence of vitamin A supplementation suggests an abnormality in vitamin A metabolism

[Kappa light chain deposition disease, presenting as Sjögren's syndrome, successfully treated by high-dose melphalan and autologous blood stem transplantation]

International audienceINTRODUCTION: Light chain deposition disease is a systemic disorder characterised by tissue deposition of monoclonal immunoglobulin light chains without tinctorial properties. It has been exceptionally reported with salivary involvement mimicking Sjögren's syndrome and peripheral neuropathy. CASE REPORT: We report a case of light chain deposition disease associated with plasma cell dyscrasia presenting as sicca syndrome with salivary glands hypertrophy and polyneuropathy successfully treated by high dose melphalan and autologous blood stem transplantation. CONCLUSION: Light chain deposition disease should be recognized as an aetiology of sicca syndrome and peripheral neuropathy. Further studies should assess the prevalence of sicca syndrome in light chain deposition disease and better characterise the neurological manifestations

Genital human Papillomavirus infection in patients with autoimmune inflammatory diseases.

International audienceTreatment advances achieved over the last few years have radically changed the management of patients with autoimmune inflammatory diseases requiring conventional or biological immunosuppressive therapy. These diseases and the drugs used to treat them increase the rate of infections, including genital infections due to the human Papillomavirus (HPV). Genital HPV infections have been extensively studied in organ transplant recipients, HIV-infected patients, and patients with congenital immune deficiencies. Although genital HPV infections usually manifest as benign lesions of the external genital organs (condylomata), they are associated with an increased risk of cancer. Very few data are available on genital HPV infections associated with autoimmune inflammatory diseases or their treatments. Here, we review the published information on this topic

Cardiac Shock Revealing Systemic Lupus Erythematosus

International audienc

Sacroiliitis in a patient with Rosai-Dorfman disease: new bone location or overlap with axial spondylarthritis?

International audienc

LupusQoL-FR is valid to assess quality of life in patients with systemic lupus erythematosus.

International audienceOBJECTIVE: To cross-culturally adapt the LupusQoL into French, to test its measurement properties and to further investigate its domain structure. METHODS: The cultural adaptation process according to guidelines and pre-testing resulted in the LupusQoL-FR. SLE patients completed the LupusQoL-FR at baseline, 15 days, 3 months and 6 months. Validity was studied through content and construct validity (factorial and Rasch analysis for structural validity, Spearman's correlation and Mann-Whitney tests for external validity). Cronbach's α and intra-class correlation coefficients were computed for reliability. The standardized response mean was computed to evaluate responsiveness. RESULTS: In all, 182 patients, age 39.6 (10.6) years, mostly outpatients [mean SELENA-SLEDAI 2.6 (3.5)] were recruited. Factor analysis with eight imposed factors was very close to the original LupusQoL. A screeplot with parallel analysis showed that LupusQoL domains could be aggregated in two physical and mental scales. Both eight- and two-factor structures showed a good Rasch fit, internal consistency (Cronbach's α: 0.85-0.95), and test-retest reliability (intra-class correlation coefficient 0.79-0.95). External convergent (correlation with SF-36, r=0.59-0.78) and divergent validity (according to SELENA-SLEDAI) were also satisfactory. CONCLUSION: The LupusQoL-FR is valid to assess quality of life in SLE patients. A two-factor structure of physical and mental aggregated scales is a valid alternative to the original eight-domain structure

Antiplatelet Antibodies Do Not Predict the Response to Intravenous Immunoglobulins during Immune Thrombocytopenia

Immune thrombocytopenia (ITP) is a rare autoimmune disease due to autoantibodies targeting platelet glycoproteins (GP). The mechanism of platelet destruction could differ depending on the specificity of antiplatelet antibodies: anti-GPIIb/IIIa antibodies lead to phagocytosis by splenic macrophages, in a Fcγ receptor (FcγR)-dependent manner while anti-GPIb/IX antibodies induce platelet desialylation leading to their destruction by hepatocytes after binding to the Ashwell–Morell receptor, in a FcγR-independent manner. Considering the FcγR-dependent mechanism of action of intravenous immunoglobulins (IVIg), we assumed that the response to IVIg could be less efficient in the presence of anti-GPIb/IX antibodies. We conducted a multicentric, retrospective study including all adult ITP patients treated with IVIg who had antiplatelet antibodies detected between January 2013 and October 2017. Among the 609 identified, 69 patients were included: 17 had anti-GPIb/IX antibodies and 33 had anti-GPIIb/IIIa antibodies. The response to IVIg was not different between the patients with or without anti-GPIb/IX (88.2% vs. 73.1%). The response to IVIg was better in the case of newly diagnosed ITP (odds ratio (OR) = 5.4 (1.2–24.7)) and in presence of anti-GPIIb/IIIa (OR = 4.82 (1.08–21.5)), while secondary ITP had a poor response (OR = 0.1 (0.02–0.64)). In clinical practice, the determination of antiplatelet antibodies is therefore of little value to predict the response to IVIg