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Loïc Guillevin

Publications and source records attributed to Loïc Guillevin.

At least 55 records · Page 3Linked to original sources
PubMed2004

[Vasculitis associated with viral infections].

VIRUSES, THE CAUSE OF VASCULITIS: Although the majority of systemic vasculitis are of unknown causes, the responsibility of a viral infection has been formally demonstrated in some of them and specific treatment can permanently cure them. Each virus incriminated accounts for a particular type of vasculitis. HEPATITIS B VIRAL INFECTION (HBV): Is the cause of polyarteritis nodosa in 36 to 50% of cases. The onset of the symptomatology is acute, usually within a few months following the infection; it is comparable to that observed in the absence of HBV infection. CRYOGLOBULINEMIA RELATED TO THE HEPATITIS C VIRUS (HCV): The clinical manifestations are those of systemic vasculitis with particular tropism for the skin (involvement generally inaugural and almost constant), peripheral nerves and the glomerula. They occur fairly late during the infection. VASCULITIS ASSOCIATED WITH HIV INFECTION: There is strong tropism for the peripheral (multi-neuritis) and central nervous system. During acute parvovirus B19 infection Vasculitis lesions have occasionally been reported following the viremic phase, generally limited to one or several flares of vascular purpura predominating on the lower limbs. FOLLOWING VARICELLA-HERPES ZOSTER INFECTION: Vasculitis occasionally develops in the form of a central neurological deficiency (locomotor deficiency with or without aphasia around one month after an ophthalmologic herpes zoster) or involving the retina or, more rarely, the skin or the kidneys. VASCULITIS ASSOCIATED WITH CYTOMEGALOVIRAL INFECTION: Predominantly observed in immunodepressed patients, vasculitis after CMV infection is diffuse and basically involving the digestive tube, notably the colon, the central nervous system and the skin. A RARE COMPLICATION OF AN HTLV1 INFECTION: Vasculitis of the retina often in the form of necrotic retinitis is often associated with spasmodic paraparessia. THERAPEUTIC STRATEGY: For many vasculitis of viral origin, corticosteroid and immunosuppressive treatments are only indicated in second intention following failure with antiviral agents and the combination of antivirals and plasma exchanges.

Adrenal Cortex Hormones↗
PubMed2004

[Stress and coping strategies in systemic lupus erythematosus].

UNDENIABLE PSYCHOLOGICAL IMPACT: Systemic lupus erythematosus (SLE), a chronic and unpredictable disease with functional disability and with a possible involvement of the central nervous system, leads to severe psychological distress. THE ROLE OF STRESS AND COPING: Many studies have investigated the place of major and minor stress and coping strategies in SLE morbidity (activity, organ damage, and physical and mental component of quality of life). Stress as a provoking factor is not proved, but stress seems to act as an exacerbating factor in the activity and to have an impact on quality of life. Coping strategies are more consistently associated with quality of life than activity. Organ damage appears to be less associated with psychosocial factors than activity or quality of life. THE NEED FOR ACTION: Despite the limitations of these studies, therapeutic interventions have to be proposed to reduce psychological distress, to improve quality of life, and maybe to moderate the progression of the disease.

Adaptation, Psychological↗
PubMed2004

[Immunomodulatory effects of intravenous immunoglobulins].

Intravenous immunoglobulins (IVIg) are therapeutic preparations of normal human IgG obtained from pools of more than 1000 healthy blood donors. They are currently used in the treatment of a wide range of auto-immune diseases, whether associated with auto-antibodies or auto-reactive T lymphocytes, as well as in the treatment of systemic inflammatory diseases. Several mechanisms of action have been identified during the last 20 years, including: (i) modulation of Fc receptors expression on leukocytes and endothelial cells; (ii) interaction with complement proteins; (iii) modulation of cytokines and chemokines synthesis and release; (iv) modulation of cell proliferation and apoptosis; (v) remyelinisation; (vi) neutralisation of circulating autoantibodies; (vii) selection of repertoires of B and T lymphocytes; (viii) interaction with other cell-surface molecules on lymphocytes and monocytes; (ix) corticosteroid sparing. These mechanisms of action are multiple and often intricate. However, they are still little known and further investigations are warranted.

Apoptosis↗
PubMed2004

Prevalences of polyarteritis nodosa, microscopic polyangiitis, Wegener's granulomatosis, and Churg-Strauss syndrome in a French urban multiethnic population in 2000: a capture-recapture estimate.

OBJECTIVE: To estimate the prevalences of polyarteritis nodosa (PAN), microscopic polyangiitis (MPA), Wegener's granulomatosis (WG), and Churg-Strauss syndrome (CSS). METHODS: Cases were collected in Seine-St. Denis County, a northeastern suburb of Paris, which has 1,093,515 adults (> or =15 years), 28% of whom are of non-European ancestry. The study period encompassed the entire calendar year 2000. Cases were identified by general practitioners, the departments of all the public hospitals and 2 large private clinics, and the National Health Insurance System. The Chapel Hill nomenclature was used to define MPA, and American College of Rheumatology criteria to define WG and CSS; PAN was diagnosed based on clinical laboratory, histological and/or angiographic findings. Three-source capture-recapture analysis was performed to correct for incomplete case ascertainment. RESULTS: A total of 75 cases were retained and capture-recapture analysis estimated that 23.8 cases had been missed by any 1 of the 3 sources. Accordingly, prevalences per 1,000,000 adults (95% confidence interval [95% CI]) were estimated to be 30.7 (95% CI 21-40) for PAN, 25.1 (95% CI 16-34) for MPA, 23.7 (95% CI 16-31) for WG, and 10.7 (95% CI 5-17) for CSS. The overall prevalence was 2.0 times higher for subjects of European ancestry than for non-Europeans (P = 0.01). CONCLUSIONS: This study provides the first prevalence estimates for these 4 vasculitides for a multiethnic, urban population. The significantly higher prevalence observed for Europeans may infer a genetic susceptibility of Caucasians. Compared with previous estimates based mostly on rural populations, the higher frequency of PAN and the lower frequency of WG might suggest specific environmental etiologic factors.

Adult↗
PubMed2004

Predicting mortality in systemic Wegener's granulomatosis: a survival analysis based on 93 patients.

OBJECTIVE: To determine predictors of survival of patients with systemic Wegener's granulomatosis (WG). METHODS: We retrospectively studied 93 patients (median age 52 years, male/female ratio 1.7) with systemic WG. All subjects received cytotoxic drugs. Survival was evaluated as a function of the main clinical and laboratory parameters and 2 disease activity scores assessed at diagnosis. Statistical analyses used the multivariate Cox proportional hazards regression model. RESULTS: The mean followup was 4.5 years; 25 (27%) patients died. According to univariate analysis, a pejorative prognostic value was attributed to serum creatinine >160 micromole/liter (P < 0.001); age >52 years (P < 0.002); absence of ear, nose, and throat (ENT) involvement (P < 0.001); and hemoglobin < or =11.8 gm/dl (P = 0.02). Multivariate analysis retained age >52 years (hazard ratio [HR] = 3.40, P = 0.04) as an independent predictor of poor outcome, whereas the presence of ENT involvement was associated with a longer survival (HR = 0.31, P = 0.02). CONCLUSION: Our results suggest that an older age and the absence of ENT involvement at diagnosis independently predict an increased risk of mortality for WG patients. These findings could indicate that the prognosis of WG might be governed by the balance between the granulomatosis as opposed to the vasculitic disease process.

Adolescent↗
PubMed2004

Immunoproliferative small intestinal disease associated with Campylobacter jejuni.

BACKGROUND: Immunoproliferative small intestinal disease (also known as alpha chain disease) is a form of lymphoma that arises in small intestinal mucosa-associated lymphoid tissue (MALT) and is associated with the expression of a monotypic truncated immunoglobulin alpha heavy chain without an associated light chain. Early-stage disease responds to antibiotics, suggesting a bacterial origin. We attempted to identify a causative agent. METHODS: We performed polymerase chain reaction (PCR), DNA sequencing, fluorescence in situ hybridization, and immunohistochemical studies on intestinal-biopsy specimens from a series of patients with immunoproliferative small intestinal disease. RESULTS: Analysis of frozen intestinal tissue obtained from an index patient with immunoproliferative small intestinal disease who had a dramatic response to antibiotics revealed the presence of Campylobacter jejuni. A follow-up retrospective analysis of archival intestinal-biopsy specimens disclosed campylobacter species in four of six additional patients with immunoproliferative small intestinal disease. CONCLUSIONS: These results indicate that campylobacter and immunoproliferative small intestinal disease are associated and that C. jejuni should be added to the growing list of human pathogens responsible for immunoproliferative states.

Anti-Bacterial Agents↗
PubMed2004

IgG reactivity with a 100-kDa tissue and endothelial cell antigen identified as topoisomerase 1 distinguishes between limited and diffuse systemic sclerosis patients.

We have analyzed antibody (Ab) reactivities of patients with limited systemic sclerosis (SSc) and anti-centromere Ab, patients with diffuse SSc and anti-topoisomerase 1 (anti-topo 1) Ab, patients with diffuse SSc without anti-topo 1 or anti-centromere Ab and age- and gender-matched healthy controls with normal human tissue and endothelial cell (EC) antigens. IgG reactivities with tissue antigens differed significantly between patients with anti-topo 1 Ab and patients with anti-centromere Ab. One 100-kDa band identified as topoisomerase 1 in macrovascular and microvascular EC extracts was recognized by IgG from patients with anti-topo 1 Ab and 50% of patients without specific Ab. IgG from patients with limited SSc and anti-centromere Ab, but not those of other patients or controls specifically recognized a 80-kDa band only in microvascular EC. Our results indicate that Ab from patients with limited or diffuse SSc with or without anti-topo 1 Ab exhibit specific and mutually exclusive reactivity patterns.

Autoantibodies↗
PubMed2004

Churg-strauss syndrome.

First described in 1951 as an allergic and granulomatous angiitis, Churg-Strauss syndrome (CSS) is a small-vessel vasculitis. Mean age at the time of diagnosis is approximately 50 years, with a sex ratio around 1. Asthma is the central feature of CSS and precedes the systemic manifestations in almost all cases, whereas 70% of the patients have maxillary sinusitis, allergic rhinitis, and/or sinus polyposis. General symptoms are frequent, and associated with pulmonary infiltrates in 38 to 77% of the patients; peripheral neuropathy, usually mononeuritis multiplex, in 64 to 75%; skin involvement in 40 to 70%; and gastrointestinal tract symptoms in 37 to 62%. Cardiac involvement is common, with pericarditis in 23% of the patients and myocarditis in 13%, and represents the primary cause of mortality. Hypereosinophilia is the main biological feature of CSS, whereas antineutrophil cytoplasm antibodies (ANCA), especially anti-myeloperoxidase (MPO), are found in one third to one half of the patients. Triggering factors, such as vaccination, desensitization, or exposure to leukotriene-receptor antagonists, have been suspected as contributing to the development of CSS, but its etiology has not yet been fully elucidated. T-helper type 2 (Th2) lymphocytes, by analogy with the pathogenesis of asthma, eosinophils infiltrating tissues, and anti-MPO ANCA are probably implicated in the pathogenesis of vasculitic lesions. CSS usually responds rapidly to corticosteroids. Adjunction of cyclophosphamide is indicated when at least one factor of poor prognosis is present. With treatment, remission is obtained in more than 80% of the patients, but it is often impossible to withdraw corticosteroids completely because of residual asthma. Relapses occur in 25% of the patients, half during the first year. The 10-year survival rate was 79% for our patients, with 73% of them requiring low-dose prednisone maintenance therapy for persistent asthma.

Journal Article↗
PubMed2004

Severe ADAMTS13 deficiency in adult idiopathic thrombotic microangiopathies defines a subset of patients characterized by various autoimmune manifestations, lower platelet count, and mild renal involvement.

The significance of ADAMTS13 deficiency in adult thrombotic microangiopathy (TMA) remains controversial. In an attempt to define the characteristics of adult TMA with severe ADAMTS13 deficiency, we determined 2 groups of patients on the basis of ADAMTS13 activity (undetectable or detectable). Clinical presentation, laboratory values, autoimmune manifestations, and outcome were compared between the groups. Patients were included retrospectively from 12 centers. All fulfilled the diagnosis criteria of TMA. Patients with a history of transplantation, cancer and chemotherapy, and Centers for Disease Control and Prevention (CDC) stage C human immunodeficiency virus (HIV) infection were not included. Forty-six patients were included. Thirty-one patients had an undetectable ADAMTS13 activity (<5%), and the remaining 15 patients had ADAMTS13 activity of >25%. Severe ADAMTS13 deficiency was associated with a plasmatic inhibitor in 17 cases (55%), suggesting an immune-mediated mechanism. Patients with undetectable ADAMTS13 were more frequently of Afro-Caribbean origin than patients with detectable ADAMTS13 activity (48.4% vs 13.3%, respectively; p = 0.03). As opposed to patients with detectable ADAMTS13 activity, patients with severe ADAMTS13 deficiency displayed various autoimmune manifestations that consisted of nondestructive polyarthritis (4 cases) associated in 1 case with malar rash and extramembranous glomerulonephritis, discoid lupus (3 cases), and autoimmune endocrinopathies, Raynaud phenomenon, and sarcoidosis-like disease (1 case each). In patients with severe ADAMTS13 deficiency, antinuclear antibodies, anti-double-stranded DNA antibodies, and anticardiolipin antibodies were positive in 22 (71%) cases, 3 (9.7%) cases, and 1 (3.2%) case, respectively. One patient fulfilled the criteria for the diagnosis of systemic lupus erythematosus. During follow-up, 1 patient with severe ADAMTS13 deficiency developed antinuclear antibodies, and 3 others developed anti-double-stranded DNA antibodies, in association with neurologic manifestations and anticardiolipin antibodies in 1 case. Patients with severe ADAMTS13 deficiency also had a lower platelet count (12 x 10(9)/L; range, 2-69 x 10(9)/L) and less severe renal failure (estimated glomerular filtration rate: 78 mL/min; range, 9-157 mL/min) than patients with detectable ADAMTS13 activity (49.5 x 10(9)/L; range, 6-103 x 10(9)/L; p = 0.0004, and 15.8 mL/min; range, 5.6-80 mL/min; p < 0.0001, respectively). End-stage renal failure occurred in 1 patient with severe ADAMTS13 deficiency and in 3 patients with detectable ADAMTS13 activity (3.2% vs 21.4%, respectively; p = 0.08). Flare-up and relapse episodes and survival were comparable between the groups. Taken together, these data indicate that adult idiopathic thrombotic thrombocytopenic purpura, as defined by severe ADAMTS13 deficiency, may occur preferentially in a particular ethnic group, and is characterized by severe thrombocytopenia, mild renal involvement, and a wide spectrum of autoimmune manifestations that may be completed during follow-up. Indeed, apparently idiopathic thrombotic thrombocytopenic purpura may be considered a specific autoimmune disease.

ADAM Proteins↗
PubMed2004

Differential diffusions of indinavir and lopinavir in genital secretions of human immunodeficiency virus-infected women.

Plasma and cervicovaginal secretion (CVS) samples were collected from 19 human immunodeficiency virus type 1-infected women on lopinavir- or indinavir-containing regimens. Lopinavir and indinavir were detectable in 29 and 93% of CVS samples, respectively, a finding that may be ascribed to these drugs' differences in protein binding and pK(a). The relationship between lopinavir and indinavir pharmacodynamics and viral evolution in the female genital tract should be assessed over time.

Adult↗
PubMed2003

Reactive hemophagocytic syndrome in adult systemic disease: report of twenty-six cases and literature review.

OBJECTIVE: To analyze specific clinical findings, underlying disorders, treatments, outcomes, and prognostic factors for reactive hemophagocytic syndrome (RHS) in systemic disease. METHODS: Data were collected using standardized forms as part of a French national survey. Adult cases without an underlying malignancy, diagnosed on bone marrow or lymph node biopsy, were included. RESULTS: Twenty-six cases (7 men, 19 women, mean age 47.4 +/- 17.7 years) were studied. Systemic diseases included systemic lupus erythematosus (n = 14), rheumatoid arthritis (n = 2), adult onset systemic Still's disease (n = 4), polyarteritis nodosa (n = 2), mixed connective tissue disease (n = 1), pulmonary sarcoidosis (n = 1), systemic sclerosis (n = 1), and Sjögren's syndrome (n = 1). RHS occurred in 2 distinct clinical settings in the course of systemic disease. RHS was associated with an active infection in 15 patients (bacterial infections, 10 cases; viral, 3 cases; tuberculosis, 1 case; and aspergillosis, 1 case) and with the onset of a systemic disease alone in 9 cases. Isolated RHS occurred in 2 cases. The overall mortality rate was 38.5%. Two factors were associated with mortality: corticosteroid treatment at the time of RHS diagnosis, and thrombocytopenia (odds ratio = 28, 95% confidence interval = 13.3-238.9). CONCLUSIONS: When RHS occurs in the course of an active systemic disease (situation only reported in cases of systemic lupus or adult Still's disease), immunosuppressive therapy should be used. In contrast, when RHS is present concomitantly with an active infection, immunosuppressive therapy needs to be lowered and antibiotic therapy should be instituted.

Adolescent↗
PubMed2003

Microscopic polyangiitis and polyarteritis nodosa: how and when do they start?

OBJECTIVE: To describe initial clinical symptoms attributable to microscopic polyangiitis (MPA) or polyarteritis nodosa (PAN). METHODS: We retrospectively reviewed the medical files of 72 patients (mean followup 6.7 years) with biopsy-proven MPA (n = 36) or PAN (n = 36). RESULTS: Initial manifestations were similar in both entities except for peripheral neuropathy (P = 0.02) and gastrointestinal tract involvement (P = 0.006), which were significantly more frequent in PAN, and general signs alone in MPA (8%; P = 0.02). The mean time to diagnosis was 9.8 +/- 19.4 months; 35% of the patients died and 26% relapsed; significantly more MPA than PAN patients relapsed (P = 0.03). Time to diagnosis >/=90 days was associated with a trend toward more patients relapsing (P = 0.12), but not with an increased risk of mortality. CONCLUSION: Initial symptoms of MPA and PAN are usually nonspecific and last for several months before the diagnosis is made. A longer time to diagnosis is associated with a tendency to a higher relapse rate.

Adolescent↗
PubMed2003

Treatment of polyarteritis nodosa and microscopic polyangiitis with poor prognosis factors: a prospective trial comparing glucocorticoids and six or twelve cyclophosphamide pulses in sixty-five patients.

OBJECTIVE: Because the optimal cyclophosphamide (CY) treatment duration for severe polyarteritis nodosa (PAN) without virus infection and microscopic polyangiitis (MPA) has not been established, we conducted a trial to compare the effectiveness of 6 versus 12 CY pulses given in combination with corticosteroids (CS). METHODS: Sixty-five (18 PAN, 47 MPA) previously untreated patients were randomized to receive 12 (n = 34) or 6 (n = 31) CY pulses combined with CS. PAN and MPA were histologically proven or met ACR criteria. All patients presented >or=1 factor of severity according to the five factor score (FFS). CY pulses were administered every 2 weeks for 1 month, then every 4 weeks. The end point of the study was the number of events (relapses and/or deaths) occurring in each group, analyzed according to an intention-to-treat strategy. The outcome was evaluated by Cox proportional hazards analysis. RESULTS: The baseline characteristics were similar for both groups. The mean (+/- SD) followup was 32 +/- 21 months. Survival analysis showed a significantly lower relapse probability (P = 0.02; hazards ratio [HR] = 0.34) and higher event-free survival (P = 0.02, HR = 0.44) for the 12 CY-pulse group while the mortality rates were not significantly different (P = 0.47). CONCLUSION: These results suggest that 6 CY pulses are less effective than 12 CY pulses to treat severe PAN and MPA, particularly with respect to the risk of relapses.

Adult↗
PubMed2003

IgM and IgG autoantibodies from microscopic polyangiitis patients but not those with other small- and medium-sized vessel vasculitides recognize multiple endothelial cell antigens.

Using a quantitative immunoblotting technique on extracts of macrovascular and microvascular endothelial cells (EC), we analyzed serum IgM and IgG reactivities of patients with active disease fulfilling the ACR and Chapel Hill criteria for the diagnosis of polyarteritis nodosa (PAN) (n = 8), PAN related to hepatitis B virus (HBV) infection (HBV-PAN) (n = 5), Wegener's granulomatosis (n = 6), microscopic polyangiitis (MPA) (n = 18), Churg-Strauss syndrome (n = 8), and patients with chronic HBV infection without PAN (n = 5) and age- and gender-matched healthy individuals (n = 45). MPA patients' IgM bound to 200-, 105-, 80-, 65-, 45-, 35-, and 33-kDa major bands, whereas IgM from controls and other patients bound predominantly to the 65-kDa band in EC extracts. MPA patients' IgG reacted mainly with 105-, 70-, 55-, and 38-kDa protein bands, whereas IgG from controls and other patients did not. Our results provide evidence that IgM and to a lesser degree IgG from MPA patients specifically recognize multiple EC antigens.

Autoantibodies↗