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P Godeau

Publications and source records attributed to P Godeau.

At least 19 recordsLinked to original sources
PubMed2002

[Value of the protein profile in the diagnosis of infectious endocarditis when hemolysis is present].

PURPOSE: Haptoglobin (H) and orosomucoid (O) are acute phase proteins that increase in a parallel manner. When hemolysis and inflammation are both present, study of the O-H couple on the protein profile may reveal an unknown hemolysis. METHODS: To determine if hemolysis is more frequent during infectious endocarditis than during septicemia without valvulopathy or during valvulopathy without septicemia. Study of three groups of patients: 26 patients with infectious endocarditis, 13 patients with septicemia and 36 patients with valvulopathy without septicemia. Studied parameters were the O-H couple, hemoglobin and rate of O. RESULTS: Hemolysis is clear in patients with endocarditis. The difference O-H is significantly more important during endocarditis than during septicemia without valvulopathy (P < 0.001) and during valvulopathy without sepsis (P < 0.001). CONCLUSION: Study of the O-H couple may be useful for the diagnosis of endocarditis showing a difficult-to-diagnose hemolysis.

Biomarkers↗
PubMed2001

A new type of acquired C1 inhibitor deficiency associated with systemic lupus erythematosus.

Acquired C1 inhibitor (C1-INH) deficiency with consequent angioedema is a rare condition that may indicate an underlying lymphoproliferative disorder. The defect is caused by increased catabolism, which is often associated with the presence of serum autoantibodies to C1-INH. The present report describes 3 patients with systemic lupus erythematosus who developed typical symptoms of acquired angioedema, characterized by recurrent swelling of subcutaneous and mucous tissues. The 3 patients demonstrated a major classical pathway-mediated complement consumption, with very low levels of C3 antigen and decreased levels of C1-INH antigen. Neither antibodies to C1-INH nor associated lymphoproliferative disease was found. No patient had clinical and biologic signs of lupus activity at the time the angioedema occurred. All patients were treated with steroids and exhibited a good response, without relapse of angioedema and with normalization of plasma levels of C1-INH. In lupus patients who present with an angioedema syndrome, acquired or hereditary angioedema must be sought by examining parameters of the classical pathway and levels of C1-INH. Our observations suggest the existence of a new form of acquired C1-INH deficiency associated with a major classical pathway-mediated complement consumption and systemic autoimmunity.

Adolescent↗
PubMed2001

Autoantibodies to receptor induced neoepitopes of fibrinolytic proteins in rheumatic and vascular diseases.

OBJECTIVE: Abnormal plasminogen activation has been implicated in vascular and rheumatic diseases. The development of an autoimmune response to neoepitopes of plasminogen and its activator (tissue-type plasminogen activator, t-PA) was explored in sera from patients with rheumatoid arthritis (RA, n = 30), Behcet's disease (n = 20), primary antiphospholipid syndrome (APS, n = 23), and idiopathic arterial (n = 33) or venous thrombosis (n = 16). METHODS: Sera diluted 1/50 were incubated with either plasminogen or t-PA bound to their natural receptors (immobilized fibrin or monocytic cells), and bound immunoglobulins were detected using a sheep peroxidase labeled anti-human Fab IgG. Controls included plates coated with fibrin or cells alone or plasminogen passively adsorbed to the plastic. Sera were considered positive when the absorbance at 405/490 nm was above the mean + 2 SD of normal sera. RESULTS: Reactivity of sera against plasminogen bound to cells (28%) or to fibrin (22%) was a predominant feature in patients with RA compared with other patient groups and controls. However, some patients with primary APS had reactivity against cell and fibrin bound plasminogen (9 and 13%, respectively). Autoantibodies against fibrin bound t-PA were detected in only 8% of patients with arterial or venous thrombosis. CONCLUSION: Conformational changes induced by molecular assembly of plasminogen on cell or fibrin surfaces result in the expression of neoepitopes recognized by autoantibodies. These autoantibodies could be markers of the proteolytic events associated with plasminogen activation in autoimmune diseases.

Adult↗
PubMed2001

[Collagenous colitis. A study of 11 cases].

BACKGROUND: Collagenous colitis (CC) is a rare large bowel inflammatory disorder. The aim of this retrospective study was to analyze extra-digestive manifestations of CC, associated systemic diseases, clinical course and response to therapeutic regimens. PATIENTS AND METHODS: Between 1989 and 1999, eleven patients were diagnosed as having CC, in two Departments of Internal Medicine and Gastroenterology, on the basis of usual criteria: chronic watery diarrhea, endoscopic examination showing normal findings and subepithelial collagen band thicker than 10 micrometer. RESULTS: Ten women and one man, age 39 to 88 years (mean: 66.6), had had their diarrhea for 1 to 240 months before diagnosis (mean: 48). Associated extra-digestive manifestations were: weight loss (3 cases out of 11), inflammatory arthralgia (4 cases), fever (2 cases), pelvispondylitis (2 cases), autoimmune thyroiditis (2 cases), and Sharp syndrome (1 cases). Laboratory abnormalities were: inflammatory syndrome (3 cases), anemia (5 cases), hypogammaglobulinemia (3 cases), and hypoalbuminemia (4 cases). Stool cultures and parasite examination were negative in all patients. Therapy used successively for CC until resolution of chronic diarrhea (uncontrolled with symptomatic treatment) was: sulfasalazine in 7 patients (beneficial (B) in 5 out of 7), 5-aminosalicylic acid in 6 (B: 2/6), corticosteroids in 2 (B: 2/2), azathioprine in 1 (B: 1/1). After a mean follow-up of 18 months (range: 1-72), resolution of CC was observed in 8 out of 11 patients. DISCUSSION: Mean characteristics of CC were: female predominance (91%), presence of extra-digestive manifestations (36%); mucosal inflammation with subepithelial collagen band and frequent association to rheumatic or autoimmune diseases suggest an immune basis for CC. Usefulness of systematic colon biopsies is underlined. Clinical course is often favorable with sulfasalazine and 5-aminosalicylate acid. Corticosteroids are rarely used.

Adult↗
PubMed2000

[Hyperhomocysteinemia and arterial or venous thrombosis. Retrospective study of 75 cases].

OBJECTIVE: Previous studies suggest that hyperhomocysteinemia may be a risk factor for arterial and venous thrombosis. We retrospectively analyzed data from 75 patients with thrombosis. PATIENTS AND METHODS: Thirty-four patients had arterial thrombosis, 22 venous thrombosis and 19 venous and arterial thrombosis. Of the 75 patients (49 men and 26 women, mean age 49 +/- 15 years) about two-thirds had recurrent episodes of thrombosis. RESULTS: Hyperhomocysteinemia was defined as serum homocysteine level above 14.1 mumol/l (mean + 2.7 SD in healthy subjects) and was found in 67 patients (89%, CI95% = 80-95). Mean total homocysteine concentration was 21.6 +/- 13.6 mumol/l for the 75 patients. About half of the patients were smokers, 35% had hypertension and 25% high serum cholesterol. There was no significant relationship between serum homocysteine level and smoking status, hypertension or serum cholesterol level. Ten patients (13%, CI95% = 7-23) had low serum cobalamin (< 150 pmol/l). Serum folates were < or = 10 nmol in 41% of the patients in the arterial thrombosis group (CI95% = 25-59), in 27% in the venous thrombosis group (CI95% = 11-50), and in 31% in the arterial and venous thrombosis group (CI95% = 13-57). Thirteen patients received vitamin B supplementation. Hyperhomocysteinemia decreased in 12/13 patients (CI95% = 64-100) and returned to normal values in 9/13 patients (69%, CI95% = 38-91). CONCLUSION: Our data show that hyperhomocysteinemia is frequently found in arterial and venous thrombosis. Further studies are needed to determine the clinical impact of homocysteine lowering therapy.

Adult↗
PubMed2000

[Severe gastrointestinal hemorrhage secondary to diffuse angiodysplasia: efficacy of estrogen-progesterone treatment].

BACKGROUND: Vascular abnormalities are being reported with increasing frequency as a cause of major lower gastrointestinal hemorrhage in the elderly. They are occasionally very difficult to treat by conventional means. CASE REPORT: A 66-year-old white man with a history of type 2 diabetes mellitus, coronary artery disease, congestive heart failure, severe peripheral arterial occlusion disease and chronic renal insufficiency presented for five years recurrent major bleeding due to gastrointestinal angiodysplasia, requiring repeated transfusions. He was treated with efficacy using ethinyl-estradiol (30 micrograms) and norethisterone acetate (1 mg) given orally once daily. After six months of treatment, transfusion requirements fell to 0 unit and the patient's hemoglobin was stable at 13 g/dl. Attempts to stop hormone therapy (by the patient himself, without complaint of side effects) led to a fall in hemoglobin. CONCLUSION: Hormonal therapy should be considered when multiple degenerative mucosal vascular bleeding lesions are beyond the reach of therapeutic endoscopy leading to high transfusion needs and when surgical risk is unacceptably high.

Aged↗
PubMed2000

A novel missense mutation (C30S) in the gene encoding tumor necrosis factor receptor 1 linked to autosomal-dominant recurrent fever with localized myositis in a French family.

OBJECTIVE: To characterize both phenotypic (clinical features and magnetic resonance imaging [MRI] findings) and genotypic aspects of autosomal-dominant recurrent fever, also known as tumor necrosis factor receptor (TNFR)-associated periodic syndrome (TRAPS), in a French family and to investigate the role of the mutated 55-kd tumor necrosis factor alpha (TNFalpha) receptor (TNFR1) in the pathogenesis of the disease. METHODS: The coding region of TNFR1 was sequenced in 2 individuals with TRAPS (the propositus and her grandfather) and in 3 clinically unaffected relatives. Expression of soluble TNFR1 (sTNFR1) was investigated in 3 of the family members carrying a C30S mutation in TNFR1, and was compared with the levels of soluble TNFR2 (sTNFR2) by enzyme-linked immunosorbent assay. The membrane TNFR1 expression was then compared with membrane TNFR2 levels at the surface of peripheral blood mononuclear cells by flow cytometric analysis. The clinical heterogeneity in this French family was investigated by searching polymorphic variants in the TNFalpha promoter by DNA sequencing. RESULTS: Both the disease course and the clinical presentation in the propositus were highly indicative of TRAPS. MRI study of the segmental inflammatory process in the limbs showed abnormal signals in the muscle and subcutaneous tissue without involvement of adjacent joints or fascia. A novel missense mutation, C30S, in the first extracellular N-terminal cysteine-rich domain (CRD1) of TNFR1 was characterized in the propositus, her affected grandfather, and her clinically unaffected father. Expression of membrane TNFR1 at the surface of monocytes and polymorphonuclear leukocytes, as well as the levels of sTNFR1 in serum when the disease was not active were not modified in the 3 individuals carrying the TNFR1 C30S mutation. In contrast, during attacks, sTNFR1 levels remained abnormally low, as compared with the levels in unrelated patients with active adult-onset systemic Still's disease. The clinical heterogeneity could not be explained by a polymorphic variant in the TNFalpha promoter. CONCLUSION: TRAPS is a distinct clinical and radiologic disease entity that is responsible for recurrent fever and migratory cellulitis-like processes with localized myositis. We have identified a novel TNFR1 mutation, C30S, that is located in the CRD1 domain in a French family affected by the disease. This mutation seems to affect the level of sTNFR1, which did not increase in the propositus during inflammatory attacks.

Adolescent↗
PubMed2000

[Menopause and hormone replacement].

INTRODUCTION: Considered until recently as a biological fate, menopause has evolved within a decade into a major public health issue at stake. Such an evolution results from various factors that deserve an exhaustive critical approach because the situation is much more complex than it appears to be at first analysis. CURRENT KNOWLEDGE AND KEY POINTS: 1) Ninety-five percent of the available epidemiological information relies on observation or cohort studies, such as case-control studies that do not allow any certitude in regard to therapy. 2) Chronic estrogen deficiency probably plays a pathogenic role in various symptoms or pathological conditions that are associated to menopause. 3) However, behind the paradigm of menopause, there is a whole psychosocial construct that classifies what remains a physiological condition within major risk factors, just as for the most serious chronic diseases. 4) Indeed, menopause cannot be considered as a well-characterized disease, and hormone replacement therapy is undeniably a complex therapeutic intervention that requires proper prescription and careful evaluation of the benefit:risk ratio. 5) While such a treatment is now considered as the gold standard for the prevention of post-menopausal osteoporosis, this does not hold true regarding cardiovascular diseases. 6) Although hormone replacement therapy may lead to the relief of various symptoms associated with menopause, it may also result in side-effects that extreme medication cannot prevent, especially since some of them are not fully known, particularly in the case of either long-term or very long-term treatments. FUTURE PROSPECTS AND PROJECTS: A more rigorous evaluation of side-effects of hormone replacement therapy in the framework of long-term controlled trials is therefore clearly required. The indications of such a treatment should only rely on objective data and not on questionable studies or impressions at clinical examination.

Aged↗
PubMed2000

[Premature cerebral vascular accidents after initiation of steroid therapy in Horton disease].

INTRODUCTION: Steroid therapy remains the standard treatment for giant cell arteritis but is sometimes incriminated in the occurrence of ischemic events, particularly in the early phase of the disease. EXEGESIS: We report four cases of ischemic events observed early after initiation of steroid therapy in giant cell arteritis. We also reviewed the literature. CONCLUSION: Though the close temporal relationship between the initiation of steroids and the occurrence of ischemic events suggests a causative link, other factors such as arteritis itself or arteriosclerosis would also play a role. Systematic prescription of an anticoagulant should be discussed at the initial phase of treatment of giant cell arteritis.

Adrenal Cortex Hormones↗
PubMed2000

Cryofibrinogenaemia: a study of 49 patients.

The purpose of this study was to characterize the clinical features and components of 30 patients with isolated cryofibrinogen (CF) versus those of 19 patients with combined CF and cryoglobulins (CG). Secondary forms of cryofibrinogenaemia associated with collagen disorders, infectious or malignant diseases, were significantly more frequent in patients with combined CF and CG than those with isolated CF (79 versus 47%, P = 0.02). Both groups of CF patients presented predominantly cutaneous symptoms (77% in isolated CF; 58% in combined CF + CG), and less frequently venous and/or arterial thrombosis (13% in isolated CF; 3% in combined CF + CG). Patients with idiopathic forms of CF, and particularly those without CG, suffered essentially from recurrent painful skin ulcers, mainly triggered by cold exposure. Patients with isolated CF had higher mean plasma concentrations of CF than those with combined CF + CG (1. 61 +/- 1.26 versus 0.82 +/- 1.18 g/l, respectively; P = 0.004), but there was no correlation between the CF plasma level and either the severity of symptoms or the sensitivity to cold. In patients with isolated CF, fibronectin was suggested (by precipitation analysis) to be a major component of the cryoprecipitate, whereas immunoglobulins were rarely present (in only three out of 30 patients). By contrast, in the majority of patients (78%) with combined CF and CG, the CF consisted mainly of immunoglobulins of the same class as those characterizing the associated CG. Analysis of the CG precipitate revealed the presence of fibronectin but not fibrinogen, alpha1-antitrypsin and alpha2-macroglobulin. In conclusion, isolated and combined cryofibrinogenaemia are associated with different clinical signs requiring different clinical management, but there is no evidence as yet for a causal role of the cryoprecipitates in the differences observed.

Adolescent↗