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E Liozon

Publications and source records attributed to E Liozon.

At least 19 recordsLinked to original sources
PubMed2001

Risk factors for visual loss in giant cell (temporal) arteritis: a prospective study of 174 patients.

OBJECTIVE: To determine the risk factors--especially the effects of thrombocytosis--for permanent visual loss in patients with temporal arteritis. METHODS: One hundred seventy-four patients with temporal arteritis (147 biopsy proven) were prospectively observed for the development of permanent visual loss. We used multivariate logistic regression analysis to determine which of 17 pretreatment characteristics were associated with visual loss. RESULTS: Visual ischemic manifestations occurred in 48 (28%) patients, including permanent visual loss in 23 (13%) patients. The independent predictors associated with an increased risk of permanent visual loss were a history of transient visual ischemic symptoms (odds ratio [OR] = 6.3; 95% confidence interval [CI]: 1.4 to 29; P = 0.02) and a higher platelet count (OR = 3.7 per SD; 95% CI: 1.8 to 7.9; P = 0.001). The presence of constitutional symptoms (OR = 0.14; 95% CI: 0.02 to 0.77, P = 0.01), polymyalgia rheumatica (OR = 0.04; 95% CI: 0.01 to 0.48, P = 0.02), and C-reactive protein level (OR = 0.35 per SD; 95% CI: 0.13 to 0.92, P = 0.03) were associated with a reduced risk. Upper limb artery involvement was excluded from the multivariate model, as no patients with that problem developed permanent visual loss. Of the 87 patients who presented with thrombocytosis (platelet count >400 x 10(9)/L), 32 (37%) developed ischemic visual symptoms, compared with 16 (18%) of those without thrombocytosis. CONCLUSIONS: An elevated platelet count is a risk factor for permanent visual loss in temporal arteritis. The finding of thrombocytosis in a patient with suspected temporal arteritis should emphasize the need for urgent treatment, with consideration of using inhibitors of platelet aggregation or anticoagulation therapy.

Aged↗
PubMed2001

[Dry mouth].

The sensation of dry mouth is a common problem, often neglected. The decrease of salivary flow causes chronic oral discomfort and functional problems and predisposes to rampant dental caries and oral candidiasis. Various methods are described to evaluate salivary gland hypofunction but no single test has sufficiently high specificity and sensitivity. Categorised questionnaires and unstimulated whole saliva flow are valuable. The causes of xerostomia are numerous, of which the principal are, drug or radiation induced xerostomia and primary an secondary Sjögren's syndrome. Treatment calls for good hydration, optimal oral hygiene and prophylaxis of candidosis. All unnecessary medications must be avoided. Oral pilocarpine is the only drug which had demonstrated beneficial effects if no contraindications exist.

Candidiasis, Oral↗
PubMed2001

[Risk factors for irreversible cerebral ischemia complications from Horton's disease: prospective study of 178 patients].

PURPOSE: To search for risk factors of developing irreversible cranial ischemic complications (ICIC) in patients with giant cell arteritis (GCA) and to explore whether two subsets of patients (high risk and low risk of developing ICIC) can be defined. METHODS: One-hundred seventy-eight consecutive patients with temporal arteritis (149 biopsy-proven) were diagnosed and followed up in a department of Internal Medicine between 1976 and 1999. The patients were separated into two groups, according to the presence or absence of ICIC, with comparison of 17 clinical and biological parameters prospectively recorded for each patient using a pre-established comprehensive questionnaire. RESULTS: ICIC occurred in 25 patients (14%), with amaurosis in 22 cases. Suggestive symptoms and/or signs of temporal arteritis were present in 92% of the patients, lasting 50 days (median) before the onset of ICIC. Forty-three patients (24%) complained of transient visual ischemic symptoms (TVIS), which preceded acute blindness in 11 cases. A multivariate logistic regression, from which 28 cases with upper limb artery involvement were excluded for technical reasons (no CCII in any case, thus predicting perfectly the lack of ischemic risk, P = 0.02), indicated that the only independent variables associated with the ischemic risk were: a history of TVIS (P = 0.05), the lack of signs of polymyalgia rheumatica (PMR; P = 0.02), lower blood levels of fibrinogen (P = 0.024) and higher mean blood platelets levels (P = 0.006). However, these five variables predicted only 30% of the variability of the model. Sensitivity, specificity, positive and negative predictive values of the model reached respectively 36, 96, 64 and 88%. Overall, 86% of the cases were correctly classified with respect to the ischemic risk. CONCLUSION: The rate of ICIC should be reduced by an earlier recognition of the usual signs of temporal arteritis. Several independent risk factors of ICIC have been identified. However, the logistic model failed to predict accurately the ischemic risk in 14% of the cases, indicating that as yet unrecognised factors probably exist that play a role in the occurrence of ICIC. Nevertheless, regarding the strong association between platelet levels and ICIC, patients with thrombocytosis should receive initially both corticosteroids and antiplatelet agents.

Aged↗
PubMed2001

[Non-simultaneous malignant lymphoma and antiphospholipid syndrome: 4 cases].

OBJECTIVE: We report four cases of non-synchronous antiphospholipid syndrome (APS) and malignant lymphoma, which highlight the complex relationship that seems to exist between these illnesses. METHODS: In a retrospective study conducted in two departments (internal medicine and clinical hematology) of a university hospital, we collected all observations of patients with both APS and malignant lymphoma diagnosed throughout the past decade. RESULTS: An association of APS with malignant lymphoma was recorded in three female and one male patient, median age 42.5 years at the time of diagnosis of the first disease. In each case, the primary APS was diagnosed, with arterial thrombotic events in three cases and venous thrombotic events in one case. One patient had isolated IgG anticardiolipin antibody, whereas the others had a combination of IgG anticardiolipin antibody and lupus anticoagulant with or without IgG anti-beta 2 glycoprotein I antibody. One patient also had an acquired inhibitor to factor VIII:C and a chronic C virus hepatitis. The mean time apparently separating the two illnesses ranged from 18 months to 9 years, but in two cases the diagnosis of APS was delayed due to a progressive, atypical, neurological onset. In two instances, the APS took place at a distance from a cured malignant lymphoma (Hodgkin's disease and nodal large cell B-cell lymphoma), whilst in the others it preceded a B-cell lymphoma (nodal and cutaneous, small cells and primary hepatic, large cells). Treatment resulted in complete haematological response in both cases, with disappearance of anticardiolipin antibody and lupus anticoagulant in the latter following a double autologous peripheral blood stem cell transplantation. In addition, late carcinomas (breast, kidney, thyroid) were seen in two patients. CONCLUSIONS: Our data indicate that the diagnosis of a malignant lymphoma should be considered in patients with a primary APS and peripheral lymph node enlargement or unexplained constitutional symptoms. Conversely, a late onset of arterial or venous thrombotic diathesis after a malignant lymphoma may indicate not only late relapse of malignant lymphoma but also a subsequent APS.

Adult↗
PubMed2001

Prevalence and characteristics of Sjögren's syndrome or Sicca syndrome in chronic hepatitis C virus infection: a prospective study.

OBJECTIVE: To describe the prevalence and clinical and laboratory characteristics of sicca syndrome and Sjögren's syndrome (SS) in chronic hepatitis C virus (HCV) infection. METHODS: Forty-five consecutive HCV infected patients referred for liver biopsy were enrolled in a prospective study. Subjective and objective criteria of xerophthalmia or xerostomia were systematically investigated and the patients classified according to 3 sets of criteria (European, Manthorpe, and Fox criteria) for the diagnosis of SS. RESULTS: Sicca syndrome was present in 28 (62%) patients; all had oral dryness and 14 had both oral and ocular dryness. Twenty-four (53%) patients had SS by the European criteria, 25 (56%) by Manthorpe criteria, and 4 (8%) by Fox criteria. Salivary gland biopsy was positive for SS (grade III or IV by Chishom classification) in 21 samples (47%); 9 samples (21%) were classified grade 0, and 15 (32%) grade I or II. No patient had anti-SSA or anti-SSB antibodies. The presence of SS or sicca syndrome was associated with older age and liver disease activity according to the METAVIR scoring system, but not with the presence of other extrahepatic manifestations or with HCV genotype. A high METAVIR activity score was only statistically associated with primary SS. CONCLUSION: HCV infection appears to account for a subgroup of patients with sicca syndrome in which half the cases meet the definition for SS according to European and Manthorpe criteria. This subgroup is characterized by the constant finding of xerostomia, the absence of classical systemic manifestations observed in primary SS, and the absence of anti-SSA or anti-SSB antibodies. Such characteristics delineate a distinctive, virus associated entity that differs from primary SS.

Adult↗
PubMed2000

[Cutaneous reactions or necrosis from interferon alpha: can interferon be reintroduced after healing? Six case reports].

PURPOSE: Alpha, beta or gamma interferon (INF) are cytokines produced by cells in response to antigenic stimulation. They are used to treat various hepatic, hematological, oncological and neurological diseases. Cutaneous reactions (rash, alopecia, labial herpes, erythema, or induration at the site of injection, and more rarely cutaneous necrosis) represent 5 to 12% of side-effects observed in patients receiving INF. The authors report six cases of local cutaneous reactions to alpha INF, five of which corresponded to cutaneous necrosis. This makes them question the relevance of INF reintroduction. METHODS: The study included 5 male and 1 female patients (mean age: 59.1 years; range: 42 to 74 years old). Three patients had chronic hepatitis C, while three others presented a blood disease. RESULTS: Cutaneous necrosis occurred after 1 to 10 months of treatment. The mean time to healing was 16.2 weeks. Reintroduction of the drug including injection in other sites did not lead to recurrence of necrosis in five out of the six cases. CONCLUSION: INF-induced cutaneous necrosis does not depend on the type of INF, the site of injection, the dose and may occur 2 months to 9 years after treatment implementation. The exact mechanisms involved in cutaneous necrosis remain unknown. Morbidity is due to a very long time to healing (4 to 6 months). Futhermore, healing sometimes requires prior surgery. Physicians should be aware of the potential occurrence of erythema in patients treated by INF, as it is the first sign of necrosis. The site of injection should then be modified. In case of necrosis, risk factors for thrombophilia, factors reducing microcirculation (DHE, beta-blockers, cigarette smoking) should be investigated. INF injections should be cautiously reintroduced in other sites with the help of a nurse in case of self-injections prior to the occurrence of necrosis. Regarding self-injections patients' training should be emphasized.

Adult↗
PubMed2000

[Drug-induced hypersensitivity syndrome in internal medicine: diagnostic and therapeutic traps. Eight observations].

PURPOSE: Drug-induced hypersensitivity syndrome (DIHS) is an acute and severe drug reaction. Manifestations include severe skin lesions, fever, nodal enlargement, blood eosinophilia and multisystemic involvement. The severe systemic manifestations of DIHS are responsible for a 10% mortality rate. The pertinence of corticosteroid therapy is discussed. METHODS: The authors report eight retrospective cases of DIHS obtained from the PMSI (Programme de Médicalisatiopn des Systèmes d'Information) between November 1991 and November 1998. RESULTS: The series consisted of five male and three female patients (mean age: 52.6 years; range: 23-83 years). The interval between the introduction of the drug and the onset of the reaction varied from two to eight weeks. Due to severe systemic manifestations, three patients were given corticosteroid therapy. Healing of skin and systemic disorders resolved with a mean delay of 4.4 weeks (range: 1 to 56 weeks). CONCLUSION: DIHS can be a diagnostic trap, as there are no diagnostic criteria for DIHS. Only the association of multiple arguments such as the time to the occurrence of symptoms, clinical similarity to many infectious illnesses, hypereosinophilia, atypical lymphocytosis, etc. may help guide diagnosis. DIHS can also be a therapeutic trap, as prompt withdrawal of the offending drug is essential to minimize morbidity. Although still controversial in the literature, the pertinence of corticosteroid therapy may be discussed in case of severe systemic effects. Patch testing can be a valuable tool to determine the responsibility of a drug; however it proves to be useful only when positive.

Adrenal Cortex Hormones↗
PubMed2000

Anticardiolipin antibody levels predict flares and relapses in patients with giant-cell (temporal) arteritis. A longitudinal study of 58 biopsy-proven cases.

OBJECTIVE: To evaluate the usefulness of anticardiolipin antibodies (aCL) in identifying flares and relapses in giant-cell arteritis. METHODS: We studied 58 consecutive patients with biopsy-proven temporal giant-cell arteritis. C-reactive protein and aCL serum levels were measured simultaneously at the time of diagnosis and at each out-patient visit until recovery. All observed episodes of a rise in C-reactive protein attributable to a precise cause, for which the simultaneous measurement of aCL was available, were analysed. RESULTS: The mean duration of clinical observation and serum aCL assessment was 34+/-18 and 24+/-11 months, respectively. Anticardiolipin antibody positivity (IgG or total antibodies > or =20 U) before treatment was found before treatment in 27 cases (46.6%) (mean 45.6+/-26 U/l, range 20-110 U). Levels of aCL decreased below 10 U with appropriate treatment in all patients except one, after a variable delay. No rise in aCL levels was recorded subsequently in any patient whose disease was controlled permanently. A significant rise in aCL was recorded in 20 of 27 (74%) of the flares or relapses of giant-cell arteritis, including seven of 12 flares in seven patients whose initial aCL level was <20 U vs none of the 28 inflammatory episodes unrelated to giant-cell arteritis (P<0.0000001). IgM aCL, infrequently found at diagnosis, was not associated with signs of disease activity. CONCLUSION: Serum aCL levels are useful in the detection of flares and relapses in giant-cell arteritis, with fairly good sensitivity (74%) and a specificity of 100%, and can be of value in distinguishing subclinical flares from infection.

Aged↗
PubMed2000

[Horton's disease and hypereosinophilic syndrome: a non-fortuitous association].

Giant cell arteritis is a T-cell dependent auto-immune vasculitis that involves a T-helper l (Th1) cell response. We report the unusual case of a woman who developed successively a biopsy-proven temporal arteritis without tissue eosinophilia at age 65, an isolated blood eosinophilia at age 69 and an hypereosinophilic syndrome at age 71, while still taking corticosteroids at the dose of 3mg/day. Considering this temporal relationship, some characteristics of her hypereosinophilic syndrome pointing to a Th2-dependent disease (absence of definite signs of myeloproliferative syndrome, elevated IgE levels and quick normalisation of eosinophil counts under corticosteroid therapy) and the existence of an unexplained blood inflammatory response at the time of HES onset, we postulate that an unbalanced T helper response led in this exceptional case to both diseases.

Aged↗
PubMed1999

[Ocular complications of Horton's disease].

Ocular manifestations of giant cell arteritis, of which permanent amaurosis overshadows all others, occur still frequently. They are usually preceeded by the classical signs of temporal arteritis, which should allow an earlier diagnosis and prompt corticosteroid treatment. Indeed, corticosteroids have proved very effective in preventing ocular complications. Once permanent amauposis is present, the treatment is still urgent, in order to avoid the involvement of the other eye and to restore some vision of the affected eye. However, once the eye is damaged, there is little hope that corticosteroid treatment will improve the vision, depending essentially upon which delay it has been started. These fearsome ocular complications argue for a better knowledge of the suggestive signs of temporal arteritis and highlight the urgency of corticosteroid treatment.

Adrenal Cortex Hormones↗
PubMed1999

Temporal artery biopsy: a diagnostic tool for systemic necrotizing vasculitis. French Vasculitis Study Group.

OBJECTIVE: To describe the clinical, biologic, and histologic features of temporal artery biopsy (TAB)-localized systemic necrotizing vasculitides (SNV), and to assess their frequency among elderly patients undergoing TAB for suspected giant cell (temporal) arteritis (GCA). METHODS: The frequency of a TAB localization of SNV was prospectively assessed in a multicenter study of elderly patients undergoing TAB for suspected GCA. All patients with SNV fulfilling the American College of Rheumatology criteria for a specific vasculitic syndrome and with evidence of vasculitis on TAB were included in a retrospective, descriptive study. RESULTS: SNV was diagnosed based on the TAB in 1.4% of the patients with suspected GCA and in 4.5% of the positive (inflamed) TAB specimens. We retrospectively selected 27 patients (18 female, 9 male; mean +/- SD age 62+/-15 years, range 22-79 years) with SNV and TAB-localized vasculitis. Only 2 of these patients were known to have SNV before TAB localization. Twenty-two patients (81%) had cephalic symptoms, including jaw claudication in 33%, clinically abnormal temporal arteries in 33%, and neuro-ophthalmologic symptoms in 11%. All patients had systemic symptoms suggestive of SNV and histologically proven NV in the TAB specimens (70%) or elsewhere in other biopsy sites (74%). Abnormal biologic results suggestive of SNV were present in 17 patients (63%). For 4 patients, the TAB-documented involvement led to initial misdiagnoses of GCA, and systemic manifestations that developed under steroid therapy revealed the correct diagnosis. The final diagnoses of the patients were polyarteritis nodosa (PAN) (n = 11), Churg-Strauss syndrome (n = 6), micropoly-angiitis (n = 3), Wegener's granulomatosis (n = 3), hepatitis B virus-related PAN (n = 2), hepatitis C virus-related cryoglobulinemic vasculitis (n = 1), and rheumatoid vasculitis (n = 1). CONCLUSION: TAB-localized SNV presents a major diagnostic dilemma because it can mimic GCA. Careful analysis of clinical, biologic, and histologic data should lead to the correct diagnosis and help guide the clinician's choice of appropriate therapy.

Adrenal Cortex Hormones↗
PubMed1998

Thymoma-associated pancytopenia: effectiveness of cyclosporine A.

Aplastic anemia is a rare complication of thymoma and is properly documented in only few cases. Here, we report the case of a previously healthy, 65-year-old patient who was found simultaneously to have a spindle-cell thymoma and severe hypoplastic anemia with a mild infiltration of the bone marrow by CD4+ and CD8+ T lymphocytes, CD16+ natural killer cells, and a decrease in blood CD4/CD8 ratio. Cultures of marrow erythroid progenitors demonstrated serum inhibitor. While steroids, cyclophosphamide and antilymphocyte globulin failed to improve hematopoiesis, cyclosporine A (Cy-A) led to a partial, stable remission that was sustained for 4 years. Since Cy-A has been associated with good responses in three cases of thymoma-associated red cell aplasia, we recommend its use in cases of thymoma-associated cytopenias refractory to steroids and cyclophosphamide.

Adrenal Cortex Hormones↗