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Biomedical subjects

P Chazerain

Publications and source records attributed to P Chazerain.

At least 19 recordsLinked to original sources
PubMed2001

Four cases of tendinopathy in patients on statin therapy.

During the last decade, statins have been widely prescribed as lipid-lowering drugs. Their overall safety profile is good. The main musculoskeletal side effects have consisted of muscle pain and weakness, peripheral neuropathy, and a few cases of drug-induced lupus. We report the first four cases of tendinopathy in patients receiving statin therapy. There were three men and one woman. The diagnoses were extensortenosynovitis at the hands (case 1), tenosynovitis of the tibialis anterior tendon (case 2), and Achilles tendinopathy (cases 3 and 4). Two patients were on simvastatin and two on atorvastatin. The tendinopathy developed 1 to 2 months after treatment initiation. The outcome was consistently favorable within 1 to 2 months after discontinuation of the drug. Similar cases have been reported to French pharmacovigilance centers. This report of four cases of tendinopathy draws attention to a possible and heretofore unrecognized side effect of a drug class that is becoming increasingly popular. Statins are effective in lowering high cholesterol levels in patients with type IIa or IIb hypercholesterolemia. They have been widely used for the last decade, particularly in the secondary and primary prevention of major coronary events. Statins act by inhibiting the enzyme hydroxy-3-methyl-glutaryl-coenzyme A (HMG-CoA) reductase. Although most patients tolerate statins extremely well, a few experience side effects requiring treatment discontinuation. Reported musculoskeletal side effects include myalgia and a few cases of rhabdomyolysis and polymyositis. Induced lupus and peripheral neuropathy are exceedingly rare.

Acute Disease↗
PubMed1999

[Diagnosis and treatment of polymyalgia rheumatica].

Polymyalgia rheumatica is a clinically defined disorder characterised by inflammatory pain in the neck, back, or shoulder or pelvic girdle muscles in a patient over 50 years of age. Results of laboratory work-up reflect only the inflammatory syndrome. Early diagnosis allows rapid initiation of low-dose corticosteroids, which dramatically improves the symptoms and avoids long, costly and difficult investigations. The cause of the disorder is poorly understood and its relationship to temporal arteritis is sometimes unclear, although the two can usually be distinguished, based on recent findings.

Adrenal Cortex Hormones↗
PubMed1999

[Spinal neurenteric cyst revealed by a cauda equina syndrome].

BACKGROUND: Intraspinal neurenteric cysts are exceptional formations which develop from incomplete separation of the neural tube and the endodermis during the third week of gestation. Symptoms generally appear before the age of 40 years and are associated with spinal malformations. Most neurenteric cysts lie in an extra-spinal position in the lower cervical and upper dorsal spine. We report a case involving the cauda equina with no associated spinal lesion. CASE REPORT: A 63-year-old woman was admitted for low back pain and right L3 radiculalgia triggered by exertion. Urinary disorders had developed over the preceding year. Physical examination found a spinal syndrome with hypoesthesia of the right para-anal area, an atonic anal sphincter and a globular bladder. Plain films showed a widened interpedicular space between L1 and L2 interpreted as the consequence of an expansive intraspinal lesion. Saccoradiculography led to the diagnosis of an intradural lesion involving L1 and L2. At magnetic resonance imaging, the lesion's signal intensity was similar to cerebrospinal fluid on T1 and T2 sequences, deforming the cauda equina and displacing the nerve roots. Surgical resection of the cyst was incomplete due to adherences to several roots and was followed by persistent radiculalgia and sphincter disorders. DISCUSSION: This case demonstrates an exceptional cause of cauda equina syndrome. Fissuration or rupture of the cyst might explain symptom exacerbation following trauma. Magnetic resonance imagining can confirm the cystic nature of the intradural lesion and help guide surgery. Resection is often incomplete with the risk of long-term recurrence.

Cauda Equina↗
PubMed1999

Anti-Sa antibody is an accurate diagnostic and prognostic marker in adult rheumatoid arthritis.

OBJECTIVES: To evaluate in various groups of patients with chronic joint disease the sensitivity and specificity of anti-Sa antibody, recently described in sera from adults with rheumatoid arthritis (RA); and to determine the prognostic significance of anti-Sa in initial sera from patients with long standing RA with or without severe joint destruction. METHODS: Serum samples from 489 patients were included. Of these, 154 were collected from patients with RA attending 2 rheumatology units. Controls were 335 patients with a variety of inflammatory joint diseases other than RA. IgG anti-Sa was detected using an immunoblotting method with purified Sa antigen from human placenta extracts. All patients were tested for the following antibodies: rheumatoid factor (RF), anti-keratin antibody (AKA), antiperinuclear factor (APF), and anti-RA 33. HLA class II DRB alleles were also determined. RESULTS: Anti-Sa was detected in 39.8% of RA sera overall, 46.7% of sera from the long standing RA group, and 23.5% of sera from the recent onset RA group (p<0.01). In patients with long standing RA, statistically significant associations were found between the presence of anti-Sa and the following variables: RF (p<0.0001), AKA (p<0.0001), APF (p<0.00001), and HLA DRB1*04 or 01 (p<0.01). In contrast, no association was found with anti-RA33. Anti-Sa was positive in 11 adult controls (7.8%) and in 26 pediatric patients with juvenile chronic arthritis (22%). The specificity of anti-Sa for RA was 92.1% in adults with well characterized rheumatic diseases and 85.9% in adults and children together. Among patients with long standing RA, those with destructive disease were more likely to test positive for anti-Sa (66.6%) than those with nondestructive disease (22.2%) (p<0.0001). Comparisons with other serologic markers for RA demonstrated that anti-Sa was sensitive (68.4%) and was also the test with the highest specificity (79%), positive predictive value (75%), and negative predictive value (71%) for discriminating between patients who do and those that do not develop late severe radiographic damage. CONCLUSION: Immunoblot-detected IgG anti-Sa is a sensitive serologic marker for RA patients with severe radiographic damage.

Adult↗
PubMed1998

Clinical usefulness of antibodies to U1snRNP proteins in mixed connective tissue disease and systemic lupus erythematosus.

OBJECTIVES: To determine whether the anti-68 kDaU1snRNP antibody is associated with mixed connective tissue disease and not with SLE; to evaluate correlations between anti-U1snRNP titers and disease activity; and to look for associations between anti-U1snRNP specificities and specific clinical features. PATIENTS AND METHODS: 40 patients with a positive double diffusion test for anti-68 kDa U1snRNP were studied, including 21 with mixed connective tissue disease, 14 with systemic lupus erythematosus and five with other connective tissue diseases. IgGs to 68 kDa U1snRNP were assayed using an ELISA. Clinical features, disease activity and antibody test findings were evaluated longitudinally in nine patients. RESULTS: Both proportions of patients with anti-68 kDa U1snRNP and titers of IgG to 68 kDa U1snRNP were similar in the mixed connective tissue disease and systemic lupus erythematosus groups. Patients with mixed connective tissue disease were significantly more likely to have anti-A U1snRNP or anti-C U1snRNP than those with systemic lupus erythematosus (P < 0.03 and P < 0.04, respectively). No significant correlations were found between any of the features of mixed connective tissue disease (e.g., Raynaud's phenomenon, myositis, or sausage digits) and a specific anti-U1snRNP antibody. During follow-up (mean, seven years; range, 1-25 years), changes occurred in the anti-U1snRNP profile and in the anti-68 kDa U1snRNP titer. These changes were not correlated with disease activity. CONCLUSIONS: IgGs to 68 kDa U1snRNP are not associated with a specific pattern of anti-RNP-positive connective tissue disease. No useful information can be gained by monitoring anti-68 kDa U1snRNP IgG titers over time. A Western blot profile including anti-A U1snRNP or anti-C U1snRNP indicates a high likelihood of U1snRNP-associated mixed connective tissue syndrome (MCTD).

Adolescent↗
PubMed1997

Thromboangiitis obliterans with inaugural rheumatic manifestations. A report of three cases.

Thromboangiitis obliterans, or Buerger's disease, is a segmental occlusive inflammatory disorder of the small- and medium-sized arteries and veins seen in young adults and associated with cigarette smoking. The lesions are most marked in the distal limbs. We report three cases in which the first manifestations were rheumatic, consisting in polyarthritis in two cases and carpal tunnel syndrome in one. Rheumatic manifestations are infrequent and rarely inaugural in thromboangiitis obliterans, although they are probably underdiagnosed. Their pathogenesis is unclear but may involve autoimmunity. Heightened awareness of the possibility that rheumatic manifestations can inaugurate thromboangiitis obliterans may allow an earlier diagnosis of this disease, which may improve the functional prognosis. However, recovery can be achieved only if the patient stops smoking.

Adult↗
PubMed1997

Polyarthritis with cutaneous mucinosis and intrasynovial mucin deposits.

We report the first case of cutaneous and articular mucinosis with presence of mucin deposits within the synovium in an HIV-positive patients. Presentation was asymmetric polyarthritis, and subcutaneous nodules developed two months later. Treatment was with hydroxychloroquine. The outcome of both the skin and joint lesions was favourable.

Adult↗
PubMed1996

Antibodies to cardiolipin and beta 2 glycoprotein I in patients with polymyalgia rheumatica and giant cell arteritis.

IgG antibodies to cardiolipin and beta 2-glycoprotein I were looked for using an enzyme-linked immunosorbent assay (ELISA) in 19 patients with giant cell arteritis (meeting 1990 American College of Rheumatology criteria), including 16 with concomitant polymyalgia rheumatica (meeting Bird's criteria) and in three patients with isolated polymyalgia rheumatica. IgG anti-cardiolipin antibodies were demonstrated in eight patients (36%) and IgG anti-beta 2-glycoprotein I antibodies in two patients (9%) including one without anti-cardiolipin antibodies. Titers of anti-cardiolipin antibodies ranged from 27 to 190 units of IgG antiphospholipid antibodies (UGPL) (mean 71 UGPL). Of the eight patients with anti-cardiolipin antibodies, two had giant cell arteritis without polymyalgia rheumatica and six had polymyalgia rheumatica with clinical (n = 2) or histologic (n = 4) evidence of giant cell arteritis. None of the three patients with polymyalgia rheumatica but no giant cell arteritis had anti-cardiolipin or anti-beta 2 glycoprotein I antibodies. The VDRL was negative in the 14 patients who had this test. Tests for lupus anticoagulant were performed routinely, always with negative results. Among giant cell arteritis patients, those who tested positive for anticardiolipin antibody had significantly higher values for the erythrocyte sedimentation rate (p < 0.006) and for serum C-reactive protein (p < 0.03) and fibrinogen values (p = 0.05), and a trend toward higher platelet counts, as compared to those who tested negative for anticardiolipin antibody. The mean daily prednisone dose at the time of sampling was significantly lower in giant cell arteritis patients with anti-cardiolipin antibodies (p < 0.05); this difference may account for the apparent correlation between anti-cardiolipin antibodies and laboratory markers for inflammation. These data, as well as findings from serial measurements, suggest that anti-cardiolipin antibodies are present early in the course of giant cell arteritis and disappear within a few weeks of initiation of corticosteroid therapy in a dose of more than 25 mg prednisone per day. In this study, only one patient without anticardiolipin antibodies developed a cerebrovascular accident. Positive tests for anti-cardiolipin antibody or anti-beta 2 glycoprotein I antibody in a patient with polymyalgia rheumatica suggest a diagnosis of concomitant giant cell arteritis, which is usually symptomatic.

Aged↗