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C Briani

Publications and source records attributed to C Briani.

At least 19 recordsLinked to original sources
PubMed2006

Peripheral neurotoxicity of pegylated interferon alpha: a prospective study in patients with HCV.

OBJECTIVE: To assess whether pegylated interferon alpha (PEG-IFNalpha) may induce peripheral neuropathy or antibodies to peripheral nerve antigens in patients with hepatitis C virus (HCV) infection. METHODS: We studied 52 patients with HCV (38 men, 14 women; mean age 44.6 +/- 10.6 years) treated with IFNalpha. Before therapy (T(0)), patients underwent quantitative viral RNA determination, HCV genotype analysis, and neurologic and electrophysiologic evaluation. At the end (T(1)) and after therapy (T(2)), patients were neurologically and electrophysiologically re-evaluated. Antibodies to gangliosides and sulfatides were assayed by ELISA at T(0) and T(1). Twenty-three patients with HCV with comparable age, viral load, and genotype, not treated with IFNalpha, were studied as controls. RESULTS: Seven patients (six in IFNalpha, one control) had peripheral neuropathy at recruitment. No significant differences in the electrophysiologic measures were detected between T(0) and T(1) (repeated-measures analysis of variance [ANOVA]) in any of the 52 patients or in those with neuropathy at T(0). No changes were found at T(2), independent of the viral response to treatment. Two patients, one with neuropathy, had antiganglioside antibodies at recruitment. Two patients, one not treated with IFNalpha, developed low antibody titers during follow-up, without symptoms or signs of neuropathy. CONCLUSIONS: Pegylated interferon alpha therapy was not associated with the occurrence (or worsening) of peripheral neuropathy or antibodies to peripheral nerve antigens in patients with hepatitis C virus.

Adolescent↗
PubMed2006

Prevalence and characteristics of peripheral neuropathy in hepatitis C virus population.

OBJECTIVE: To assess the prevalence of peripheral neuropathy (PN) and its correlation with cryoglobulinemia (CG) in an unselected, untreated referral hepatitis C virus (HCV) population. PATIENTS AND METHODS: Two hundred and thirty four patients (120 women and 114 men) with untreated HCV infection were consecutively enrolled by seven Italian centres. Clinical neuropathy was diagnosed when symptoms and signs of peripheral sensory or motor involvement were present. Median, ulnar, peroneal, and sural nerves were explored in all patients and distal symmetric polyneuropathy was diagnosed when all explored nerves or both lower limb nerves were affected. Mononeuropathy and mononeuropathy multiplex were diagnosed when one nerve or two non-contiguous nerves with asymmetrical distribution were affected. Screening for CG was done in 191 unselected patients. RESULTS: Clinical signs of PN were observed in 25 of the 234 patients (10.6%). Electrophysiological PN was found in 36 (15.3%). CG was present in 56/191 patients (29.3%). The prevalence of CG increased significantly with age (p<0.001) and disease duration (p<0.05). PN was present in 12/56 (21%) patients with CG and 18/135 (13%) without CG (p=NS). PN increased significantly with age (p<0.001) and logistic regression analysis confirmed age as the only independent predictor of PN (OR 1.10 for each year; 95% CI 1.04 to 1.15; p<0.001). CONCLUSIONS: Electrophysiological examination detected subclinical neuropathy in 11 patients (4.7%). Statistical analysis showed that CG was not a risk factor for PN whereas PN prevalence increased significantly with age.

Adolescent↗
PubMed2006

Update on idiopathic inflammatory myopathies.

The inflammatory myopathies are a group of acquired diseases, characterized by an inflammatory infiltrate of the skeletal muscle. On the basis of clinical, immuno-pathological and demographic features, three major diseases can be identified: dermatomyositis (DM); polymyositis (PM); and inclusion body myositis (IBM). New diagnostic criteria have recently been introduced, which are crucial for discriminating between the three different subsets of inflammatory myopathies and for excluding other disorders. DM is a complement-mediated microangiopathy affecting skin and muscle. PM and IBM are T cell-mediated disorders, where CD8-positive cytotoxic T cells invade muscle fibres expressing MHC class I antigens, thus leading to fibre necrosis. In IBM, vacuolar formation with amyloid deposits are also present. This article summarizes the main clinical, laboratory, electrophysiological, immunological and histologic features as well as the therapeutic options of the inflammatory myopathies.

Autoantibodies↗
PubMed2006

Clinical implications of autoantibody screening in patients with autoimmune myositis.

OBJECTIVE: To evaluate the clinical usefulness of serum autoantibody profiling in patients with autoimmune myositis. METHODS: We retrospectively studied 74 consecutive patients: 68 had definite or probable myositis according to Bohan-Peter criteria, six suffered from antisynthetase syndrome with subclinical myopathy. Myositis specific antibodies (MSA) (anti-ARS, -SRP, -Mi-2) were determined by RNA immunoprecipitation or immunoblot, myositis associated antibodies (MAA) (anti-RoRNP, -U1RNP, -PM/Scl, -Ku) by immunoblot. RESULTS: Forty-three patients (58%) were positive for MSA: anti-Jo-1 in 15/27 polymyositis (PM) (55%), 4/33 dermatomyositis (DM) (12%), 1/8 overlap (12%) and 2/6 antisynthetase syndrome (33%); anti-ARS non-Jo-1 in 1/27 PM (4%), 2/33 DM (6%) and 4/6 antisynthetase syndrome (67%); anti-Mi-2 in 1/27 PM (4%) and 11/33 DM (33%); anti-SRP in 3/27 PM (11%) and 1/33 DM (3%). One patient was anti-Jo-1/Mi-2 positive, one anti-Jo-1/SRP positive. Moreover, 27 patients (36%) were positive for MAA: anti-Ro/SSA in 8/27 PM (30%), 7/33 DM (21%), 1/8 overlap (12%), and 3/6 antisynthetase syndrome (50%); anti-U1RNP in 1/27 PM (3.7%), 1/33 DM (3%), and 2/8 overlap (25%); anti-PM/Scl in 2/8 overlap (25%), anti-Ku in 2/8 overlap (25%). Anti-Jo-1 was predominantly associated with PM, anti-Mi-2 was almost exclusively found in DM patients. Anti-ARS antibodies were closely associated with interstitial lung disease and polyarthritis; notably, anti-ARS non-Jo-1 was more frequent in patients without overt muscle alterations. Anti-Ro/SSA antibody was not associated with any disease subset, but significantly more frequent in antisynthetase syndrome. CONCLUSIONS: Searching for MSA and MAA in patients with autoimmmune myositis is recommended because of its diagnostic and clinical value. Anti-ARS non-Jo-1 antibodies seem to preferentially target patients with pulmonary fibrosis without overt myopathy.

Adolescent↗
PubMed2005

Positive and negative effects of thalidomide on refractory cutaneous lupus erythematosus.

BACKGROUND: Thalidomide is used in cutaneous lupus erythematosus (CLE) refractory to conventional therapies. Peripheral neuropathy (PN) is the most severe side effect, but the incidence of PN and its relation to thalidomide dose are still unclear. OBJECTIVE: To prospectively evaluate the efficacy as well as the occurrence of PN in CLE patients treated with thalidomide, and to assess whether PN, when occurs, correlates with thalidomide dose and/or length of treatment. METHODS: Fourteen female patients with CLE in low-dose thalidomide therapy were followed for up to 24 months. Prior to, and regularly during treatment patients underwent rheumatological, dermatological, neurological and electrophysiological evaluations. A decline in sural SNAP of 50% or more from baseline value was considered as criterion of sensory axonal PN. RESULTS: All patients showed a dramatic improvement of skin manifestations. Ten patients (71.4%) developed a sensory axonal PN. The median time free from this complication was 14 months. No correlations were found between age of the patients nor thalidomide cumulative dose and occurrence of PN (Mann-Whitney U Test; p>0.16). Other adverse effects were: tremor, paresthesias, somnolence, amenhorrea, constipation and thoracic pain. CONCLUSIONS: Low does thalidomide is efficacious in treating CLE, but PN is a common complication whose occurrence does not seem to correlate with total thalidomide dose, whereas with the duration of therapy. A closer electrophysiological follow-up is therefore recommended in the long-term treatment.

Adult↗
PubMed2005

Neurological complications of celiac disease and autoimmune mechanisms: preliminary data of a prospective study in adult patients.

Antibodies to gangliosides and Purkinje cells have been reported in patients with celiac disease (CD) with neuropathy and ataxia, respectively. Whether these antibodies are pathogenic is not clear. The response of neurological symptoms and antibody titers to a gluten-free diet is still controversial. The objective of our study was to assess whether neurological manifestations in CD patients correlate with antibody titers and a gluten-free diet.Thirty-five CD patients (9 males, 26 females, mean age 37.1 +/- 12.6 yrs) were followed prospectively. At initial evaluation, 23 were on a gluten-free diet, 12 were not. At recruitment and during follow-up, patients underwent neurological and electrophysiological evaluation. IgG, IgM, and IgA anti-ganglioside antibodies were assayed by ELISA; anti-neuronal antibodies were assessed by immunohistochemistry and Western blot. Four patients, all males, had electrophysiological evidence of neuropathy; three had been on a gluten-free diet for several months, and one was newly diagnosed. One had reduced tendon reflexes; another complained of distal paresthesias. With regard to anti-ganglioside antibodies, three patients had a moderate increase in antibodies without symptoms or signs of neuropathy. No patients had ataxia or cerebellar dysfunction, although in four patients reactivity to neuronal antigens was found. In 17 patients, an electrophysiological follow-up (mean duration of follow-up, 9 months) showed no changes. In conclusion, the preliminary results of this prospective study indicate that neuropathy, usually subclinical, may accompany CD. Antibody titers do not seem to correlate with neurological symptoms/signs or diet. Ongoing follow-up will help confirm these data and clarify the role, if any, of antibodies in neurological involvement in CD.

Adult↗
PubMed2004

Anti-ganglioside antibodies in children with coeliac disease: correlation with gluten-free diet and neurological complications.

BACKGROUND: Emerging evidence points to humoural mechanisms in neurological complications of coeliac disease. Immunoglobulin G anti-ganglioside antibodies have been reported in coeliac disease patients with neuropathy, suggesting an immune response to peripheral nerve antigens. No data are so far available on anti-ganglioside antibodies in coeliac disease children or on antibody modifications after gluten-free diet. AIM: To evaluate the presence of antibodies to ganglioside antigens in children with coeliac disease, their modification after gluten-free diet, and possible correlations with neurological manifestations. METHODS: Sera from 42 coeliac disease children, before and after gluten-free diet, were tested by enzyme-linked immunosorbent assay for the presence of antibodies (immunoglobulin M, immunoglobulin A, immunoglobulin G) to gangliosides. Thirty-five sera of age-matched children with dyspepsia were used as control. RESULTS: High anti-ganglioside antibodies titres were present in two patients. In one patient, antibody titre reversed after gluten-free diet, whereas in the other one the titre increased after diet. Neither one complained of neurological symptoms. CONCLUSIONS: Anti-ganglioside antibodies do not seem to correlate with gluten ingestion or with neurological manifestations in children with coeliac disease. Mechanisms different from gluten exposure may be implicated in the antibody production. An ongoing prospective study will help clarify the role, if any, of these antibodies in coeliac disease.

Adolescent↗
PubMed2004

Thalidomide neurotoxicity: prospective study in patients with lupus erythematosus.

The authors prospectively followed 14 patients treated with thalidomide for cutaneous lupus erythematosus (CLE), in order to evaluate the occurrence of peripheral neuropathy (PN) and to assess whether PN correlates with thalidomide dose. The patients were followed for up to 24 months with neurologic and electrophysiologic evaluations. Seven patients (50%) developed sensory axonal PN. The median time free from PN was 14 months. PN occurred after 10 months in the majority of patients. No correlations were found between thalidomide cumulative dose and occurrence of PN (Mann-Whitney U test; p > 0.16).

Adult↗
PubMed2004

Thalidomide sensory neurotoxicity: a clinical and neurophysiologic study.

The clinical and neurophysiologic data from 65 patients taking thalidomide were reviewed. Thalidomide sensory neurotoxicity was found to be cumulative dose dependent but occurs only when the total dose is relatively high (>20 g). The risk of developing sensory neuropathy is around 10% below this threshold but increases with higher doses.

Adult↗
PubMed2004

Thiethylperazine-induced parkinsonism: in vivo demonstration of dopamine D2 receptors blockade.

Thiethylperazine (Torecan) is a piperazine phenothiazine employed to relieve vertigo. Its use may be associated with extrapyramidal side effects (dystonia, akathisia, tardive dyskinesia) (Sulkava, 1984), but parkinsonism has rarely been described. We describe a woman who, 1 month after the onset of thiethylperazine treatment, developed parkinsonism that disappeared 2 months after withdrawal of the drug. However, cerebral single-photon emission computed tomography (SPECT) with the dopamine (DA) D2 receptors ligand 123I-iodobenzamide (123I-IBZM) revealed a persistent reduced DA D2 receptors activity (by 45%) in the basal ganglia (BG), which may be clinically not effective.

Basal Ganglia↗
PubMed2004

Pregnancy in rare autoimmune rheumatic diseases: UCTD, MCTD, myositis, systemic vasculitis and Beçhet disease.

The physiological adaptation of the immune system to pregnancy can potentially affect the course of all autoimmune rheumatic diseases (ARD), conversely the autoimmune processes characteristic of these conditions may compromise the foetal outcome. Unfortunately, very few reports on pregnancy outcome in patients with rare ARD are available. In this paper, we briefly review the data published until now on these disorders. Some general guidelines which were elaborated for more prevalent ARD seem to be valid also for such rare conditions: 1) patients should be correctly informed on the risk of becoming pregnant; 2) pregnancies should be planned when the disease is in remission since it increases the probability of successful maternal and foetal outcome; 3) patients should be regularly monitored during gestation and postpartum by a multidisciplinary team including rheumatologist, obstetrician, and neonatologist; 4) in the case of disease relapse an adequate treatment, even aggressive if necessary, should be recommended since active disease can be more detrimental for foetus than drugs; 5) pregnancies complicated by the onset of rare ARD have a particularly severe prognosis; in these cases a prompt treatment and very close clinical surveillance are indicated.

Autoimmune Diseases↗
PubMed2002

Combined analysis of CSF betaA42 peptide and tau protein and serum antibodies to glycosaminoglycans in Alzheimer's disease: preliminary data.

Neuropathological hallmarks of Alzheimer's disease (AD) are amyloid plaques and neurofibrillary tangles, containing betaA(42) peptide and tau protein, respectively. Amyloid plaques contain also glycosaminoglycans (GAGs). Whereas cerebrospinal fluid (CSF) levels of betaA(42) peptide and tau protein have been demonstrated as potential markers of Alzheimer's disease (AD), no data are available for GAGs. We determined (Elisa) tau and betaA(42) CSF levels, as well as serum antibodies to GAGs in 9 AD patients, and the values were analyzed in relation to age and severity of the disease. Beta-A42 and tau CSF levels were significantly reduced and increased, respectively, in AD patients when compared to controls, but they did not correlate with the severity of the disease. Despite their role in amyloidogenesis, we did not find evidence for the use of GAGs as diagnostic marker of AD.

Aged↗
PubMed2000

Antibodies to chondroitin sulfates A, B, and C: clinico-pathological correlates in neurological diseases.

Anti-chondroitin sulfates (ChSs) antibodies have been reported in neuropathy and neurodegenerative diseases. Differences in specificities may account for their association with different diseases. Sera from 303 neurological patients were tested for antibodies to ChSs A, B, C. Titers >/=51,200 were found in 16 patients (eight peripheral neuropathy, three motor neuron disease, four multiple sclerosis, one myelitis). Three patients also had anti-sulfatides antibodies, which in two cases cross-reacted with ChSs. By indirect immunofluorescence, positive sera stained nuclei on normal human peripheral nerve sections. These findings indicate that human anti-ChSs antibodies are broadly reactive and not specific to any neurological disease.

Absorption↗
PubMed1999

Effect of complex polyphenols and tannins from red wine (WCPT) on chemically induced oxidative DNA damage in the rat.

BACKGROUND: Flavonoids are polyphenolic antioxidants occurring in vegetables and fruits as well as beverages such as tea and wine which have been thought to influence oxidative damage. AIM OF THE STUDY: We wanted to verify whether a complex mixture of wine tannins (wine complex polyphenols and tannins, WCPT) prevent chemically-induced oxidative DNA damage in vivo. METHODS: Oxidative DNA damage was evaluated by measuring the ratio of 8-hydroxy-2'-deoxyguanosine (80HdG)/ 2-deoxyguanosine (2dG) x 10(-6) in hydrolyzed DNA using HPLC coupled with electrochemical and UV detectors. RESULTS: We treated rats with WCPT (57 mg/kg p.o.) for 14 d, a dose 10-fold higher than what a moderate wine drinker would be exposed to. WCPT administration significantly reduced the ratio of 80HdG/2dG x 10(-6) in liver DNA obtained from rats treated with 2-nitropropane (2NP) relative to controls administered 2NP only (33. 3 +/- 2.5 vs. 44.9 +/- 3.2 x 10(-6) 2dG; micro +/- SE; p<0.05). On the contrary, pretreatment with WCPT for 10 d did not protect the colon mucosa from oxidative DNA damage induced by 1, 2-dimethylhydrazine (DMH). 2NP and DMH are hepatic and colon carcinogens, respectively, capable of inducing oxidative DNA damage. CONCLUSIONS: WCPT have protective action against some types of chemically-induced oxidative DNA damage in vivo.

1,2-Dimethylhydrazine↗
PubMed1998

Antibodies to chondroitin sulfate C: a new detection assay and correlations with neurological diseases.

Antibodies to chondroitin sulfate C (ChS C) have been previously associated with sensory axonal neuropathy. Investigation of these antibodies has, however, been limited by the lack of a sensitive and reliable test for their detection. We developed a new enzyme-linked immunoassorbent assay (ELISA), where biotinylated ChS C was made to adhere to avidin-coated microwells. The new ELISA showed a much greater sensitivity than other currently available ELISAs for detection of anti-ChS C antibodies. A total of 480 sera (466 patients and 14 normal volunteers) were tested at increasing dilutions for anti-ChS C antibody activity. Normal subjects had IgM anti-ChS C antibody titers of up to 3,200 and mildly elevated titers of 6,400 were seen in a variety of diseases. Eleven patients had titers of 12,800 or higher. These included seven patients with sensory axonal neuropathy, three with amyotrophic lateral sclerosis and one with corticobasal ganglionic degeneration. These studies indicate that anti-ChS antibodies do occur in patients with axonal sensory neuropathy, but are not limited to that disease.

Antibodies, Monoclonal↗
PubMed1998

Positive correlation of CTG expansion and pharyngoesophageal alterations in myotonic dystrophy patients.

Alteration of the pharyngoesophageal musculature is a common finding in patients with myotonic dystrophy (MD), regardless of the presence of dysphagia. The aim of the present study was to determine whether a specific pattern of swallowing abnormalities could be identified in MD patients, and the possible correlation with the size of CTG repeats. Fifteen MD patients, 8 of whom were asymptomatic for dysphagia, underwent a videofluoroscopic study of swallowing. Alterations of the pharyngoesophageal phase of swallowing were detected in 12 of 15 patients, 6 without clinical evidence of dysphagia. Incomplete relaxation of the upper esophageal sphincter (UES) and esophageal hypotonia were the most common alterations. We found a significant correlation between the number of radiological alterations and the size of CTG repeats. A typical radiological pattern of swallowing has also been identified. The role of videofluoroscopy in evaluation of MD patients is briefly discussed.

Adult↗