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Nicolò Pipitone

Publications and source records attributed to Nicolò Pipitone.

9 recordsLinked to original sources
PubMed2006

Interleukin-10 promoter polymorphisms in giant cell arteritis.

OBJECTIVE: To investigate potential associations between interleukin-10 (IL-10) promoter polymorphisms and susceptibility to, and clinical features of, giant cell arteritis (GCA). METHODS: A total of 140 patients with biopsy-proven GCA who were residents of Reggio Emilia, Italy, and 200 population-based controls from the same geographic area were genotyped for promoter polymorphisms of the IL-10 gene, by molecular methods. The patients were subgrouped according to the presence or absence of polymyalgia rheumatica (PMR) and ischemic complications (any or all of the following: vision loss, jaw claudication, cerebrovascular accidents, or aortic arch syndrome). RESULTS: The distribution of the C/A 592 genotype differed significantly between the GCA patients and the controls (P(corr) = 0.003). Carriers of the A592 allele (A/A or C/A) were significantly more frequent among the GCA patients than among the controls (P(corr) = 0.004, odds ratio [OR] 2.0 [95% confidence interval (95% CI) 1.3-3.1]). Homozygosity for the A592 allele was significantly more frequent among the GCA patients than among the controls (P(corr) = 0.002, OR 3.4 [95% CI 1.6-7.2]). The distribution of the A/G 1082 genotype was similar in GCA patients and controls. In the haplotype analysis, the frequency of the ATA haplotype was significantly higher in GCA patients than in the controls (P = 0.0001), whereas the frequencies of the ACC and GTA haplotypes were significantly lower (P = 0.0001 for both comparisons). No significant associations were found for comparisons of GCA patients with and those without PMR or GCA patients with and those without ischemic complications. CONCLUSION: Our findings show that the -592 C/A promoter polymorphism of the IL-10 gene is associated with susceptibility to GCA.

Aged↗
PubMed2006

New approaches in the treatment of Adamantiades-Behçet's disease.

PURPOSE OF REVIEW: To update clinicians on the recent advances in the treatment of Adamantiades-Behçet's disease. RECENT FINDINGS: Interferon-alpha-2a and infliximab have proved able to induce prompt remission in the vast majority of Adamantiades-Behçet's patients with DMARD-resistant uveoretinitis. Efficacy of interferon-alpha-2a has also been reported for mucocutaneous lesions, arthritis, and (more anecdotally) for neuro-Behçet, while results from small case series suggest that infliximab is beneficial for mucocutaneous lesions and (more anecdotally) for arthritis and gastro-intestinal manifestations. Two cases of neuro-Behçet treated with infliximab showed a complete resolution. Finally, in a randomized controlled trial of patients with mucocutaneous, arthritic manifestations, or both, etanercept effectively suppressed mucocutaneous lesions.A different approach is tolerization by oral administration of the 336-351 peptide of the human heat shock protein 60 (thought to have a pathogenic role in Adamantiades-Behçet's disease-associated uveitis), linked to recombinant cholera B-toxin B-subunit. Preliminary results have shown that tolerization is safe and effective in preventing relapses of uveitis. SUMMARY: Biologic agents have proved effective in patients resistant to conventional treatment. However, disease subsets characterized by severe morbidity and mortality such as vasculo-Behçet and neuro-Behçet still pose major therapeutic challenges. Further studies are needed to devise better treatment strategies for severe Adamantiades-Behçet's disease.

Antibodies, Monoclonal↗
PubMed2006

Relationship between interleukin 6 promoter polymorphism at position -174, IL-6 serum levels, and the risk of relapse/recurrence in polymyalgia rheumatica.

OBJECTIVE: To assess the role of -174 G/C promoter polymorphism of interleukin 6 (IL-6) in the susceptibility to polymyalgia rheumatica (PMR). We also investigated whether this polymorphism modulates the circulating level of IL-6 and the risk of relapse/recurrence in a series of patients with PMR followed up prospectively. METHODS: A prospective study of 112 consecutive, untreated patients with isolated PMR (i.e., without evidence of giant cell arteritis) who were followed up for at least 24 months. This cohort represented all patients diagnosed over a 5-year period in one Italian rheumatological secondary referral center. Patients were monitored for clinical signs/symptoms and acute-phase reactants. All PMR patients and 112 population-based controls from the same geographic area were genotyped for IL-6 polymorphism at position -174 by molecular methods. IL-6 serum levels were measured in 67 PMR patients and 43 population-based controls. RESULTS: The distribution of the G/C 174 genotype was similar in PMR patients and controls. No significant associations with IL-6 promoter polymorphism at position -174 were found when PMR patients with and without relapse/recurrence were compared. Controls homozygous for the C allele had higher serum IL-6 levels than the carriers of the G allele (4.5 +/- 3.7 pg/ml vs 1.8 +/- 2.1 pg/ml, p = 0.01). Patients homozygous for the allele C had significantly higher values of IL-6 during followup than patients carrying GC or GG genotypes. CC homozygosity was significantly more frequent in patients with persistently elevated levels of IL-6 than in those without. The presence of persistently elevated IL-6 levels, but not the CC genotype, was associated with an increased frequency of relapse/recurrence. CONCLUSION: Our findings show that the 174 G/C promoter IL-6 polymorphism is not implicated in susceptibility to PMR. However, CC genotype characterized PMR patients with persistently elevated levels of IL-6 who are at higher risk of developing relapse/recurrence. A genetically modulated pattern of IL-6 production could affect the longterm outcome of patients with PMR.

Aged↗
PubMed2005

Positron emission tomography (PET): evaluation of chronic periaortitis.

OBJECTIVE: To evaluate the presence and extent of large-vessel inflammation in patients with chronic periaortitis (CP) using (18)F-fluorodeoxyglucose-positron emission tomography (FDG-PET). METHODS: A consecutive case series consisting of 7 patients with CP seen over a 3-year period and a control group of 14 patients with malignancy were evaluated with FDG-PET. For every case we selected 2 age- and sex-matched controls who underwent PET imaging for malignancy. The diagnosis of CP was made by means of computed tomography. PET imaging was performed at diagnosis before therapy was started. Measurement of vascular uptake was graded using a 4-point semiquantitative scale. RESULTS: All patients had evidence of grade 2+ or 3+ vascular uptake in the abdominal aorta and/or iliac artery. No controls showed vascular uptake greater than 1+. Vascular uptake in the thoracic aorta and/or in its branches was seen in 3 (43%) of 7 patients. Vascular uptake in abdominal aorta and/or iliac artery was observed in patients with CP but not in controls (100% versus 0%). There was also a significantly more frequent FDG uptake in the large thoracic arteries in case-patients compared with controls (43% versus 0%; P = 0.03). CONCLUSION: FDG-PET scan shows in patients with CP the presence of a large-vessel vasculitis involving abdominal aorta and common iliac arteries, which in some patients is also extended to thoracic aorta and/or its branches.

Adult↗
PubMed2005

Risk factors for visual loss in an Italian population-based cohort of patients with giant cell arteritis.

OBJECTIVE: To evaluate the frequency of visual manifestations at presentation in an Italian population-based cohort of patients with biopsy-proven giant cell arteritis (GCA), and to investigate predictors for the development of permanent visual loss. METHODS: We identified 136 Reggio Emilia (Italy) residents with biopsy-proven GCA diagnosed between 1986 and 2002. Medical records of these 136 patients were reviewed, and demographic, clinical, and laboratory data were collected.Multivariate analysis with multiple logistic regression models was performed to identify the best predictors of visual loss. RESULTS: Visual manifestations developed in 41 patients (30.1%). Partial or total visual loss was observed in 26 patients (19.1%). Anterior ischemic optic neuropathy was seen in 24 patients, and 2 patients had central retinal artery occlusion. Unilateral vision loss occurred in 19 patients, and bilateral visual loss in 7. In 25 patients, visual loss developed before glucocorticoid therapy for GCA was started. The age at disease onset was significantly higher in patients with permanent visual loss compared with those without it. The frequency of systemic signs/symptoms and erythrocyte sedimentation rate (ESR) and C-reactive protein values at diagnosis were significantly lower in patients with permanent visual loss. By multivariate logistic regression, the only statistically significant predictor for the development of permanent visual loss was the absence of high levels of ESR at diagnosis (tertile 2: Odds ratio [OR] 0.08; tertile 3: OR 0.11). Other predictors included in the model were the absence of systemic manifestations (OR 0.24), an older age at disease diagnosis (quintile 5: OR 5.60), and the presence of an elevated platelet count at diagnosis (OR 4.99), however they were only of borderline statistical significance. CONCLUSION: The proportion of Italian patients with GCA that developed visual loss was similar to that reported from other countries. The patients with low inflammatory response had a higher risk of visual loss.

Age of Onset↗
PubMed2005

Are steroids alone sufficient for the treatment of giant cell arteritis?

Glucocorticosteroids are the cornerstone of treatment of giant cell arteritis. An initial dose of prednisone or its equivalent of at least 40-60mg per day as single or divided dose is usually adequate. Glucocorticosteroids may prevent, but usually do not reverse, visual loss. A treatment course of 1-2 years is often required. Some patients, however, have a more chronic-relapsing course and may require low doses of glucocorticosteroids for several years. Glucocorticosteroid-related adverse events are common. In studies on immunosuppressant agents, methotrexate has been used as a glucocorticosteroid-sparing drug with conflicting results. This drug may, however, be given to patients who need high doses of glucocorticosteroids to control active disease and who have serious side effects. A recent pilot study found that infliximab was efficacious in patients with glucocorticosteroid-resistant giant cell arteritis. However, randomized controlled trials are required to define the role of anti-tumor necrosis factor-alpha agents in the treatment of giant cell arteritis. Finally, low-dose aspirin has been shown in a recent retrospective study to decrease the rate of cranial ischemic complications secondary to giant cell arteritis. It is conceivable that the definition of different patterns of inflammation in giant cell arteritis in the future might facilitate the design of differentiated therapeutic approaches.

Clinical Trials as Topic↗
PubMed2005

Interleukin-6 promoter polymorphism at position -174 in giant cell arteritis.

OBJECTIVE: To investigate potential associations between the -174 G/C interleukin-6 (IL-6) promoter polymorphism and susceptibility to and clinical features of giant cell arteritis (GCA), particularly in patients with or without polymyalgia rheumatica (PMR) and with or without ischemic complications. METHODS: One hundred and twenty-six patients with biopsy-proven GCA who were residents in Reggio Emilia, Italy, and 112 population-based controls from the same geographic area were genotyped for IL-6 polymorphism at position -174 by molecular methods. Patients were divided in subgroups according to presence or absence of PMR and ischemic complications (visual loss, jaw claudication, cerebrovascular accidents, aortic arch syndrome). RESULTS: Distribution of the G/C 174 genotype was similar in patients with GCA and controls. No significant associations with the IL-6 promoter polymorphism at position -174 were found when GCA patients with or without PMR or with or without ischemic complications were compared. Further, IL-6 genotypes did not significantly affect levels of C-reactive protein or other inflammatory markers at diagnosis. CONCLUSION: Our findings show that the 174 G/C promoter IL-6 polymorphism does not seem to be implicated in susceptibility to and clinical expression of GCA.

Aged↗
PubMed2004

[Arthritides in the elderly].

The arthritides of the elderly comprise a fairly heterogeneous group of diseases. They include conditions that affect exclusively or predominantly the elderly (such as, for instance, remitting seronegative symmetric synovitis with pitting edema) and conditions affecting any age group, but which can present with peculiar features in the elderly, like rheumatoid arthritis and the seronegative arthropathies. Therefore, in order to arrive at a correct diagnosis, a knowledge of the specific features of these disorders is required. In addition, the treatment of elderly patients differs from that of other age groups in that elderly subjects appear to have an increased susceptibility to adverse reactions. This susceptibility is related both to the different metabolism of aged subjects, including the impairment of the renal function, and to the multiple therapies that such subjects often receive. In view of the ever increasing elderly population in the western world, all physicians, over and beyond the limited circle of rheumatologists, should be knowlegeable about the principles of diagnosing and treating senile arthritis.

Adrenal Cortex Hormones↗