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R La Corte

Publications and source records attributed to R La Corte.

At least 19 recordsLinked to original sources
PubMed2006

In patients with antisynthetase syndrome the occurrence of anti-Ro/SSA antibodies causes a more severe interstitial lung disease.

We studied the clinical features and autoantibody profile in 21 patients with antisynthetase syndrome (AS) comparing to 48 patients with classical polymyositis and dermatomyositis without AS. At presentation, the AS group showed more frequently the presence of interstitial lung disease (ILD), arthritis/arthralgia, mechanic's hand and anti-Ro/SSA antibodies. Patients without AS had more frequent proximal weakness and cutaneous erythematosus rash. Interestingly, the AS patients with associated anti-Ro/SS-A antibodies seem to be predisposed to the development of a more severe ILD, expressed as HRCT total score > or = 7. During a follow up of about 3 years (range 6-110 months), the presence of anti-Jo-1 antibody alone or in association with anti-Ro/SSA did not influence survival or a more severe prognosis of ILD.

Adolescent↗
PubMed2004

Clinical manifestations of Behçet's disease in 137 Italian patients: results of a multicenter study.

OBJECTIVE: To determine the type and frequency of clinical features of Behçet's disease in a population of Italian patients. METHODS: We retrospectively studied 137 Italian patients (76 males and 61 females, age at onset 29.6 +/- 12.2 [mean +/- SD] years) seen consecutively in nine different referral centers. The duration of follow-up at study entry was 10.9 +/- 8.2 years. Virtually all patients fulfilled the classification criteria developed by the International Study Group for Behçet's disease. The clinical manifestations of the patients were recorded by the attending physicians using specifically designed forms. RESULTS: The most frequent manifestations at disease onset were oral (78.3%) and genital aphthae (29.2%) followed by inflammatory ocular involvement (20%) and arthritis (14.2%). The commonest (>50% of cases) manifestations observed throughout the disease course were oral aphthae (99.3%), genital aphthae (62.8%), various cutaneous lesions including erythema nodosum (81.8%), and inflammatory ocular disease (60.6%). Panuveitis and posterior uveitis/retinitis occurred more frequently in males compared with females (28.9% versus 11.5% and 57.9% versus 36.1%, respectively; p < 0.05). 61.6% of our patients were HLA-B51 positive. CONCLUSION: Behçet's disease in Italian patients is characterized by a variety of clinical manifestations in agreement with the medical literature. Panuveitis and posterior uveitis/retinitis occur more frequently in male patients.

Adult↗
PubMed2000

Wegener's granulomatosis associated with antiphospholipid syndrome.

We report a case of Wegener's granulomatosis (WG) with pulmonary hemorrhage also satisfying the criteria for antiphospholipid antibody syndrome (APS). This association has, to the best of our knowledge, never been described before. Pulmonary hemorrhage may be an early manifestation of several immune and idiopathic disorders such as ANCA-associated vasculitis. Several case-reports of APS patients with capillaritis have been described. A possible explanation is that microvascular thrombosis with subsequent increase in vascular permeability facilitates perivascular IgG and complement deposition leading to development of capillaritis. Whether the vascular disease is secondary to thrombosis or vasculitis or both is important in choosing the proper management strategy. We suggest that anticardiolipin antibodies (aCL) should be detected in ANCA-associated vascularitis because they may contribute to life-threatening events superimposed on vascular damage.

Adult↗
PubMed1999

Long-lasting remission and successful treatment of acquired factor VIII inhibitors using cyclophosphamide in a patient with systemic lupus erythematosus.

Acquired deficiency of clotting factor VIII (FVIII) is a rare bleeding diathesis seldom encountered in systemic lupus erythematosus (SLE). Reduction of FVIII activity by autoantibodies can cause potentially life-threatening situations. Herein, an SLE patient with a positive lupus anticoagulant (LAC) test who abruptly developed metrorrhagia 4 yr after diagnosis is reported. Coagulation tests revealed FVIII activity reduced to 3% and a prolonged aPTT. FVIII inhibitor(s) were found to be as high as 3.0 Bethesda Units. Plasmapheresis, immunoglobulins, prednisolone and FVIII plasma concentrates induced the cessation of metrorrhagia, but the clotting tests were barely improved. One month later, extensive ecchymosis appeared and worsened, despite re-administration of the previous therapy. Pulse cyclophosphamide followed by oral administration was then started with normalization of coagulation parameters and long-lasting disease remission.

Administration, Oral↗
PubMed1999

Prophylaxis and treatment of NSAID-induced gastroduodenal disorders.

A significant percentage of patients taking nonsteroidal anti-inflammatory drugs (NSAIDs) experience some type of adverse gastrointestinal symptoms, lesions of the gastroduodenal tract being clinically the most relevant. NSAIDs cause gastrointestinal damage by 2 independent mechanisms: a topical effect, which is pH and pKa related, and a systemic effect mediated by cyclooxygenase (COX) inhibition with a reduction in prostaglandin synthesis. Using endoscopy, gastroduodenal lesions identified include subepithelial haemorrhages, erosions and ulcers. The prevalence of ulceration in NSAID users has been reported as being between 14 and 31% with a 2-fold higher frequency of gastric ulcers compared with duodenal ulcers. Among the strategies used to decrease the risk of ulcer development are: (i) the use of analgesics other than NSAIDs; (ii) use of the lowest possible dosage of NSAID; (iii) the use of a COX-2 selective NSAID; (iv) the use of low doses of corticosteroids instead of NSAIDs; (v) avoidance of concomitant use of NSAIDs and corticosteroids; and (vi) use of preventive therapy. In an attempt to reduce the incidence of NSAID-induced gastrointestinal lesions, the following approaches have been proposed: (i) use of the prostaglandin analogue misoprostol, which is an antiulcer drug which has been proven to be as effective in the prevention of NSAID-induced gastric and duodenal ulcers as in the reduction of serious upper gastrointestinal complications; (ii) histamine H2 receptor antagonists (H2 antagonists), e.g. ranitidine, cimetidine and famotidine, which are useful in the prevention of NSAID-induced duodenal ulcers during long term treatment, but not in the prevention of NSAID-induced gastric ulcers; (iii) proton pump inhibitors, e.g omeprazole, and pantoprazole, whose efficacy in preventing NSAID-associated ulcers has been recently demonstrated; and (iv) barrier agents, e.g. sucralfate, which cannot be recommended as prophylactic agents to prevent NSAID-induced gastropathy. The first step in the treatment of NSAID-associated ulcers lies in a reduction in the dosage of the NSAID or discontinuation of the drug. If NSAID treatment cannot be withdrawn, a proton pump inhibitor appears to be the most effective treatment in healing ulcers, accelerating the slow healing observed with H2 antagonists.

Adrenal Cortex Hormones↗
PubMed1998

Nonsteroidal antiinflammatory drug use and gallstone disease prevalence: a case-control study.

OBJECTIVES: Conflicting results on the relationship between gallstone disease and the use of nonsteroidal antiinflammatory drugs (NSAIDs) have been reported, but studies on the effect of NSAID use in populations not selected on the basis of a high risk for gallstone development are still lacking. METHODS: We conducted a case-control study involving 216 patients, regular NSAID users (43 men and 173 women) consecutively admitted to a rheumatology department, suffering from rheumatoid arthritis (n = 147), osteoarthritis (n = 49), and ankylosing spondylitis (n = 20). Two-hundred sixteen patients who were not NSAID users, matched for gender, age, and body mass index, consecutively admitted to a medical department for various medical pathologies, acted as a control group. All patients underwent upper abdomen ultrasonography. RESULTS: The overall prevalence of gallstones was similar in the two groups: 24.0% in NSAID users (15.7% actual stones and 8.3% previous cholecystectomy) and 21.3% in controls (13.9% gallstones and 7.4% cholecystectomy). The prevalence of gallstone disease was significantly higher in women than in men, and the mean age was higher in gallstone patients than in gallstone-free patients, in both groups. No significant differences in type and duration of arthritis condition, type and dose of NSAID taken, and duration of treatment between gallstone patients and gallstone-free patients were found. On logistic regression analysis only female gender, aging, and family history of gallstone disease were significantly associated with the presence of gallstones, whereas no relationship between NSAID use and gallstone disease was found. CONCLUSIONS: Chronic NSAID ingestion does not seem to prevent gallstones in arthritis patients; in these patients gallstone disease is associated with classic risk factors (female gender and age).

Age Factors↗
PubMed1998

[Pancreatic duct antibodies and subclinical insufficiency of the exocrine pancreas in Sjögren's syndrome].

In previous studies we reported evidence of subclinical exocrine pancreatic insufficiency in primary or secondary Sjögren's syndrome (SSI, SSII) and rheumatoid arthritis (RA). In present study we evaluated the occurrence of pancreatic duct antibodies (PDA), and their relationship to exocrine pancreatic function in 36 women. Of these patients, 12 were classified as SSI, 12 as SSII, and 12 as RA. Exocrine pancreatic function was evaluated using the Secretin-Caerulein test (S.Cae test). The indirect immunofluorescent technique was used to evaluate patient sera for PDA. S.Cae test results, compared to controls, showed a statistically significant decrease in duodenal juice volumes, bicarbonates and enzymes in 58.3% of SSI, in 58.3% of SSI and in 30% of RA, according to our previous trials. PDA were found in two patients, the former with SSI and the latter with SSII, both asymptomatic with regard to pancreatic diseases but with impaired exocrine pancreatic function as evaluated by S.Cae test. We discuss the possible causes of these results.

Adult↗
PubMed1997

CD4-positive T-lymphocytes infiltrate the bronchial mucosa of patients with Sjögren's syndrome.

To investigate the degree and the type of inflammation in the bronchial mucosa in patients with Sjögren's syndrome, we examined lobar bronchial biopsies obtained from 10 patients with Sjögren's syndrome (six with primary and four with secondary) and eight control subjects. Histochemistry with hematoxylin-eosin was performed both to identify the number of mononuclear cells and eosinophils and to measure the thickness of the basement membrane. Immunohistochemistry was performed to identify neutrophils (neutrophil-elastase), macrophages (CD68), and T-lymphocyte subpopulations (CD4 and CD8) in the submucosa. Subjects with Sjögren's syndrome presented a greater number of CD4-positive T-lymphocytes than did the normal control subjects (p = 0.0129). Instead, eosinophils, neutrophils, macrophages, CD8 positive T-lymphocytes, and basement membrane thickness were similar in the two groups. There were no differences in cell counts between patients with primary and those with secondary Sjögren's syndrome and between symptomatic and asymptomatic patients. No correlation was found between cell counts, symptoms, lung volumes, and disease duration. This study has shown that patients with Sjögren's syndrome have an increased number of CD4 positive T-lymphocytes in the bronchial mucosa outside of the bronchial glands, supporting the concept that, in the airways. Sjögren's syndrome involves also extraglandular tissues.

Adult↗
PubMed1997

[Functional reserve of the exocrine pancreas in Sjögren's syndrome].

Exocrine pancreatic function was studied in a homogeneous group of 33 female patients aged 42-67 years. Of these patients, 11 were classified as rheumatoid arthritis (RA), 11 as Sjögren's syndrome I (SSI) and 11 as Sjögren's syndrome associated with RA (SSII). Clinical features, laboratory tests and special instrumental techniques excluded gastroenteric-hepatobiliary causes of pancreatic diseases. These patients were subjected to direct pancreatic stimulation with secretin and caerulein (S. Cae test). Test results, compared to control-group (10 voluntary healthy females) showed, in the last 30 m of stimulation, a statistically significant decrease (p < 0.05) in duodenal juice volume, bicarbonates and trypsin in 6 cases (54.5%) of SSI and in 3 cases (27.2%) of RA. SSII S. Cae test showed a decrease of volume and bicarbonates in 6 patients (54.5%) and in only 4 of these (36.4%) it was associated with a concomitant decrease in trypsin levels. Authors discuss the subclinical exocrine pancreatic function in relationship to sicca-syndrome, possible immunological factors and primary disease of pancreatic ducts.

Adult↗
PubMed1996

Colon involvement in systemic sclerosis: clinical-radiological correlations.

About one third of all patients with systemic sclerosis (SS) presents colon abnormalities, although these may be underestimated because they frequently remain asymptomatic for a long time. Thirty-five patients (33 women and 2 men; mean age 56.5 years; mean disease duration 11.9 years) affected by SS (25 with limited and 10 with diffuse pattern of skin involvement) were investigated using barium enema to detect radiological changes in the colon, and to correlate them with other visceral involvement, autoantibody profile, abdominal symptoms and duration of the disease. Ten patients (28.6%) showed X-rays abnormalities (excluding isolated diverticula), wide-mouthed sacculations being the most frequent finding. Our data confirm that the colon is frequently involved in SS, even in the limited form of the disease. The most relevant finding was the dissociation between clinical symptoms and radiological features which proved to be more evident among the patients with limited SS. No correlations were found between the radiological picture and any other parameter, thus suggesting that careful evaluation of the colon should be performed in any patient suffering from the disease.

Adult↗
PubMed1996

Endoscopic aspects of gastroduodenal mucosa due to NSAIDs.

The role of endoscopy in NSAID-related gastroduodenal pathologies is reviewed. If an accepted and largely used algorithm in which the role of endoscopy is exactly identified is not available, current strategy for the management of gastroduodenal toxicity gives indication for endoscopy immediately after the onset of symptoms, anaemia and evidence of bleeding, overt or occult. The endoscopic patterns of lesions in patients taking NSAID are characteristics patterns of erosive and ulcerative lesions. Endoscopy can recognize early lesions, allowing us to prevent a more advanced mucosal damage.

Aged↗
PubMed1996

Ultrastructural damage of gastric epithelium in patients taking NSAIDs.

As far as concerns ultrastructural lesions in the gastric epithelium following NSAIDs, a review has been made of existing data and ideas for future research concerning the ultrastructural field are advanced. Specific ultrastructural damage of the gastric epithelial cells has been recognized in patients taking NSAIDs: this pattern of damage appears characterized by a proliferative phenomen of "desquamation" of contiguous epithelial cells. Studies in animal models indicate that the first-level of epithelial damage involves a mitochondrial derangement and an alteration of tight junctions and cytoskeletal. The length of time of local drug action on the gastric mucosa could be the reason for the characteristic morphological presentation seen in vivo. If ulcers are the result of an imbalance between cell necrosis and cell regeneration, the high progression speed of cell necrosis to contiguous cells should play a basic role in the genesis of ulcers.

Animals↗
PubMed1996

Therapy of NSAIDs-induced gastropathy.

NSAID-induced gastropathy is the most frequent side effect due to NSAID use. The resulting clinical event is usually of little significance and only in a small percentage of cases results in serious side effects. Nevertheless, the large worldwide use of NSAIDs makes, even a rare side effect, numerically consistent. The pathogenesis of NSAID-induced gastropathy is related to two main mechanisms: an initial topical effect which is pH dependent and a systemic effect which is, more slowly developing, and mainly correlated to the inhibition of prostaglandin synthesis. The therapy of NSAID-gastropathy is almost completely identified with the therapy of NSAID ulceration because of its frequent relation to the development of potentially serious complications. In the case of symptomatic ulcer development the first therapeutic step is NSAID suspension and, in such a case all "antiulcer" drugs are efficient. When the NSAID can not be discontinued, omeprazole seems to be the most efficient drug; H2 blockers can promote ulcer healing but at a slower rate; sucralfate shows an efficacy similar to H2 blockers; misoprostol is useful in the prevention of NSAID-gastropathy. However, it is not so efficient in the treatment of established lesions and shows poor efficacy in the reduction of dyspeptic symptoms. For each one of these drugs it is necessary to obtain further data.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed1995

Bronchial hyperreactivity in systemic sclerosis patients: influence of associated Sjögren's syndrome.

OBJECTIVE: To determine the frequency and relative risk of bronchial hyperreactivity to methacholine in systemic sclerosis patients with or without associated Sjögren's syndrome. METHODS: A prospective study of 56 patients with systemic sclerosis (42 with the diffuse and 14 with the limited variant; 24 with associated Sjögren's syndrome), 57 with primary Sjögren's syndrome, and 61 healthy controls. RESULTS: Bronchial hyperreactivity (BH) was present in 6.5% of the healthy controls, 25% of the systemic sclerosis patients without associated Sjögren's syndrome, 42.2% of those with primary Sjögren's syndrome, and in 50% of those with systemic sclerosis with associated Sjögren's syndrome. The presence of BH did not correlate with age, disease duration, chest radiograph abnormalities, respiratory, and immunological data. The subgroup of subjects with the limited variant of systemic sclerosis more frequently had associated BH than did those with the diffuse variant of the disease; coexisting Sjögren's syndrome further increased this frequency. CONCLUSIONS: In agreement with previous studies, we have confirmed the high prevalence of bronchial hyperreactivity in primary Sjögren's syndrome; systemic sclerosis likewise appears to be associated with an increased frequency of bronchial hyperreactivity compared with healthy control subjects. There is evidence also that the coexistence of Sjögren's syndrome and systemic sclerosis further increases the frequency and the calculated relative risk of developing bronchial hyperreactivity.

Bronchi↗
PubMed1990

Increased bronchial responsiveness in primary and secondary Sjögren's syndrome.

We examined one group of 33 patients with primary Sjögren's syndrome, one group of 17 patients with secondary Sjögren's syndrome, i.e. associated with other connective tissue diseases, and one group of 14 patients with connective tissue diseases but without Sjögren's syndrome. In each patient we obtained chest radiographs and measured lung volumes, carbon monoxide diffusing capacity and airway responsiveness to methacholine. We observed no difference in chest radiograph abnormalities, in lung volumes and in carbon monoxide diffusing capacity among the three groups. However, we found a slight but significant increase of bronchial responsiveness in patients with primary and secondary Sjögren's syndrome compared with patients with connective tissue disorders but without Sjögren's syndrome. Thus PD20FEV1 methacholine was 1.07 mg (1.2) (geometric mean and GSEM) in primary Sjögren's syndrome, 0.91 mg (1.4) in secondary Sjögren's syndrome (NS), and 2.24 mg (1.09) in patients with connective tissue diseases but without Sjögren's syndrome (t = 2.59 and t = 2.8, both p less than 0.05, vs primary and secondary Sjögren's syndrome, respectively). These results show that some patients with Sjögren's syndrome have mild bronchial hyperresponsiveness, which may be related to the specific airway abnormalities of this disease.

Bronchial Provocation Tests↗