Multicenter study of the safety/efficacy of misoprostol in the prevention and treatment of NSAID-induced gastroduodenal lesions.

Gastrointestinal symptoms and lesions are often associated with the clinical use of non-steroidal antiinflammatory drugs (NSAIDs). An open-label, single arm multicenter Italian study evaluated if misoprostol, a prostaglandin E1 analogue with gastroduodenal mucosal protective activity, was effective in the prevention and treatment of NSAID-induced gastroduodenal lesions. Patients affected by rheumatoid arthritis (RA) or osteoarthritis (OA), in treatment with NSAIDs and suffering from gastric symptoms or gastroduodenal lesions related to NSAID use, were admitted to the study. Gastrointestinal and arthritic symptoms were assessed before and after 4 weeks co-administration of an NSAID (the most frequent was diclofenac, used in 35% of the RA and in 22% of the OA patients, followed by piroxicam and tenoxicam respectively) + misoprostol (200 mcg two times daily in 58% of the cases, 200 mcg three times daily in 39%, 200 mcg four times daily in 3%). On admission and after 4 weeks of therapy a gastrointestinal endoscopy was performed to evaluate the condition of the gastroduodenal mucosa. Final results showed that: (i) NSAID-related gastric lesions were more frequent than duodenal lesions; (ii) when patients were given misoprostol and NSAIDs, 96% of them did not develop gastric lesions and 97% did not develop duodenal lesions; (iii) even when NSAID therapy was continued, gastric or duodenal lesions induced by NSAIDs healed or in any case did not worsen in 92% and 91% respectively of the cases; (iv) during the period of coadministration of NSAIDs+misoprostol, NSAID-related UGI symptoms disappeared or improved in 77% of the cases.(ABSTRACT TRUNCATED AT 250 WORDS)

History of hypertrophic osteoarthropathy (HOA).

Hypertrophic osteoarthropathy (HOA) was first described in 1868 as "hyperostosis of the entire skeleton". It has also been mistaken for acromegaly. In 1887-1888 the first description was given of a dermatological disorder "cutis verticis girata" which coexisted with the peculiar bone anomalies of HOA. In 1890 HOA was named "osteoarthropatie hypertrophiante pneumique". Later a distinction was made between the rare idiopathic (or primary) form, also called "pachydermoperiostosis" and the more common secondary form due to concomitant disorders involving the lungs and pleura. The primary form usually develops shortly after puberty or during adolescence and has not been found associated with underlying disease. Secondary HOA was initially called "hypertrophic pulmonary osteoarthropathy" because it is frequently associated with various malignancies or chronic infections of the lung and pleura. Later, since the site of primary disease may be elsewhere, involving the gut and the cardiovascular, hepatobiliary and endocrine systems, this designation fell into disuse. In some cases of secondary HOA, the osteoarthropatic and facial skin changes subside after pneumonectomy or other procedures. A disease resembling human HOA has been also described in dogs.

Nerve growth factor in the synovial fluid of patients with chronic arthritis.

Cytokines regulate nerve growth factor (NGF) synthesis during inflammatory processes. Since cytokines are also involved in the inflammatory processes of autoimmune rheumatic diseases, we examined levels of NGF in patients with rheumatoid or other types of chronic arthritis. NGF was present in the synovial fluid and synovium of patients with chronic arthritis, but was undetectable in control fluids. We conclude that NGF might be involved in the pathogenesis of arthritis.

Collagenopathic cardiopathies.

Collagenopathic cardiopathies are a subject of extreme etiologic, pathogenetic and clinical interest. These disorders are associated with congenital or acquired anomalies of the connective tissue and because of the diffusion and nearly total distribution of this tissue, have a higher frequency than what has been previously estimated. The collagenopathic cardiopathies, can be divided into two main groups: one deriving from hereditary connective tissue diseases, and the other from acquired connective tissue diseases. The first group has a Mendelian type of transmission whereas the other appears to be secondary to various kinds of stimuli (viral, immunologic etc.) although polygenic factors are present. Of the first group we considered Marfan's syndrome, the Ehlers-Danlos syndrome, osteogenesis imperfecta, pseudoxanthoma elasticum, cutis laxa and the diseases of the fundamental substance with particular reference to mucopolysaccharidosis type 1H (Hurler's syndrome). In all of these disorders a specific metabolic disturbance is responsible for the cardiovascular damage which is expressed, depending on the specific genetic component in a more or less serious form. Among the acquired diseases of the connective tissue, we examined rheumatoid arthritis, systemic lupus erythematosus, polydermatomyositis, scleroderma; of the reactive arthritis, rheumatic fever; of the seronegative forms, spondyloarthritis, ankylosing spondylitis and Reiter's syndrome, mixed connective tissue disease and Lyme's disease. It must be emphasized that all of these disorders share relatively common pathogenetic characteristics which point to the importance of the presence of various types of antigens, immune complexes and the significant role of some of the histocompatibility antigens, as well as possible disturbances of cell-mediated immunity.(ABSTRACT TRUNCATED AT 250 WORDS)

Prevalence and clinical associations of anticardiolipin antibodies in systemic lupus erythematosus: a prospective study.

The main objectives of the present study were to determine the prevalence of IgG and IgM anticardiolipin antibody (aCL) isotypes in systemic lupus erythematosus (SLE) in order to analyze their possible association with the clinical manifestations of the disease. Clinical features of 64 consecutive and unselected SLE patients were prospectively studied. Sera from the same patients taken during each clinical manifestation were tested for the presence of aCL. The prevalence of aCL was 43.75% for the IgG isotype and 9.4% for the IgM isotype. A strong linkage between the presence of these antibodies and the occurrence of both thrombosis and abortions was found: a weaker association with neurological events and thrombocytopenia was also demonstrated. The titre of aCL appeared to be linked with the probability of having the clinical manifestations associated with these autoantibodies. Our results suggest that thrombosis and abortion, and possibly thrombocytopenia and central nervous system involvement, may be associated with the presence of aCL at the time when these clinical events develop in SLE patients.

Cytotoxic drugs in systemic autoimmune diseases.

Inhibition of cell proliferation, together with the depression of synthesis of non-specific and specific cellular products, are the modes of action of cytotoxic drugs. In systemic autoimmune diseases these actions result in immunosuppressive and anti-inflammatory effects. The adoption of cytotoxic treatment, as well as the choice of the cytotoxic agent and therapeutic strategy in individual patients, depend on the disease status, on the patient's tolerance to previously administered drugs and on the theoretical risk of major side effects. The oncogenic risk and its relationship with the cumulative dose or the duration of traditional administration schedules must be taken into account, even if this is not constant for all cytotoxic drugs. Both in life-threatening and in seriously disabling systemic autoimmune diseases cytotoxic drugs are employed, according to general guidelines, to induce complete or partial remission of active disease in patients intolerant or refractory to corticosteroids and/or to other disease-modifying drugs. Combinations of cytotoxic drugs and other non-specific immunosuppressive agents as well as innovative therapeutic regimens (pulse therapy, alternation of treatments) have been used with encouraging results: in the future cytotoxic drugs may perhaps be used in association with specific immunosuppressive agents in a complementary combination to halt pathologic processes in systemic autoimmune diseases.

Iron overload and lysosomal stability in beta zero-thalassaemia intermedia and trait: correlation between serum ferritin and serum N-acetyl-beta-D-glucosaminidase levels.

Increased iron storage represents a characteristic condition in patients with beta zero-thalassaemia intermedia. Iron overload is an important factor in cellular damage. Recent studies have shown an enhanced lysosomal fragility due to increased iron storage. 13 patients with beta-thalassaemia intermedia, aged 17-44 years, were studied. Both serum ferritin and serum N-acetyl-beta-D-glucosaminidase levels were evaluated in all subjects studied. A significant linear correlation (P less than 0.05) between serum ferritin and serum N-acetyl-beta-D-glucosaminidase levels were found.

[Familial Mediterranean fever. Description of a case observed by us]. / La febbre familiare mediterranea. Descrizione di un caso di nostra osservazione.

Familial mediterranean fever (FMF) is an hereditary disorder characterized by attacks of febrile serosal inflammation involving pleura or peritoneum and synovium, followed usually by insidious onset of amyloidosis. In other patients amyloidosis of AA-type is the only finding of the disease. This disorder is common in Jews of Sephardi and Ashkenazi ancestry, Arabs, Armenians and Turks. In this work the clinico-biological features and the therapeutical aspects of a patient, suffering from FMF, of Italian ancestry are presented.