Nociceptive related microRNAs and their role in rheumatoid arthritis.

Rheumatoid Arthritis (RA) is an autoimmune disease with unknown etiology and a global incidence around 1%, a positive family history increases the risk of RA roughly three to five times. Pain is one of the first symptoms to appear in this disease. MicroRNAs (miRNAs) belong to the class of small non-coding RNAs; they regulate multiple cellular processes including embryonic development, cellular proliferation, differentiation and apoptosis among others. A great deal of evidence points to the employment of miRNAs as therapeutic targets and biomarkers for several pathologies. The main objective of this Review is to assess how miRNAs participate in the pathogenesis of RA. Two advanced searches were conducted in databases, one using "micro-RNA" and "rheumatoid arthritis" as key words, and another one with "micro-RNA", "pain" and "nociception". In this Review, we describe how six miRNAs: miR-16-5p, miR-23b-3b, miR-124-3p, miR-146a-5p, miR-155-5p and miR-223-3p, involved in the modulation and transmission of the nociceptive input are unregulated in RA patients. Key molecular pathways involved in nociception, inflammation and autoimmune responses, are regulated by these miRNAs; the NF-κB, TNF-α, interleukins and TLR4. By means of gene repression, the miRNAs here described modulate the nociceptive process as well as the autoimmune response that characterize this disease.

[Polyarthritis flare in patient with ankylosing spondylitis treated with infliximab]. / Poliartrite febbrile in paziente affetto da spondilite anchilosante in trattamento con infliximab.

Over the last ten years, the treatment of seronegative spondyloarthropathies has changed dramatically with the introduction of the anti-tumor necrosis factor alpha (TNFα) agents. Nevertheless, there is a growing number of studies describing several adverse reactions in patients treated with biological agents. In the present report we describe the case of a 22-year-old male patient with ankylosing spondylitis who developed a "paradoxic" adverse reaction, while receiving infliximab.

[Gitelman syndrome associated with chondrocalcinosis: description of two cases]. / Sindrome di Gitelman associata con condrocalcinosi: descrizione di due casi.

Gitelman syndrome is a rare inherited tubulopathy, characterized by hypomagnesemia, hypokalemia, metabolic alkalosis, hypocalciuria and hyperreninemic hyperaldosteronism. The clinical spectrum is wide and includes: cramps, myalgias, muscle weakness, until episodes of carpo-podalic spasm, tetania, rhabdomyolysis and paralysis. Some cases have been described in literature underlining the association of this condition with chondrocalcinosis, as a typical example of hypomagnesemia-induced crystal deposition disease. The therapy of Gitelman syndrome consists on the administration of defective electrolytes, although not always effective. We describe two cases of Gitelman syndrome associated with chondrocalcinosis showing the wide range of presentation of this clinical condition.

[Severe drug hypersensitivity syndrome due to sulphasalazine in patient with rheumatoid arthritis]. / Grave sindrome da ipersensibilità a farmaci indotta da sulfasalazina in paziente con artrite reumatoide.

Drug Hypersensitivity Syndrome, also known as Drug Rash with Eosinophilia and Systemic Symptoms is a severe adverse reaction characterized by clinical manifestations including fever, skin eruption, lymphoadenopathy, associated with eosinophilia, leukocytosis and multiple visceral involvement, with 10% of mortality due to development of multiple organ failure. This reaction usually occurs between two and six-eight weeks after the beginning of the treatment and may not resolve with interruption of the suspected drug. Sulfonamides, anticonvulsant, allopurinol are the most frequently involved molecules, but recently cases have been described also with gabapentin and strontium ranelate. In the present report we describe a case of a patient with rheumatoid arthritis who presented severe drug hypersensitivity syndrome, with liver and kidney involvement due to sulphasalazine.

[The ultrasound assessment of the psoriatic arthritis: from joint to skin]. / L'ecografia nella valutazione della artrite psoriasica: dalla articolazione alla cute.

There is a growing number of papers investigating the diagnostic potential of ultrasonography in the assessment of patients with psoriatic arthritis and supporting its higher sensitivity over clinical examination in the diagnosis of synovitis, enthesitis and tenosynovitis. Less attention has been paid on both skin and nail, frequently involved in this condition. The aim of this paper is to show the potential of ultrasound in a multi-target assessment (joints, tendons, entesis, skin and nails) in patients with psoriatic arthritis, using the last generation ultrasound equipment.

Megatherapy combining I(131) metaiodobenzylguanidine and high-dose chemotherapy with haematopoietic progenitor cell rescue for neuroblastoma.

Despite the use of aggressive chemotherapy, stage 4 high risk neuroblastoma still has very poor prognosis which is estimated at 25%. Metabolic radiotherapy with I(131) MIBG appears a feasible option to enhance the effects of chemotherapy. Seventeen patients having MIBG-positive residual disease received 4.1-11.1 mCi/kg of I(131) MIBG 7-10 days before initiating the high-dose chemotherapy cycle consisting of busulphan 16 mg/kg and melphalan 140 mg/m(2) followed by PBSC infusion. We compared the toxicity in these patients to that seen in 15 control subjects with neuroblastoma who underwent a PBSC transplant without MIBG therapy. We observed greater toxic involvement of the gastrointestinal system in children treated with I(131) MIBG: grade 2 or 3 mucositis developed in 13/17 patients treated with I(131) MIBG and in 9/15 treated without it. Grade 1-2 gastrointestinal toxicity occurred in 12/17 children given MIBG and in 5/15 of the controls. One child receiving I(131) MIBG developed transient interstitial pneumonia. Another child who also received I(131) MIBG after PBSC rescue developed fatal pneumonia after the third course of metabolic radiotherapy. Our experience indicates that MIBG can be included in the high-dose chemotherapy regimens followed by PBSC rescue for children with residual neuroblastoma taking up MIBG. Attention should be paid to avoiding lung complications. Prospective studies are needed to demonstrate the real efficacy of this treatment.