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Copyright of Ginecologia.ro is the property of MEDICHUB MEDIA, S.R.L. and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Ginecologia.ro is the property of MEDICHUB MEDIA, S.R.L. and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

We present the case o f a 73 year-old woman w ith multiple cardiovascular risk factors which had been administered Rosuvastatin 20 mg/day for approximately 2 months, The patient presented to the emergency department for onset of myalgia, loss of muscle strength and fatigue. Clinical examination revealed tetramelic proximal muscle weakness, tetramelic hypotonia and symmetrically diminished reflexes. Atrophy of the shoulder girdle muscles was noted, especially the deltoid and trapezius muscles bilaterally. Initial Wood work was unremarkable save for severe muscle enzyme elevation ("30 x normal values) and kidney failure. Electromyography was undertaken and it showed a myopathic pattern at the level of the proximal muscles. The patient was diagnosed at this stage w ith myopathy of unknown origin possibly triggered by statin administration and a muscle biopsy was requested. At the same tim e a panel fo r determining autoimmune myositis antibody titers was ordered. Left bicep brachialis biopsy revealed a severe necrotizing inflammatory myositis with active lesions and elements suggestive for dermatomyositis. Mi-2 serum antibodies turned out positive from the panel ordered which are high in specificity for dermatomyositis (without other pathological elements). Serum tumor markers and abctomino-petvic ultrasonography showed no elements of neoplasia. The patient was treated with corticosteroids under which symptoms and serum enzymes steadily decreased. The patient was referred to a rheumatology clink for steroid sparing immunosuppressive treatment initiation. Abdomino-pefvic computed tomography and oncological follow-up was recommended as dermatomyositis of paraneoplastic origin is common in this age group. [ABSTRACT FROM AUTHOR]

Introduction, Neurogenic detrusor oweractivitv(NDQ) is the condition where the detrusor overactivity is caused by a disturbance of nervous control mechanism with evidence of a relevant neurological disorder. The overall burden o f NDO is quite high: 65% of M ultiple Sclerosis (MSj patients have signs of NDO, and about 50% o f subjects w ith MS confront w ith urge urinary incontinence; for traumatic Spinal Cord Injury (SCI), about 80% of these patients are developing NDO, w ith a prevalence of urge urinary incontinence of approximately 50%, EAU Guidelines 2015 recommend higher doses or combination of antimuscarinic agents as an option to maximize the outcome of therapy in patients w ith neurological impairment. For patients who abort anticholinergic drugs due to the adverse events or for those who are unresponsive to antimuscarinic agents, the use of botulinum toxin A administered as intradetrusor injections has emerged as an effective alternative. Material and method. The goal was to assess the efficacy of botulinum toxin a for the treatment o f NOO. From the patients reffered to us with MS or SCI, 22 patients with urodynamicaly diagnosed NDO were included in the study, with at least 1 episode o f urinary incontinence per 24 hours on a 2 Day bladder diary. They underwent intravesical therapy w ith Botulinum toxin, We used Botox 200 u, which was injected cystoscopies ily into the detrusor muscle in 30 different sites, sparing the bladder trigone. The patients were followed at 3 months w ith urodynamic tests and the parameters (MCC and MDP) were significantly improved in all patients. In terms o f clinical outcomes, they reported a decrease in the urinary incontinence episodes, frequency and urgency episodes. No major adverse events were reported. The second follow-up is scheduled at 6 months and is under way. Conclusion. Botulinum toxin A appears to be a feasible second line treatment for patients w ith neurogenic detrusor overactivity non responsive or who fail to tolerate anticholinergic medication. [ABSTRACT FROM AUTHOR]