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To prospectively compare erectile function at 12 months, utilizing the abbreviated International Index of Erectile Function-5 (IIEF-5) score, for men treated with an immediate repair versus a delayed repair.
This was a prospective randomized study conducted at 2 tertiary level institutions in Jamaica, the University Hospital of the West Indies (UHWI) and the Kingston Public Hospital (KPH). All cases of penile fracture were recruited from the emergency room (ER) of both hospitals between the period January 2015 to January 2017 and all patients were over 18 years of age.
Information on demographics, length of time since the injury, mechanism of injury and risk factors for erectile dysfunction (Diabetes mellitus, Hypertension, Dyslipidemia, Smoking) was collected. Erectile function was objectively assessed utilizing the abbreviated International Index for Erectile Function-5 (IIEF-5), and scores at initial presentation were taken to represent the premorbid erectile function.
A block randomization sequence was created and cases were allocated 1:1 to either immediate repair (group 1) or delayed repair (group 2). Allocation sequence numbers were kept concealed in sequentially numbered folders and access was only granted to the principal investigator.
For Group 1 (Immediate repair)
Patients were admitted to hospital and underwent emergency repair via a subcoronal circumferential degloving approach.
For Group 2 (Delayed repair)
Patients were not admitted. Instead, they were discharged from hospital and given an elective surgery date 7 - 10 days after the injury. Oral Diclofenac Sodium 50mg was prescribed to be taken as needed and instructions to abstain from any sexual activity.
All patients were then re-examined at 6 weeks for quality assurance. They were then instructed that resumption of sexual activity would be safe.
Routine clinic visits were scheduled at 3 months, 6 months, and 12 months. IIEF-5 scores were obtained from all patients at 12months.
Immediate repair, Delayed repair, Lidocaine, Ceftriaxone, Diclofenac Sodium
Kingston Public Hospital
Ministry of Health, Jamaica
Published on BioPortfolio: 2018-03-06T21:56:17-0500
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The reconstruction of a continuous two-stranded DNA molecule without mismatch from a molecule which contained damaged regions. The major repair mechanisms are excision repair, in which defective regions in one strand are excised and resynthesized using the complementary base pairing information in the intact strand; photoreactivation repair, in which the lethal and mutagenic effects of ultraviolet light are eliminated; and post-replication repair, in which the primary lesions are not repaired, but the gaps in one daughter duplex are filled in by incorporation of portions of the other (undamaged) daughter duplex. Excision repair and post-replication repair are sometimes referred to as "dark repair" because they do not require light.
A DNA repair enzyme that catalyzes DNA synthesis during base excision DNA repair. EC 184.108.40.206.
The repair of DOUBLE-STRAND DNA BREAKS by rejoining the broken ends of DNA to each other directly.
Repair of DNA DAMAGE by exchange of DNA between matching sequences, usually between the allelic DNA (ALLELES) of sister chromatids.
DNA repair proteins that include the bacterial MutL protein and its eukaryotic homologs. They consist of a conserved N-terminal region with weak ATPase activity, an endonuclease motif, and a C-terminal domain that forms MutL homodimers or heterodimers between MLH1 and the PMS1, MISMATCH REPAIR ENDONUCLEASE PMS2; or MLH3 proteins. These complexes function in DNA repair pathways, primarily DNA MISMATCH REPAIR, where MutL/MLH1 and the MUTS DNA MISMATCH-BINDING PROTEIN are targeted to damaged DNA.
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