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- Demirci, Umit, et al.
(författare)
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Urovaginal fistula formation after gynaecological and obstetric surgical procedures: Clinical experiences in a Scandinavian series.
- 2013
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Ingår i: Scandinavian journal of urology and nephrology. - : Informa UK Limited. - 1651-2065 .- 2168-1805 .- 2168-1813. ; 47:2, s. 140-144
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Tidskriftsartikel (refereegranskat)abstract
- Abstract Objective. The aim of this retrospective study was to review what kinds of surgical procedures are most frequently complicated by urovaginal fistulae, to find out how they were diagnosed and managed, and to study the outcome after surgical reconstruction. Material and methods. Nineteen women who underwent fistula repair at Sahlgrenska University Hospital between 2003 and 2009 were retrospectively studied by reviewing the medical records. Results. For 17 of the 19 patients hysterectomy was the causative procedure. Fourteen patients developed vesicovaginal and five developed ureterovaginal fistula. Urethrocystoscopy was sufficient for the diagnosis in nearly 50% of the patients and when combined with methylene blue instillation 90% of all fistulae were found. Several patients sought medical advice due to vaginal leakage following gynaecological surgery without the doctor suspecting a fistula, and for these patients the diagnosis was delayed. Eighteen patients were operated on with an abdominal approach and one with a vaginal approach, in all cases a minimum of 3 months after primary surgery. The reconstruction technique included the interposition of vascularized tissue. None of the patients reported leakage or relapse at follow-up after fistula repair. Conclusions. Hysterectomy was the most common cause behind the formation of urovaginal fistulae. Misinterpretation of symptoms after gynaecological surgery was common even in cases where the symptoms were indicative of a urovaginal fistula. Delayed fistula repair after a minimum of 3 months, via the abdominal route and with the interposition of vascularized tissue, yielded an excellent final outcome.
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| 2. |
- Kindblom, Jenny, 1971, et al.
(författare)
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Increased adipogenesis in bone marrow but decreased bone mineral density in mice devoid of thyroid hormone receptors.
- 2005
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Ingår i: Bone. - : Elsevier BV. - 8756-3282. ; 36:4, s. 607-16
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Tidskriftsartikel (refereegranskat)abstract
- Mice deficient for all known thyroid hormone receptors, TRalpha1-/-beta-/- mice, display a clear skeletal phenotype characterized by growth retardation, delayed maturation of long bones and decreased trabecular and total bone mineral density (BMD; -14.6 +/- 2.8%, -14.4 +/- 1.5%). The aim of the present study was to investigate the molecular mechanisms behind the skeletal phenotype in TRalpha1-/-beta-/- mice. Global gene expression analysis was performed on total vertebrae from wild-type (WT) and TRalpha1-/-beta-/- mice using DNA microarray and the results were verified by real-time PCR. The mRNA levels of six genes (AdipoQ, Adipsin, Fat-Specific Protein 27 (FSP 27), lipoprotein lipase (LPL), retinol-binding protein (RBP) and phosphoenolpyruvate carboxykinase (PEPCK)) expressed by mature adipocytes were increased in TRalpha1-/-beta-/- compared with WT mice. An increased amount of fat (225% over WT) due to an increased number but unchanged mean size of adipocytes in the bone marrow of TRalpha1-/-beta-/- mice was revealed. Interestingly, the mRNA levels of the key regulator of osteoclastogenesis, receptor activator of NF-varkappab ligand (RANKL), were dramatically decreased in TRalpha1-/-beta-/- mice. In conclusion, TRalpha1-/-beta-/- mice demonstrated increased expression of adipocyte specific genes and an increased amount of bone marrow fat. Thus, these mice have increased adipogenesis in bone marrow associated with decreased trabecular bone mineral density (BMD). One may speculate that these effects either could be caused by an imbalance in the differentiation of the osteoblast and the adipocyte lineages at the expense of osteoblastogenesis, or by independent effects on the regulation of both osteoblastogenesis and adipogenesis.
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