Bladder augmentation in children: where have we been and where are we going?

Mitchell, Michael E.

doi:10.1046/j.1464-410x.92.s1.6.x

Cited by 24 publications

(12 citation statements)

References 97 publications

(94 reference statements)

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“…Chronic bladder diseases cause reduced contractility and compliance, form heavy scar tissue, and significantly reduce bladder volume (end-stage bladder disease). To treat invasive malignancies or end-stage bladder diseases, a partial or total cystectomy is often used, followed by the creation of a neo-bladder or a continent urinary reservoir with an intestinal segment or gastric flap [1] to restore bladder function and increase its volume. However, using bowel tissue for this purpose commonly causes complications, such as excess mucus secretion, urinary tract infection, stone formation, and, most importantly, increased risk for malignancy, particularly adenocarcinoma, because of histological changes in the intestinal mucosa after long-term exposure to urine.…”

Section: Introductionmentioning

confidence: 99%

Urine-derived stem cells for potential use in bladder repair

et al. 2014

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Engineered bladder tissues, created with autologous bladder cells seeded on biodegradable scaffolds, are being developed for use in patients who need cystoplasty. However, in individuals with organ damage from congenital disorders, infection, irradiation, or cancer, abnormal cells obtained by biopsy from the compromised tissue could potentially contaminate the engineered tissue. Thus, an alternative cell source for construction of the neo-organ would be useful. Although other types of stem cells have been investigated, autologous mesenchymal stem cells (MSCs) are most suitable to use in bladder regeneration. These cells are often used as a cell source for bladder repair in three ways - secreting paracrine factors, recruiting resident cells, and trans-differentiation, inducing MSCs to differentiate into bladder smooth muscle cells and urothelial cells. Adult stem cell populations have been demonstrated in bone marrow, fat, muscle, hair follicles, and amniotic fluid. These cells remain an area of intense study, as their potential for therapy may be applicable to bladder disorders. Recently, we have found stem cells in the urine and the cells are highly expandable, and have self-renewal capacity and paracrine properties. As a novel cell source, urine-derived stem cells (USCs) provide advantages for cell therapy and tissue engineering applications in bladder tissue repair because they originate from the urinary tract system. Importantly, USCs can be obtained via a noninvasive, simple, and low-cost approach and induced with high efficiency to differentiate into bladder cells.

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Section: Introductionmentioning

confidence: 99%

Urine-derived stem cells for potential use in bladder repair

et al. 2014

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“…Such microenvironmental effects may be highly dependent on the tissue origin of cells. Augmentation cystoplasties, bladder reconstruction procedures in which gastrointestinal tissue is used to repair the urinary bladder (reviewed in depth by Mitchell [1]), are an example of the tissue-specific microenvironment response. Such cystoplasties have an approximately 600-fold increased risk of malignancy in the anastomosed gastrointestinal tissue compared to the risk of bladder cancer in the general population [2].…”

Section: Introductionmentioning

confidence: 99%

Increased cancer risk of augmentation cystoplasty: Possible role for hyperosmolal microenvironment on DNA damage recognition

Dixon¹,

Chu²,

Henry³

et al. 2009

Mutation Research/Fundamental and Molecular Mechanisms of Mutag

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Patients who have had surgical bladder augmentation have an increased risk of bladder malignancy, though the mechanism for this increased risk is unknown. Hyperosmolal microenvironments such as the bladder may impair DNA damage signaling and repair; this effect may be more pronounced in tissues not normally exposed to such conditions. Comparing gastric and colon epithelial cell lines to transitional epithelial cell lines gradually adapted to an osmolality of 600mOsm/kg with either sodium chloride or urea, cell lines of gastrointestinal origin were inhibited in their ability to activate ATM and downstream effectors of DNA damage signaling and repair such as p53, Nbs1, replication protein A (RPA), and γH2AX following the induction of DNA damage with etoposide. In contrast, bladder cell lines demonstrated a preserved ability to phosphorylate ATM and its effectors under conditions of hyperosmolal urea, and to a lesser extent with sodium chloride. The bladder cell lines' ability to respond to DNA damage under hyperosmolal conditions may be due in part to protective mechanisms such as the accumulation of intracellular organic osmolytes and the uroplakincontaining asymmetric unit membrane as found in transitional epithelial cells, but not in gastrointestinal cells. Failure of such protective adaptations in the tissues used for augmentation cystoplasties may place these tissues at increased risk for malignancy.

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“…Bladder augmentation is necessary in only 15% of cases. [1][2][3] In these patients secondary VUR can be resolved by the increase in bladder capacity and compliance and the decrease in high intravesical pressure achieved by bladder augmentation. There is no uniform concept and practice in the literature as to whether reimplantation of the refluxing ureters is necessary during augmentation cystoplasty in children with dysfunctional bladder, or whether augmentation alone is sufficient for the treatment of secondary VUR.…”

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confidence: 99%