[Show abstract][Hide abstract] ABSTRACT: Vulvovaginitis has a known association with urinary tract infections (UTIs) in girls. We hypothesize that vulvovaginitis is a major contributor to UTIs in prepubertal girls by increasing periurethral colonization with uropathogens.
Periurethral swabs and urine specimens were obtained from a total of 101 girls (58 with vulvovaginitis and 43 without vulvovaginitis). Specimens were cultured for bacterial growth. The dominant organism in the periurethral swabs and urine cultures was recorded and antibiotic sensitivity profiles were compared.
Periurethral swabs from children with vulvovaginitis were associated with a statistically significant increase in uropathogenic bacteria (79% Enterococcus species or Escherichia coli) as the dominant culture compared with swabs from girls without vaginitis (18%) (p < 0.05). In children with vulvovaginitis, 52% of the urine cultures were positive for UTIs, and the dominant organism in the urine cultures matched the species and antibiotic sensitivity profile of the corresponding periurethral swab. Only 11% of the urine cultures from girls without vulvovaginitis were positive for UTIs.
Vulvovaginitis may cause UTIs by altering the perineal biome such that there is increased colonization of uropathogens.
No preview · Article · Dec 2014 · Therapeutic Advances in Urology
[Show abstract][Hide abstract] ABSTRACT: Objective
To determine whether age of toilet training is associated with dysfunctional voiding in children.
Materials and methods
We compared patients referred to the urologic clinics for voiding dysfunction with age-matched controls without urinary complaints. Characteristics including age and reason for toilet training, method of training, and encopresis or constipation were compared between both groups.
Initiation of toilet training prior to 24 months and later than 36 months of age were associated with dysfunctional voiding. However, dysfunctional voiding due to late toilet training was also associated with constipation.
Dysfunctional voiding may be due to delayed emptying of the bowel and bladder by children. The symptoms of dysfunctional voiding are more common when toilet training early, as immature children may be less likely to empty in a timely manner, or when training late due to (or in association with) constipation.
Full-text · Article · Oct 2014 · Research and Reports in Urology
[Show abstract][Hide abstract] ABSTRACT: The objective of this review article is to present the current literature on medical expulsive therapy (MET) and help guide practitioners in the appropriate use of MET for treatment of stone disease. Kidney stones can be treated with multiple modalities including medical therapy, ureteroscopy, shock wave lithotripsy (SWL), percutaneous nephrostolithotomy, open/laparoscopic stone removal, and/or combinations of these modalities. The choice of intervention depends on patient factors, anatomical considerations, surgeon preference, and stone location and characteristics. MET is an excellent treatment modality in the appropriately selected patient. The AUA/EAU guidelines suggest MET as a reasonable treatment choice in select patients. A review of the data suggests the use of alpha antagonist and calcium channel blockers can improve stone expulsion rates. Most data suggests alpha antagonists as superior to calcium channel blockers. There are numerous available alpha antagonists, all of which have supporting data for their use in MET. Evidence suggests that MET can decrease colic events, narcotic use, and hospital visits. MET may also reduce medical costs and prevent unnecessary surgeries and the associated risks. Further, there is a role for alpha antagonists and calcium channel blockers in improving stone passage and decreasing pain in those subjects treated with other modalities (i.e. SWL and ureteroscopy). Despite this evidence, MET remains underutilized as a treatment modality.
No preview · Article · Feb 2014 · Indian Journal of Urology
[Show abstract][Hide abstract] ABSTRACT: Background / Purpose:
Post-therapy bladder neck contractures can be a challenge to treat. Some reports of transurethral injection of scars with various agents have shown promise. We compare use of intralesional injection with mitomycin C and tacrolimus combined with TUIBN in a 10-patient cohort.
At a median of 7.5 months follow up, it seems that intralesional injection combined with transurethral incision can provide potency.
[Show abstract][Hide abstract] ABSTRACT: Urethral strictures are from periurethral spongiofibrosis that develops as a result of urethral trauma, disease, or iatrogenic injury. The spongy tissue that surrounds the strictured urethra has an altered ratio of collagen, with increased collagen type I relative to type III. We evaluated the ability of a urethral catheter that was coated with halofuginone (HF), a potent type I collagen inhibitor, to prevent spongiofibrosis formation in a rat model.
HF was coated on silicone catheters and release kinetics were measured. Success of impregnation was evaluated with scanning electron microscopy, serial weights, and drug elution data. Urethral strictures were induced in rats using electrocautery. Half the animals had placement of an HF-coated catheter while the others had uncoated silicone controls. Animals were sacrificed at predetermined time points, and urethral tissue was either processed for staining with Masson trichrome and anti-alpha-1 collagen or digested to determine HF concentration. Serum drug levels were also determined in treated animals. Slides were graded by a pathologist who was blinded to treatment to determine collagen deposition.
HF was coated successfully on silicone catheters. Local urethral concentration of HF was tenfold higher than serum concentration in treated rats. Animals with HF-coated catheters had no new type I collagen deposition after urethral injury. Control animals had increased periurethral collagen type I deposition, typical of urethral stricture formation.
HF can be coated successfully on silicone catheters. HF successfully inhibits periurethral type I collagen deposition after urethral injury. This may become an important therapy to prevent urethral stricture formation or recurrence after endoscopic therapy.
No preview · Article · Jan 2011 · Journal of endourology / Endourological Society
[Show abstract][Hide abstract] ABSTRACT: Metabolic syndrome (MetS) is a complex entity consisting of multiple interrelated factors including insulin resistance, central adiposity, dyslipidemia, endothelial dysfunction and atherosclerotic disease, low-grade inflammation, and in males, low testosterone levels. MetS has been linked to a number of urologic diseases including nephrolithiasis, benign prostatic hyperplasia and lower urinary tract symptoms, erectile dysfunction, male infertility, female incontinence, and prostate cancer. This article reviews the relationships between MetS and these entities. Urologists need to be cognizant of the impact that MetS has on urologic diseases as well as on overall patient health.
Full-text · Article · Jan 2010 · Reviews in urology
[Show abstract][Hide abstract] ABSTRACT: By removing UV-induced lesions from DNA, the nucleotide excision repair (NER) pathway preserves the integrity of the genome. The UV-damaged DNA-binding (UV-DDB) protein complex is involved in the recognition of chromatin-embedded UV-damaged DNA, which is the least understood step of NER. UV-DDB consists of DDB1 and DDB2, and it is a component of the cullin 4A (CUL4A)-based ubiquitin ligase, DDB1-CUL4A(DDB2). We previously showed that DDB1-CUL4A(DDB2) ubiquitinates histone H2A at the sites of UV lesions in a DDB2-dependent manner. Mutations in DDB2 cause a cancer prone syndrome, xeroderma pigmentosum group E (XP-E). CUL4A and its paralog, cullin 4B (CUL4B), copurify with the UV-DDB complex, but it is unclear whether CUL4B has a role in NER as a separate E3 ubiquitin ligase. Here, we present evidence that CUL4A and CUL4B form two individual E3 ligases, DDB1-CUL4A(DDB2) and DDB1-CUL4B(DDB2). To investigate CUL4B's possible role in NER, we examined its subcellular localization in unirradiated and irradiated cells. CUL4B colocalizes with DDB2 at UV-damaged DNA sites. Furthermore, CUL4B binds to UV-damaged chromatin as a part of the DDB1-CUL4B(DDB2) E3 ligase in the presence of functional DDB2. In contrast to CUL4A, CUL4B is localized in the nucleus and facilitates the transfer of DDB1 into the nucleus independently of DDB2. Importantly, DDB1-CUL4B(DDB2) is more efficient than DDB1-CUL4A(DDB2) in monoubiquitinating histone H2A in vitro. Overall, this study suggests that DDB1-CUL4B(DDB2) E3 ligase may have a distinctive function in modifying the chromatin structure at the site of UV lesions to promote efficient NER.