Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0403608 (ureter)
 9,655 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Exocrine secretions of 16 of 22 pancreas allografts were drained into the urinary tract. Seven of these 16 patients have functioning allografts, six with pancreaticocystostomies and one with duct-to-ureter anastomosis. A notable problem has been a chronic metabolic acidosis, along with weight loss and hypotension, secondary to chronic bicarbonate loss and volume depletion through the urinary pancreatic fistula. This occurred as early as one week posttransplant, and intermittently thereafter up to four years. The syndrome was aggravated by episodes of renal dysfunction (acute tubular necrosis or rejection), and febrile syndromes. An inverse relationship between serum and urine bicarbonate concentrations existed, with a correlation coefficient, r = -0.746, (P less than 0.05). A negative correlation was also noted between serum bicarbonate and serum creatinine, r = 0.726, (P less than 0.05). Hyperchloremic metabolic acidosis with normal anion gap occurred despite periods of marginal pancreas allograft function resulting from ongoing rejection. Treatment consisted of intravenous and/or oral bicarbonate supplementation, and bicarbonate dialysis for uremic patients. In addition, one patient was first seen with severe balanitis and urethritis due to documented activation of trypsinogen and chymotrypsinogen, presumably caused by recurrent episodes of urinary tract infection. Urinary assay revealed a 10(2-3) increase in activated trypsin and chymotrypsin in comparison with other asymptomatic allograft recipients. Conversion to ductal enteric drainage led to resolution of both the balanitis and bicarbonate wasting. Measurement of urinary amylase levels were gross indicators of graft viability since no correlation could be found between these levels, onset of hyperglycemia, and eventual graft rejection confirmed by pathological examination.
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PMID:Pancreatic allograft exocrine urinary tract diversion. Pathophysiology. 243 6

Symptomatic clinical changes and urodynamic changes are apparent in the female urinary tract system during pregnancy, the menstrual cycle and following the menopause. The sex hormones exert physiological effects on the female urinary tract, from the ureters to the urethra, with oestrogens having an additional influence on the structures of the pelvic floor. High affinity oestrogen receptors have been identified in bladder, trigone, urethra and pubococcygeus muscle of women. Oestrogen pretreatment enhances the contractile response of animal detrusor muscle to alpha-adrenoceptor agonists, cholinomimetics and prostaglandins, as well as enhancing the contractile response to alpha-agonists in ureter and urethra. Progesterone on the other hand decreases tone in the ureter, bladder and urethra by enhancing beta-adrenergic responses. The dependence on oestrogens of the tissues of the lower urinary tract contributes to increased urinary problems in postmenopausal women. Urinary symptoms due to atrophic mucosal changes respond well to oestrogen replacement therapy. However, because they recur when treatment is stopped, continuous therapy with low dose natural oestrogens is recommended. Oestrogens may be of benefit in postmenopausal women with stress incontinence, but the doses necessary for clinical effect are higher than for the treatment of atrophic urethritis. The practice of adding a progestagen to long term oestrogen therapy to reduce the risk of endometrial carcinoma may, however, exacerbate stress incontinence by decreasing urethral pressure. Cyclical therapy with oestrogens may therefore be more appropriate particularly in women who are not suitable for surgery or have a mild degree of stress incontinence, along with other conservative measures such as pelvic floor exercises and alpha-adrenoceptor agonists. The place of oestrogen therapy in motor urge incontinence has not been determined. The risk of developing endometrial carcinoma as a result of long term high dose oestrogen replacement therapy must be borne in mind but remains to be clarified. However, oestriol has less of a uterotrophic effect compared to other oestrogens in standard therapeutic doses and is to be preferred. Side effects are usually dose related and tend not to be a problem with low dose therapy.
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PMID:Sex hormones and the female urinary tract. 306 38

Suboperative observations of 73 patients have shown that lower polar renal vessels are often associated with other abnormalities (congenital fibrosis and segmentary hypoplasia of the parapelvic portion of the ureter resulting in the development of hydronephrosis, chronic urethritis, atrophy of the muscle layer and secondary stenosis of the ureter). The operation of choice is resection of the pyeloureteral segment and part of the pelvis followed by antevasal anastomosis.
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PMID:[Surgical treatment of compression of the parapelvic portion of the ureter by the lower polar renal vessels in children]. 370 52

The imaging appearances of prostate cancer are well described in the radiology literature, but little has been written about the detection and appearance of the complications of therapy for this disease. The most frequently used treatments for prostate cancer are surgical therapy (eg, radical retropubic prostatectomy, radical perineal prostatectomy), radiation therapy (eg, brachytherapy, external-beam radiation therapy, three-dimensional conformal radiation therapy, intensity-modulated radiation therapy), and cryoablative therapy, each of which may lead to complications with characteristic imaging appearances. Possible complications include lymphocele formation; injuries to the ureter, rectum, and urethra; prostatic necrosis; vesicourethral anastomotic leak and stricture; urethral stricture, necrosis, and fistula; radiation proctitis; transient bladder outlet obstruction; radiation-induced urethritis; urinary incontinence; and erectile dysfunction. With improvements in surgical techniques and advances in technology, complications of therapy for prostate cancer are decreasing but still occur with sufficient frequency to warrant familiarity on the part of radiologists. Knowledge of the diverse spectrum of these complications and their characteristic radiologic features facilitates prompt diagnosis and treatment.
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PMID:Complications of prostate cancer treatment: spectrum of imaging findings. 1548 40

Polypoid cystitis and its more chronic phase papillary cystitis, which results as a reaction to injury to the bladder mucosa, is a benign lesion mimicking various papillary urothelial neoplasms. Analogous lesions occur throughout the urothelial tract and are referred to as polypoid urethritis, polypoid ureteritis, and polypoid pyelititis when present in the urethra, ureter, and renal pelvis, respectively. For simplicity, these lesions in different sites and papillary cystitis will typically be referred to as polypoid cystitis in this manuscript. A search of the consultation files from our institution from January 2000 to July 2007 was performed. Of 155 cases diagnosed as polypoid cystitis, we identified 41 cases that were diagnosed as papillary urothelial neoplasms by contributing pathologists and only sent to us, typically at the request of the urologist after the case had be signed out. For cases where information was available, clinical symptoms included bladder obstruction (n=7), gross hematuria (n=6), colovesicular fistula (n=4), follow-up status posttreatment of bladder and ureter carcinoma (n=4), bladder/urethral stones (n=2), benign prostate hyperplasia (n=2), follow-up after radiation for prostate cancer (n=2), long-standing urinary stents (n=2), and voiding dysfunction (n=1). Original diagnoses included noninvasive low grade papillary urothelial carcinoma (n=23), noninvasive high grade papillary urothelial carcinoma (n=6), papillary urothelial neoplasm of low malignant potential (n=5), papilloma (n=3), urothelial neoplasia (n=2), carcinoma in situ (n=1), and squamous carcinoma (n=1). The mean age at diagnosis was 63 years (range, 19 to 93 y; median 63 y). Male to female ratio was 3.1 to 1. Clinical symptoms varied with the most common manifestations, including gross hematuria, bladder/urethral stones, history of prostate cancer treated with radiation, follow-up after bladder/ureter carcinoma treatment, long-term urinary stents, and colovesicular fistulas. At cystoscopy, lesions were variably described as polypoid, trabeculations, bullous polyps, and diffuse erythema and edema. The locations of polypoid cystitis were bladder (n=34), ureteral orifice (n=2), urethra (n=2), renal pelvis (n=2), and undesignated (n=1). Architecturally, 31 cases had isolated papillary fronds with in 1 case branching papillary structures. The base of the papillary stalks were characterized as both broad and narrow (n=24), only broad (n=9), and only narrow (n=3). The overlying urothelium of polypoid cystitis was diffusely and focally thickened in 8 cases and 5 cases, respectively. Umbrella cells were identified in 32 cases. Acute and chronic inflammation was present in 28 cases, moderate in 15, and mild in 13 cases. Eleven cases showed chronic inflammation, mild in 10, and moderate in 1 case. Reactive urothelial atypia was noted in 26 cases with mitotic figures present in 22 cases, frequent in 3 and rare in 19 cases. Stroma edema was seen in 32 cases with fibrosis within the polypoid stalks seen in 16 cases. The key to correctly diagnosing polypoid/papillary cystitis is to recognize at low magnification the reactive nature of the process with an inflamed background that is edematous or densely fibrous with predominantly simple, non-branching, broad-based fronds of relatively normal thickness urothelium, and not focus at higher power on the exceptional frond that may more closely resemble a urothelial neoplasm either architecturally or cytologically. In cases where the diagnosis of papillary neoplasia is not straightforward and there is a question of polypoid cystitis, pathologists should seek clinical history that might suggest a reactive process. Because the urologist can more often better recognize the inflammatory nature of the lesion than the pathologist, the pathologist should hesitate diagnosing urothelial neoplasia when the cystoscopic impression is that of an inflammatory lesion.
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PMID:Polypoid/papillary cystitis: a series of 41 cases misdiagnosed as papillary urothelial neoplasia. 1837 18