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PubMed1998

A psychophysical study of discomfort produced by repeated filling of the urinary bladder.

Psychophysical studies were performed in 10 healthy, female volunteers using urinary bladder distension (UBD) as a visceral stimulus. Stimulus methodology was similar to that used clinically for obtaining cystometrograms with a fixed-rate (100 cc/min normal saline) filling of the urinary bladder, occasional pauses and simultaneous measure of bladder pressure using a catheter-transducer assembly. During bladder filling, subjects were asked to report sensations by verbal report and by using an electronic, hand-held, visual-analog-scale device. Sensations evoked by UBD were generally localized to the suprapubic region. UBD produced cardiovascular responses which increased with repeated trials. Sensation intensity increased with repeated UBDs as indicated by global pain ratings. Intravesical pressure and volume correlated with sensation intensity. The volume of distending fluid needed to produce a report of discomfort was highly variable from trial to trial and did not change significantly with repeated UBDs. The intravesical pressure which produced a report of discomfort was less variable and significantly decreased with repeated UBDs. The change in intravesical pressure and volume needed to produce discomfort was inversely correlated with initial intravesical pressure measures. Similar to findings in other organ systems, these findings demonstrate that repeated presentations of a visceral stimulus may lead to an increase in physiological and perceptual responses to pain.

Adult↗
PubMed2000

Effects of NS1608 on MaxiK channels in smooth muscle cells from urinary bladder.

Using the patch-clamp technique, we have characterized membrane currents in single detrusor smooth muscle cells from rat and human urinary bladder. From the voltage- and Ca(2+)-dependence of the current as well as the single channel conductance we conclude that rat and human urinary bladder smooth muscle cells express MaxiK channels. In smooth muscle cells from rat urinary bladder we tested the action of NS1608 on current through these MaxiK channels. Application of 10 microm NS1608 increased the amplitude of the current and this increase could be explained by a shift in the activation voltage of the MaxiK channels approximately 100 mV towards more negative potentials. Charybdotoxin as well as paxilline, well known blockers of MaxiK channels, were able to reduce current through MaxiK channels in our cell preparation. In addition, application of 10 microm NS1608 hyperpolarized the membrane potential of the investigated cells. This hyperpolarization could be antagonized by the application of paxilline. We conclude that application of NS1608 results in the opening of MaxiK channels under physiological conditions that leads to a hyperpolarization of the cells. This hyperpolarization in turn could relax urinary bladder smooth muscle cells. MaxiK channels in these cells could therefore play a role in directly controlling muscle tone by regulating the membrane potential. This opens up the possibility of MaxiK channels being targets for the treatment of urge incontinence.

Animals↗
PubMed2003

The role of cholinesterases in rat urinary bladder contractility.

This study examines the effects of inhibition of acetylcholinesterase (AChE) and butyrylcholinesterase (BuChE) on acetylcholine (ACh)-induced contraction in rat urinary bladder smooth muscle. Neostigmine, a non-selective ChE inhibitor, caused concentration-dependent contractions in rat urinary bladder strips, whereas tetraisopropylpyrophosphoramide (iso-OMPA; a BuChE inhibitor) failed to affect the resting tone of the preparations. Neostigmine (1 microM) markedly augmented the contractile responses to ACh. Although iso-OMPA (10 microM) also potentiated ACh-induced contraction, the effect was less than that evoked by neostigmine. The activities of AChE in rat urinary bladder strips were significantly (P<0.05) higher than those of BuChE. These results indicated that AChE, rather than BuChE, plays an important role in controlling ACh-induced contractions of rat urinary bladder.

Acetylcholinesterase↗
PubMed1991

[A case of malignant pheochromocytoma of the urinary bladder].

A 31-year-old man was admitted to our hospital because of miction pain and gross hematuria in August, 1988. Cystoscopic examination revealed a solid mass in the bladder. The histological diagnosis was pheochromocytoma of urinary bladder by biopsy. He had a history of syncope on urination several times. Abnormal elevation of serum noradrenaline was observed in hormonal studies and abnormal accumulation was seen in the bladder by 131I-MIBG scintigraphy. Total cystectomy, lymphadenectomy and urinary diversion were performed in November, 1988. Pathological diagnosis was pheochromocytoma of the urinary bladder with metastasis to both iliac lymph nodes.

3-Iodobenzylguanidine↗
PubMed1985

Urinary bladder MR imaging. Part I. Normal and benign conditions.

The normal urinary bladder and several benign entities of the bladder were examined in 50 patients by magnetic resonance (MR) imaging. Specific features assessed included appearance of the bladder wall, optimal repetition (TR) and echo delay (TE) parameters for bladder-wall demonstration, and differentiation among various benign abnormalities, including bladder-wall hypertrophy, inflammation, and mucosal congestion, on MR images. The bladder wall in the 30 healthy subjects was best displayed using a TR = 2 sec, TE = 56 msec image, which gave 60% contrast between the bladder wall and urine and 48% contrast between the bladder wall and fat. Demonstration of bladder-wall hypertrophy required similar imaging; bladder distention was necessary to demonstrate the thickness of the bladder wall. Congestion and inflammation were best demonstrated on TR = 2 sec, TE = 56 msec images, which gave 45% contrast. Normal and/or hypertrophic bladder wall were distinguished from inflammation and congestion on the basis of signal intensity variations and/or T1 and T2 relaxation parameters.

Adult↗
PubMed1987

Thiazides stimulate calcium absorption in urinary bladder of winter flounder.

Thiazides inhibit voltage-independent NaCl absorption in the urinary bladder of the winter flounder presumably by blocking an electroneutral mucosal Na/Cl co-transporter. As thiazides stimulate calcium absorption in mammalian distal convoluted tubule while inhibiting NaCl absorption, we studied the effects of hydrochlorothiazide (HCTZ) on unidirectional 45Ca fluxes and intracellular electrical potential in short-circuited bladders to examine possible mechanisms of HCTZ effects on calcium transport. Basal secretory calcium flux was, on average, slightly larger than absorptive flux, reflecting small net calcium secretion. Mucosal addition of HCTZ (10(-4) M) stimulated absorptive calcium flux by 46% while the secretory flux was unaltered. Thus, HCTZ tended to induce net calcium absorption. Pre-treatment with serosal ouabain (10(-4) M) attenuated the HCTZ-induced increase in absorptive calcium flux. Moreover, HCTZ hyperpolarized the mucosal membrane potential by 18% as measured by conventional open-tip microelectrodes. These effects of HCTZ are consistent with the hypothesis that HCTZ indirectly stimulates Na/Ca exchange located at the serosal membrane. In conclusion, HCTZ in flounder urinary bladder, as in mammalian distal convoluted tubule, simultaneously inhibits NaCl absorption and stimulates calcium absorption. This study expands on the functional similarities between the flounder urinary bladder and the mammalian distal convoluted tubule.

Animals↗
PubMed1990

[Study of the intracellular contractile mechanism of the urinary bladder smooth muscle using skinned fiber technique].

The intracellular contractile mechanism of the urinary bladder smooth muscle was studied using the saponin-treated skinned fiber in which cell membrane was chemically removed. The chemically skinned bladder muscle showed a tension development which was dependent on Ca2(+)-concentration. The minimal Ca2(+)-concentration for the tension development was 2 X 10(-7) M Ca2+. The maximal tension was induced at 10(-5) M. This maximal tension was approximately the same as the K(+)-induced tension development observed in the intact muscle. In addition, SDS-polyacrylamide gel electrophoresis showed that the contractile proteins were still preserved in the saponin-treated bladder smooth muscle. The Ca2(+)-concentration-tension response curve shifted to the left with an increase in MgATP concentration (from 3 mM to 7 mM), indicating that the sensitivity of the skinned muscle was affected by MgATP. Mg2+ above 6 mM caused a slow tension development by itself in the absence of Ca2+. Ca2(+)-induced tension development was blocked by the addition of W-7 (calmodulin antagonist). This result suggested that calmodulin (Ca2(+)-binding protein) regulates the actin-myosin interaction in the urinary bladder smooth muscle. Caffeine solution (25 mM) caused a rapid tension development in the skinned bladder smooth muscle which was loaded with Ca2(+)-concentration, however, this tension development decreased when the loaded Ca2(+)-concentration exceeded 10(-6) M. It seems from this result that "Ca-induced-Ca release mechanism" also exists in the urinary bladder smooth muscle.

Adenosine Triphosphate↗
PubMed1998

Infrequent involvement of microsatellite instability in urinary bladder carcinomas of the NON/Shi mouse treated with N-butyl-N-(4-hydroxybutyl)nitrosamine.

Variation in the frequency of microsatellite instability (MSI) has been reported in different kinds of human malignant tumors, with less than one-third of invasive urinary bladder carcinoma cases estimated to be affected. Here we investigated the MSI for 27 microsatellite sequences in invasive urinary bladder carcinomas of the NON/Shi mouse induced by N-butyl-N-(4-hydroxybutyl)nitrosamine. A total of 28 urinary bladder carcinomas of both transitional cell and squamous cell types were studied. All were invasive (greater than pT3) and high-grade and 10 of them had metastasis. Only two (11%) of 18 primary bladder carcinomas without metastasis foci showed alterations in one or two loci. None of 10 pairs of urinary bladder carcinomas and metastasis foci demonstrated any alterations. In conclusion, MSI which represents a defect in the DNA mismatch repair system is infrequent and therefore unlikely to be a critical step in genesis of invasive mouse urinary bladder carcinomas.

Animals↗
PubMed2000

Multinucleated giant cells in submucosal layer of human urinary bladder: an immunohistochemical and electron microscopic study.

Multinucleated giant cells (MGC) detected in the submucosal layer of human urinary bladder mainly associated with transitional cell carcinoma were examined immunohistochemically and ultrastructurally. The cases examined totaled 29, namely 14 cases with transitional cell carcinoma and another 15 cases mostly with malignancy in other organs. Histologically, MGC were smooth, irregular or dendritic in shape, and tended to increase in number in the vicinity of cancer or marked inflammation. They were consistently positive for not only vimentin, but also MB-2, and CD34, and were mostly positive for proliferating cell nuclear antigen (PCNA), but not MIB-1 (Ki-67) and HLA-DRalpha antigens. On occasion, antibodies to alpha-smooth muscle actin (alpha-SMA), muscle actin (M-actin), CD68 (KP-1) and alpha subunit of S-100 protein also yielded positive reactions. Interestingly, aggregated short bulbous processes were ultrastructurally observed on their surface in parts. These findings suggested that MGC in the submucosal layer of human urinary bladder were MB-2 and CD34-positive multipotential mesenchymal cells with no mitotic activity expressing fibroblastic (vimentin), myofibroblastic (alpha-SMA), or histiocytic (CD68) markers mostly in the vicinity of malignancy, and that these MGC were formed by fusion of mononuclear cells expressing identical markers with those of MGC. Further investigations are needed to clarify the exact function of MGC in human urinary bladder.

Adult↗
PubMed2000

Primary localized amyloidosis of the urinary bladder: a case series of 31 patients.

OBJECTIVE: To evaluate the presentation and prognosis of primary localized amyloidosis of the urinary bladder. PATIENTS AND METHODS: The medical records of 31 patients with primary localized amyloidosis of the urinary bladder were reviewed. Immunohistochemical amyloid typing was performed on bladder biopsy specimens from 27 patients. RESULTS: The median age of the 22 men and 9 women was 55 years. Twenty-four patients (77%) presented with gross hematuria (associated with irritative urinary tract symptoms in 6 patients), and 7 (23%) had only irritative lower urinary tract symptoms. Multiple bladder areas were involved in 20 patients (65%), a single area was involved in 8 (26%), and diffuse involvement was present in 3 (10%). Twenty-four patients had immunoglobulin light chain, and 3 had transthyretin-related amyloid. Local recurrences were common. None of the patients developed systemic amyloidosis. CONCLUSION: Primary localized amyloidosis of the urinary bladder can be easily confused with a neoplasm. Immunohistochemical amyloid typing is important. Transthyretin-related amyloid of the bladder requires no further work-up. Repeated work-ups for systemic amyloidosis are unnecessary for patients with light chain-related amyloidosis of the urinary bladder. Early eradication with fulguration or laser therapy is indicated. Cystoscopic follow-up is necessary.

Adult↗
PubMed1984

The effects of nicotine on spontaneous contractions of cat urinary bladder in situ.

Nicotine and dimethyl-phenylpiperazinium (DMPP) increased intravesicular pressure and then transiently depressed the spontaneous activity of the urinary bladder in chloralose anaesthetized cats. Adrenaline (5-10 micrograms kg-1), noradrenaline (5-20 micrograms kg-1) and isoprenaline (40-50 micrograms kg-1) which depressed spontaneous urinary bladder activity, were antagonized by the beta-receptor blocking agent propranolol (1 mg kg-1). Phenylephrine (10-30 micrograms kg-1) was ineffective on the urinary bladder though it increased the systemic blood pressure. This latter effect was blocked by the alpha-receptor blocking agent phentolamine (2 mg kg-1). Acetylcholine (2-8 micrograms kg-1) caused a marked fall in systemic blood pressure, which was potentiated by physostigmine, but failed to produce any response on the intravesicular pressure even after physostigmine (50-100 micrograms kg-1) treatment. ATP (2 mg kg-1) produced an increase in intravesicular pressure accompanied by a fall in systemic blood pressure. The increased intravesicular pressure was antagonized by quinidine (20 mg kg-1); however, the fall in blood pressure remained unaltered. The increased intravesicular pressure induced by nicotine (20-40 micrograms kg-1) or DMPP (50-100 micrograms kg-1) was not affected by phentolamine (2 mg kg-1), propranolol (1 mg kg-1) or guanethidine (15-20 mg kg-1). Physostigmine (50-100 micrograms kg-1), hemicholinium 3 (2 mg kg-1) or atropine (1 mg kg-1) were also unable to affect the response to nicotine. Hexamethonium (1 mg kg-1), reduced the amplitude of spontaneous bladder contractions and quinidine (20 mg kg-1) abolished the effect of nicotine. 7 Bilateral sectioning of the cervical sympathetic or hypogastric nerves did not alter the effect of nicotine or DMPP. Higher spinal cord transection (Cl-C2) blocked the spontaneous, as well as the nicotine- and DMPP-induced, contractions of the bladder. 8 It is concluded that the increase in intravesicular pressure induced by nicotine is atropineresistant and is not mediated either through adrenergic or cholinergic mechanisms. It is probable that a purinergic mechanism is involved, via the activation of P2-receptors present in the urinary bladder.

Adenosine Triphosphate↗
PubMed1999

Baroreceptor-heart rate reflex sensitivity enhancement after urinary bladder distention in essential hypertensives.

Our objective was to determine if urinary bladder distention modifies the sensitivity of the baroreceptor-heart rate reflex in hypertensive and control subjects. The baroreceptor-heart rate reflex sensitivity was measured in 15 male patients (mean age 37+/-8 years) with mild untreated hypertension (mean 163+/-8/ 95+/-12 mmHg) and 17 age- and sex-matched control subjects before and after urinary bladder distention. Bladder filling was performed infusing saline heated to 37 degrees C via a urinary catheter; the volume infused in each patient corresponded to that which caused the urge to void without reaching the pain threshold. The baroreceptor-heart rate reflex sensitivity was determined correlating the variations of the systolic pressure and of the peak blood flow velocity in the common carotid artery with the variations of the ECG RR' interval of the following heart beat, both during spontaneous and phenylephrine-induced fluctuations of the haemodynamic variables. After bladder distention the diastolic pressure of the hypertensive subjects increased significantly (95+/-12 vs. 100+/-12 mmHg: P < 0.02), whereas the heart rate decreased (RR= 873+/-70 vs. 926+/-80 ms; P < 0.005). These parameters were unchanged in the normotensive subjects (84+/-9 vs. 83+/-8 mmHg and 914+/-158 vs. 913+/-140 ms, respectively). The baroreceptor-heart rate reflex sensitivity, measured on the basis of spontaneous pressure and carotid blood flow velocity fluctuations in relationship to RR changes, decreased in the normotensive subjects after bladder distention (10.7+/-4.6 vs. 9.4+/-2.7 ms/mmHg; P < 0.05 and 423+/-99 vs. 356+/-102 ms/kHz; P < 0.01, respectively), whereas it increased in the hypertensive patients (6.9 +/- 3.6 vs. 8.3 +/- 2.8 ms/mmHg; P < 0.03, and 332 +/- 86 vs. 381+/-97 ms/kHz; P < 0.03 respectively). After bladder distention and phenylephrine administration the baroreceptor-heart rate reflex sensitivity, measured by the correlation between systolic pressure and RR interval, increased only in the hypertensive group (10.2+/-5.4 vs. 15.2+/-7.7 ms/mmHg; P < 0.005). In conclusion urinary bladder distention provokes in hypertensives but not normotensive controls a brisk parasympathetic response of the component of the baroreceptor-heart rate reflex which controls heart rate.

Adult↗
PubMed1997

Effects of allocryptopine, an alkaloid isolated from Glaucium arabicum on rat isolated ileum and urinary bladder.

1. The alkaloid, allocryptopine, was isolated from the chloroform extract of Glaucium arabicum. 2. The effect of allocryptopine on urinary bladder and ileal smooth muscles was investigated in this study. 3. Allocryptopine, in concentrations from 1 x 10(-5) to 3 x 10(-3) M caused a concentration-dependent contraction of rat isolated urinary bladder and a concentration-dependent relaxation of rat ileal smooth muscles. 4. Theophylline (10(-5) M) shifted to the left the allocryptopine concentration-effect curve on ileum and increased the maximum inhibitory effect of allocryptopine. 5. Methylene blue (10(-3) M) had no significant effect on the concentration-effect curve of allocryptopine of the ileum. 6. Phentolamine (10(-6) M) shifted to the right the allocryptopine concentration-effect curve of urinary bladder. 7. These observations suggest that allocryptopine induces a relaxing effect on the ileum by inhibiting phosphodiesterase enzyme, and thus elevating cellular cAMP and its contractile effect on the urinary bladder by affecting alpha-adrenergic receptors in this tissue.

Alkaloids↗
PubMed2003

Predicting disease outcome of non-invasive transitional cell carcinoma of the urinary bladder using an artificial neural network model: results of patient follow-up for 15 years or longer.

BACKGROUND: Patients with non-invasive (Ta/T1) transitional cell carcinoma (TCC) of the urinary bladder are often observed without progression in the long-term follow-up period, although many of them experience recurrence of disease. It is difficult to accurately predict the disease outcome of each patient with Ta/T1 TCC using conventional prognostic criteria. In this study, we examined the usefulness of artificial neural networks (ANNs) to predict the long-term disease outcome of patients with TCC of the urinary bladder. METHODS: A retrospective, prognostic study of 90 patients with Ta/T1 TCC of the urinary bladder, diagnosed by transurethral resection of the bladder tumor between April 1981 and March 1985, and then followed up for 15 years or longer, was carried out. Data were analyzed using the Bayesian network tool of SPSS Neural Connection 2.1. The input neural data consisted of tumor stage, grade, tumor number, age, gender, tumor architecture and estimates of mean nuclear volume. The data set was randomly divided into 68 training and 22 testing examples for the prediction of disease progression and tumor recurrence within 15 years. RESULTS: During 15 years follow-up, tumor recurrence was noted in 42/90 (47%) Ta/T1 tumors. The ANN model could not predict tumor recurrence. Conversely, disease progression was noted in 17/90 (19%) Ta/T1 tumors, and, in the test set, 4/22 (18%) Ta/T1 tumors underwent disease progression. The sensitivity of the ANN model to predict progression was 100% (specificity 67%; positive predictive value 40%; negative predictive value 100%). Patients who were judged to have a favorable prognosis using ANN analysis did not progress within the 15-year follow-up period. CONCLUSION: The results of the ANN study indicate that long-term progression-free survival of patients with non-invasive TCC of the urinary bladder can be precisely predicted. A favorable prognosis using ANNs would be one of the exclusion criteria for immediate or future total cystectomy.

Adult↗
PubMed1988

Carcinoma in situ of the urinary bladder--the Singapore experience.

Carcinoma in situ of the urinary bladder has been described since 1952. However, it was not well recognised as a clinical entity until recently when we are more aware of its clinical significance, that a large proportion progresses to muscle invasive cancer and becomes life threatening, and therefore more aggressive management is needed. From 1980 to 1984 over a period of 5 years, we studied the records of 130 patients with transitional cell carcinoma of the urinary bladder. Eighty-two (63%) were staged as superficial carcinoma while 48 (37%) were diagnosed as muscle invasive cancer (Tables II, III & IV). Out of the 82 cases of superficial carcinoma, 12 (11%) were found to have associated carcinoma in situ of the bladder. Diagnosis depends on a high index of suspicion, urinary cytology and biopsies of not only the obvious papillary or solid tumours but also any abnormal bladder mucosa and random bladder biopsy. Management is a problem and controversial. We have been using intensive intravesical chemotherapy with thiotepa and mitomycin, and if there is evidence of deep muscle invasion, then more aggressive therapy such as cystectomy would be advised. Management of these 12 cases and the problems we encountered are discussed.

Carcinoma in Situ↗
PubMed1997

Study of the effect of external urethral sphincter contraction on the mechanical activity of the ureterovesical junction and urinary bladder: recognition of the sphinctero-ureterovesical reflex.

OBJECTIVES: To study the effect of external urethral sphincter (EUS) contraction on the urinary bladder and ureterovesical junction (UVJ). METHODS: The study was comprised of 9 healthy volunteers (7 men, 2 women; mean age 40.8 +/- 6.6 years). A manometric catheter was introduced into each of the two UVJs and urinary bladder. The EUS was made to contract by voluntary squeezing and by electromyographic stimulation with a needle electrode inserted into the sphincter. The response of the bladder and the UVJs to EUS contraction was determined before and after anesthetization of the EUS, bladder, and the two UVJs, each at a different time. RESULTS: On voluntary squeezing or electromyographic needle stimulation of the EUS, the pressure in both the UVJs and the urinary bladder showed a significant drop (P < 0.05 in both instances). There was no pressure response in the UVJs or in the urinary bladder 10 minutes after separate anesthetization of either the EUS or the UVJs and the bladder; however, 2 hours later, the pressure response was similar to that before anesthesia (P > 0.05). CONCLUSIONS: Bladder and UVJ relaxation on EUS contraction postulate a reflex relationship that was reproducible and absent on anesthetization of either of the suggested two arms of the reflex: the EUS on one end and the bladder and UVJs on the other end. We call this reflex the "sphinctero-ureterovesical reflex." Further studies are needed to evaluate the possible role of this reflex in the micturition mechanism and disorders.

Adult↗
PubMed1985

Tumour localization of radiolabelled monoclonal antibody in mice bearing human urinary bladder (T24) carcinoma xenografts.

Selectivity of mouse monoclonal antibody 7E9 (IGG3) directed against human urinary bladder carcinoma cells has been examined by indirect membrane immunofluorescence, using a panel of 31 human cell lines. The 7E9 monoclonal antibody discriminated between urinary bladder carcinoma cells and normal urothelium or cells of non-urothelial origin, although occasional reactions with bladder carcinoma-unrelated cell types were observed. The 7E9 antibody was purified by protein A affinity chromatography, labeled with 131I and used for gamma scintigraphy in nude mice xenografted with human urinary bladder carcinoma T24. The 7E9 antibody was capable of locating the T24 xenografts in nude mice; it localized preferentially in the T24 tissue compared to normal mouse tissues. The T24 xenografts could not be detected by gamma scintigraphy with 131I-labelled monoclonal antibody against human mammary carcinoma cells and two other control antibodies. Likewise, the 131I-labelled 7E9 antibody was not capable of locating human mammary carcinoma xenografts in nude mice.

Animals↗
PubMed2003

Large cell neuroendocrine carcinoma of the urinary bladder with lymphoepithelioma-like features.

The group of undifferentiated carcinomas of the urinary bladder encompasses small cell undifferentiated carcinoma, giant cell carcinoma, lymphoepithelioma-like carcinoma (LELC), and large cell neuroendocrine carcinoma (LCNEC). These tumors are either pure or can be associated with other components, such as transitional cell carcinoma, squamous cell carcinoma, and adenocarcinoma. We report a case of LCNEC of the urinary bladder in a 54-year-old woman. Histologically, the tumor showed features of LELC; immunohistochemically, the tumor cells reacted to chromogranin A, NSE, and synaptophysin. In addition to these neuroendocrine markers, tumor cells were positive for cytokeratin CAM 5.2 and AE1/AE3, and there was focal positivity for vimentin. In situ hybridization for the detection of Epstein-Barr virus was negative. Despite radical cystourethrectomy and six courses of chemotherapy, the patient developed metastases invading the left inguinal lymph nodes 11 months postoperatively. Currently, 16 months postoperatively, the patient has developed metastases spreading into the lymph nodes of the right ischiorectal fossa; therefore, she is receiving a new cyclus of chemotherapy. There are only three previously reported cases of LCNEC of the urinary bladder, and the significance of neuroendocrine differentiation in non-small cell carcinomas at this location remains to be established. However, LELC appears to be a separate clinicopathological entity with sensitivity to chemotherapy and a relatively favorable prognosis. The differentiation between LELC and LCNEC with prominent inflammatory reaction could be of therapeutic relevance. However, in our case, this was possible using immunohistochemistry only.

Antineoplastic Combined Chemotherapy Protocols↗