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Bladder cancer

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Steven C. Campbell, M.D., Ph.D.; Associate Editor(s)-in-Chief: Shanshan Cen, M.D. [1]

Synonyms and keywords: Carcinoma of bladder, cancer of bladder，carcinoma of the bladder, cancer of the bladder, malignant neoplasm of bladder, bladder neoplasm, bladder tumor, bladder tumour, malignant tumor of bladder, malignant tumour of bladder, carcinoma of urinary bladder, cancer of urinary bladder，carcinoma of the urinary bladder, cancer of the urinary bladder, malignant neoplasm of urinary bladder, urinary bladder neoplasm, urinary bladder tumor, urinary bladder tumour, malignant tumor of urinary bladder, malignant tumour of urinary bladder

Overview

Overview

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Farima Kahe M.D. [2]Steven C. Campbell, M.D., Ph.D.

Overview

Bladder cancer refers to any of several types of malignant growths of the urinary bladder. Bladder cancer may be classified according to cell types into several subtypes: transitional cell carcinomas, squamous cell carcinomas, adenocarcinomas, small cell carcinoma, lymphoma, and sarcoma. The prevalence of bladder cancer is approximately 130.5 per 100,000 individuals in the United States. Males are more commonly affected with bladder cancer than females. Common risk factors in the development of bladder cancer are smoking, occupational exposure to chemicals, chronic bladder irritation, chemotherapy, radiation therapy, arsenic, personal history of cancer in the urinary tract, congenital bladder anomalies, and aristolochic acids. The most common symptoms of bladder cancer include hematuria, urinary frequency , urinary urgency, difficulty urinating, and dysuria. Common complications of bladder cancer include metastasis, anemia, hydronephrosis, urethral stricture, and urinary incontinence. The predominant therapy for bladder cancer is surgical resection. Adjunctive chemotherapy, radiation therapy, and immunotherapy may be required. Prognosis is generally good, and the 5-year survival rate is approximately 77.4%. The prognosis varies with the stages of tumor; carcinoma in situ have the most favorable prognosis.

Classification

Bladder cancer may be classified according to cell types into several subtypes: transitional cell carcinomas, squamous cell carcinomas, adenocarcinomas, small cell carcinoma, lymphoma, and sarcoma.

Pathophysiology

Genes involved in the pathogenesis of bladder cancer include HRAS, Rb1, PTEN/MMAC1, NAT2, and GSTM1. On gross pathology, flat lesions or papillary lesions are characteristic findings of non-invasive transitional cell carcinomas; a large infiltrative mass or a multifocal, flat to papillary lesion with delicate fronds are characteristic findings of invasive transitional cell carcinomas. On microscopic histopathological analysis, loss of cell polarity, nuclear crowding, and cytologic atypia are characteristic findings of flat lesion; fibrovascular stalks, umbrella cells, and eosinophilic cytoplasm are characteristic findings of papillary lesion; invasion beyond the basement membrane is the characteristic finding of invasive transitional cell carcinomas.

Causes

There are no established causes for bladder cancer.

Differential Diagnosis

Bladder cancer must be differentiated from renal cancer, renal stones, prostate cancer, and cystitis.

Epidemiology and Demographics

The prevalence of bladder cancer is approximately 130.5 per 100,000 individuals in the United States. The incidence of bladder cancer is approximately 20.3 per 100,000 individuals in the United States. The incidence of bladder cancer increases with age; the median age at diagnosis is 73 years. Males are more commonly affected with bladder cancer than females. Bladder cancer usually affects individuals of the white race. African American, Asian, and Hispanic individuals are less likely to develop bladder cancer.

Risk Factors

Common risk factors in the development of bladder cancer are smoking, occupational exposure to chemicals, chronic bladder irritation, chemotherapy, radiation therapy, arsenic, personal history of cancer in the urinary tract, congenital bladder anomalies, and aristolochic acids.

Screening

According to the the U.S. Preventive Service Task Force (USPSTF), there is insufficient evidence to recommend routine screening for bladder cancer.

Natural History, Complications and Prognosis

Common complications of bladder cancer include metastasis, anemia, hydronephrosis, urethral stricture, and urinary incontinence. Prognosis is generally good, and the 5-year survival rate is approximately 77.4%. The prognosis varies with the stages of tumor; carcinoma in situ have the most favorable prognosis.

History and Symptoms

The most common symptoms of bladder cancer include hematuria, urinary frequency , urinary urgency, difficulty urinating, and dysuria.

Physical Examination

Common physical examination findings of bladder cancer include cachexia, pallor, and a pelvic mass may be palpated.

Staging

Bladder cancer may be classified into several subtypes based on TNM system.

Laboratory Findings

Laboratory findings consistent with the diagnosis of bladder cancer include blood in the urine, abnormal cells in the urine, and elevated tumor markers.

X Ray

Chest X-ray may be performed to detect metastases of bladder cancer to the lungs.

CT Scan

CT scan may be helpful in the diagnosis of bladder cancer.

MRI

MRI may be helpful in the diagnosis of bladder cancer.

Ultrasound

There are no ultrasound findings associated with bladder cancer.

Other Imaging Findings

There are no other imaging findings associated with bladder cancer.

Other Diagnostic Studies

There are no other diagnostic study findings associated with bladder cancer.

Biopsy

Biopsy is helpful in the diagnosis of bladder cancer.

Medical Therapy

The predominant therapy for bladder cancer is surgical resection. Adjunctive chemotherapy, radiation therapy, and immunotherapy may be required.

Surgery

Surgery is the mainstay of treatment for bladder cancer.

Primary prevention

Primary prevention strategies of bladder cancer include cease smoking, avoid aristolochic acids, and avoid exposure to industrial chemicals and arsenic.

Secondary prevention

There are no secondary preventive measures available for bladder cancer.

References

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Historical Perspective

Historical Perspective

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Farima Kahe M.D. [2]

Overview

Association between bladder cancer and environmental carcinogens is first discovered in 1895. First cystectomy is performed as a treatment for bladder cancer in in 1877. Radium is first used as a treatment of bladder tumors in 1903. Neoadjuvant chemotherapy including methotrexate, vinblastine, doxorubicin, and cisplatin (MVAC) is first described in 1985. FDA approved the use of live bacterium, Bacillus Calmette-Guérin (BCG) for treatment and prevent the recurrence of superficial tumors in 1990.

Historical Perspective

Discovery

  • Cystoscope was first discovered by Maximilian Nitze, a German urologist, in 1877.[1]
  • Association between bladder cancer and environmental carcinogens is first discovered in 1895.
  • Urine cytology is first described in 1945.[2]
  • Micropapillary bladder cancer is first described in 1982.[3]
  • Approximately 356,000 new bladder cancer cases of bladder cancer are reported in 2002 worldwide.[4]

Landmark Events in the Development of Treatment Strategies

References

  1. ↑ Wood JW, Casiano RR (2012). “Inverted papillomas and benign nonneoplastic lesions of the nasal cavity”. Am J Rhinol Allergy. 26 (2): 157–63. doi:10.2500/ajra.2012.26.3732. PMC 3906506. PMID 22487294.
  2. ↑ Griffiths, T. R. L. (2013). “Current perspectives in bladder cancer management”. International Journal of Clinical Practice. 67 (5): 435–448. doi:10.1111/ijcp.12075. ISSN 1368-5031.
  3. ↑ Heudel, Pierre; El Karak, Fadi; Ismaili, Nabil; Droz, Jean-Pierre; Flechon, Aude (2009). “Micropapillary bladder cancer: a review of Léon Bérard Cancer Center experience”. BMC Urology. 9 (1). doi:10.1186/1471-2490-9-5. ISSN 1471-2490.
  4. ↑ Ploeg M, Aben KK, Kiemeney LA (June 2009). “The present and future burden of urinary bladder cancer in the world”. World J Urol. 27 (3): 289–93. doi:10.1007/s00345-009-0383-3. PMC 2694323. PMID 19219610.
  5. ↑ LENZ M, CAHILL GF (October 1947). “The treatment of cancer of the bladder by radium needles”. Am J Roentgenol Radium Ther. 58 (4): 486–92. PMID 20273482.
  6. ↑ Balar A, Bajorin DF, Milowsky MI (June 2011). “Management of invasive bladder cancer in patients who are not candidates for or decline cystectomy”. Ther Adv Urol. 3 (3): 107–17. doi:10.1177/1756287211407543. PMC 3159398. PMID 21904567.
  7. ↑ Sagaster P, Flamm J, Flamm M, Mayer A, Donner G, Oberleitner S, Havelec L, Lepsinger L, Ludwig H (July 1996). “Neoadjuvant chemotherapy (MVAC) in locally invasive bladder cancer”. Eur. J. Cancer. 32A (8): 1320–4. PMID 8869093.
  8. ↑ Porten SP, Leapman MS, Greene KL (2015). “Intravesical chemotherapy in non-muscle-invasive bladder cancer”. Indian J Urol. 31 (4): 297–303. doi:10.4103/0970-1591.166446. PMC 4626913. PMID 26604440.
  9. ↑ Askeland EJ, Newton MR, O’Donnell MA, Luo Y (2012). “Bladder Cancer Immunotherapy: BCG and Beyond”. Adv Urol. 2012: 181987. doi:10.1155/2012/181987. PMC 3388311. PMID 22778725.
  10. ↑ Als AB, Sengelov L, Von Der Maase H (2008). “Gemcitabine and cisplatin in locally advanced and metastatic bladder cancer; 3- or 4-week schedule?”. Acta Oncol. 47 (1): 110–9. doi:10.1080/02841860701499382. PMID 17851853.
Classification

Classification

Steven C. Campbell, M.D., Ph.D.; Associate Editor(s)-in-Chief: Farima Kahe M.D. [1] Shanshan Cen, M.D. [2]

Overview

Bladder cancer may be classified according to the cell types into several subtypes include transitional cell carcinomas, squamous cell carcinomas, adenocarcinomas, small cell carcinoma, lymphoma, and sarcoma.

Classification

Bladder cancer may be classified according to the cell types into several subtypes as following:[1][2][3][4]

References

  1. ↑ Pasin E, Josephson DY, Mitra AP, Cote RJ, Stein JP (2008). “Superficial bladder cancer: an update on etiology, molecular development, classification, and natural history”. Rev Urol. 10 (1): 31–43. PMC 2312342. PMID 18470273.
  2. ↑ Montironi R, Lopez-Beltran A (April 2005). “The 2004 WHO classification of bladder tumors: a summary and commentary”. Int. J. Surg. Pathol. 13 (2): 143–53. doi:10.1177/106689690501300203. PMID 15864376.
  3. ↑ Humphrey PA, Moch H, Cubilla AL, Ulbright TM, Reuter VE (July 2016). “The 2016 WHO Classification of Tumours of the Urinary System and Male Genital Organs-Part B: Prostate and Bladder Tumours”. Eur. Urol. 70 (1): 106–119. doi:10.1016/j.eururo.2016.02.028. PMID 26996659.
  4. ↑ Bertz S, Hartmann A, Knüchel-Clarke R, Gaisa NT (February 2016). “[Specific types of bladder cancer]”. Pathologe (in German). 37 (1): 40–51. doi:10.1007/s00292-015-0129-5. PMID 26782034.

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Pathophysiology

Pathophysiology

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [2]; Associate Editor(s)-in-Chief: Farima Kahe M.D. [3] Shanshan Cen, M.D. [4] Steven C. Campbell, M.D., Ph.D.

Overview

Genes involved in the pathogenesis of bladder cancer include HRAS, Rb1, PTEN/MMAC1, NAT2, and GSTM1. On gross pathology, flat lesions or papillary lesions are characteristic findings of non-invasive transitional cell carcinomas; a large infiltrative mass or a multifocal, flat to papillary lesion with delicate fronds are characteristic findings of invasive transitional cell carcinomas. On microscopic histopathological analysis, loss of cell polarity, nuclear crowding, and cytologic atypia are characteristic findings of flat lesion; fibrovascular stalks, umbrella cells, and eosinophilic cytoplasm are characteristic findings of papillary lesion; invasion beyond the basement membrane is the characteristic finding of invasive transitional cell carcinomas.

Pathogenesis

  • Under normal conditions, the bladder, the lower part of the kidneys, the ureters, and the proximal urethra are lined with a specialized mucous membrane referred to as transitional epithelium (also called urothelium).[1]
  • Most cancers that form in the bladder, the lower part of the kidneys, the ureters, and the proximal urethra are transitional cell carcinomas (also called urothelial carcinomas) that derive from transitional epithelium.
  • Urothelial carcinomas may be non-invasive or invasive.
  • Urothelial carcinomas with mixed epithelial features are invasive tumors that have different types of cells mixed with the cancer cells.

Genetics

  • Genetic mutations involved in the pathogenesis of bladder cancer include:[2]
  • HRAS mutation
  • Rb1 mutation
  • PTEN/MMAC1 mutation
  • NAT2 slow acetylator phenotype
  • GSTM1 null phenotype

Gross Pathology

  • Non-invasive urothelial carcinoma[3][4]
  • On gross pathology, flat lesions or papillary lesions are characteristic findings of non-invasive urothelial carcinoma.
  • Invasive urothelial carcinoma[5]
  • On gross pathology, a large infiltrative mass or a multifocal, flat to papillary lesion with delicate fronds are characteristic findings of invasive urothelial carcinoma.

Microscopic Pathology

  • Flat lesions
  • On microscopic histopathological analysis, loss of cell polarity, nuclear crowding, and cytologic atypia are characteristic findings.
  • On microscopic histopathological analysis, fibrovascular stalks, umbrella cells, and eosinophilic cytoplasm are characteristic findings.
  • Invasive urothelial carcinoma
  • On microscopic histopathological analysis, invasion beyond the basement membrane is the characteristic finding.[5]
Image showing muscle invasive urothelial carcinoma [1]


References

  1. ↑ Bladder Cancer. Canadian Cancer Society 2015. http://www.cancer.ca/en/cancer-information/cancer-type/bladder/bladder-cancer/urothelial-carcinoma/?region=ab Accessed on October, 1 2015
  2. ↑ National Cancer Institute. Physician Data Query Database 2015. http://www.cancer.gov/types/bladder/hp/bladder-treatment-pdq#link/_359_toc Accessed on October, 1 2015
  3. ↑ 3.0 3.1 Cheng L, Cheville JC, Neumann RM, Bostwick DG (2000). “Flat intraepithelial lesions of the urinary bladder”. Cancer. 88 (3): 625–31. PMID 10649257.
  4. ↑ Cheng L, Cheville JC, Neumann RM, Bostwick DG (1999). “Natural history of urothelial dysplasia of the bladder”. Am J Surg Pathol. 23 (4): 443–7. PMID 10199474.
  5. ↑ 5.0 5.1 Pons F, Orsola A, Morote J, Bellmunt J (2011). “Variant forms of bladder cancer: basic considerations on treatment approaches”. Curr Oncol Rep. 13 (3): 216–21. doi:10.1007/s11912-011-0161-4. PMID 21360040.
  6. ↑ McKenney JK, Amin MB, Young RH (2003). “Urothelial (transitional cell) papilloma of the urinary bladder: a clinicopathologic study of 26 cases”. Mod Pathol. 16 (7): 623–9. doi:10.1097/01.MP.0000073973.74228.1E. PMID 12861056.
  7. ↑ Picozzi S, Casellato S, Bozzini G, Ratti D, Macchi A, Rubino B; et al. (2013). “Inverted papilloma of the bladder: a review and an analysis of the recent literature of 365 patients”. Urol Oncol. 31 (8): 1584–90. doi:10.1016/j.urolonc.2012.03.009. PMID 22520573.

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Causes

Causes

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Shanshan Cen, M.D. [2]

Overview

There are no established causes of bladder cancer.

Causes

  • There are no established causes of bladder cancer.
  • To view the list of risk factors in the development of bladder cancer, please click here.

References

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Differentiating Bladder cancer from other Diseases

Differentiating Bladder cancer from other Diseases

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Shanshan Cen, M.D. [2]

Overview

Bladder cancer must be differentiated from renal cancer, renal stones, prostate cancer, and cystitis.

Differential Diagnosis

The most common presentation of bladder cancer is hematuria; however in the advanced cases, the presentation can be bladder mass.

Bladder cancer must be differentiated from other causes of hematuria as in the below table:

Diseases Clinical manifestations Para-clinical findings Gold standard
Symptoms Physical examina
Lab Findings Diagnosi
Low back pain Fever Nausea/

Vomiting

Urinary symptoms Hypertension Pitting edema Other
Dysuria Frequency Oliguria
Glomerular diseases IgA nephropathy[1][2] (Berger nephropathy) + – – – + + + – – Biopsy:

IgA deposited in a diffuse granular pattern in the mesangium

Biopsy
    Hereditary nephritis[3][4] (Alport syndrome) – – – – – – + –
    • Cataract
    • Hearing loss
    		 Biopsy: Genetic analysis
    Post-streptococcal glomerulonephritis[5][6] +/- + – – + + + +

    Biopsy

    		Biopsy
    Focal segmental glomerular sclerosis[7][8][9] – – – – – – + + Biopsy
    • Segmental solidification in the perihilar region and peripheral areas, especially the tubular pole
    • Coarsely granular deposits -of IgM and C3
    		 Biopsy
    Rapidly progressive glomerulonephritis[10][11][12] + + + – – – + – Biopsy: Biopsy
    Lupus nephritis[13][14] – + – – – – + +
    • Foamy dark urine
    • Weight gain
    		 Biopsy,
    • Different pathologies, CLICK HERE for more information.
    		 Biopsy
    Fabry disease – – – – – – + + – Biopsy Biopsy
    Disease Low back pain Fever Nausea/

    Vomiting

    		Dysuria Frequency Oliguria Hypertension Pitting edema Other Lab Findings Diagnosis method Gold standard
    Tubulointerstitial diseases[15][16][17] + + + – – – – – Rash Biopsy: Renal biopsy
    Nephrolithiasis[18][19] + ± + ± ± ± – –
    • Radiating pain to groin
    		 Abdominal CT scan without contrast
    Reflux nephropathy (hydronephrosis) + + – – – – – + –
    Malignancy Renal cell carcinoma (RCC)[20][21] – – – – – – ± ± –
    Nephroblastoma (Wilms tumor)[22][23] – – – – – – – –

    Biopsy:

    		Biopsy
    Bladder cancer[27][28][29] – – – – ± ± – – Suprapubic pain Ultrasound, CT scan, Biopsy Biopsy
    Prostate cancer[30][31] ± – – – ± ± – – – Ultrasound, CT scan, Biopsy Biopsy
    Disease Low back pain Fever Nausea/

    Vomiting

    		Dysuria Frequency Oliguria Hypertension Pitting edema Other Lab Findings Diagnosis method Gold standard
    Familial diseases Polycystic kidney disease[32][33] + – – – – – + + Ultrasound:
    • Unilateral or bilateral cysts

    CT:

    • Hyperdense appearance,
    • Septations
    • Calcifications

    Genetic testing demonstrates:

    • Frame insertions/deletions
    • Non-canonical splice site alterations
    • Combined missense changes

    Biopsy:

    • Interstitial fibrosis
    • Tubular atrophy
    • Thickening and lamellation of tubular basement membranes
    		 Ultrasound
    Vascular diseases Renal vein thrombosis[34][35] + + + – – – – – Renal venography: Gold standard
    Wegner’s granulomatosis polyangiitis[36][37][38][39] – – – – – +/- + + CT chest:

    Biopsy:

    		Biopsy
    Henoch-Schönlein purpura[40][41] – – – – – +/- +/- + Biopsy:

    IgA deposited in a diffuse granular pattern in the mesangium

    		Renal biopsy, and clinical syndrome
    Disease Low back pain Fever Nausea/

    Vomiting

    		Dysuria Frequency Oliguria Hypertension Pitting edema Other Lab Findings Diagnosis method Gold standard
    Lower urinary tract diseases Benign prostatic hyperplasia +/- – – + + – – –
    • Nocturia
    • Other voiding symptoms
      • Slow urinary stream
      • Splitting or spraying of the urinary stream
      • Intermittent urinary stream
      • Hesitancy
      • Straining to void
      • Terminal dribbling
    • Urinalysis to rule out UTI
    • Elevated BUN/Cr
    • High PSA values
    • Urine cytology to screen for bladder cancer
    • Biopsy to rule out cancer
    		 Biopsy
    Urolithiasis[42][43][44] + +/- + + + + – – Abdominppelvic CT scan without contrast Abdominppelvic CT scan without contrast
    Disease Low back pain Fever Nausea/

    Vomiting

    		Dysuria Frequency Oliguria Hypertension Pitting edema Other Lab Findings Diagnosis method Gold standard
    Infectious diseases Pyelonephritis[45][46] + + + + + + – – CT and ultrasound: –
    Cystitis[47][48] – – – + + + – – Ultrasound:
    • Presence of gas in the bladder wall.
    • Also, help to detect the presence of a tumor or a stone.
    		 Urine culture
    Prostatitis[49][50] – + – + + + – –
    • Body aches
    		 Ultrasound:
    • Focal hypoechoic region located in the peripheral part of the prostate

    CT scan:

    		–
    Urethritis[51][52] -/- + – + + + – –

    CT scan:

    • Diffuse, circumferential urothelial wall thickening and contrast-enhancement
    • Periureteric or perinephric fat stranding.
    		 Urine culture
    Urogenital trauma Inserted bladder or ureteral catheters – – – + + + – –
    • Retrograde urethrogram (RUG)
    • Retrograde urethrogram (RUG)

    Lower abdominal mass can be classified to the gynecological and non-gynecological causes. Bladder cancer in the advanced cases can present as a bladder mass. Below table discusses lower abdominal mass causes:

    References

    1. ↑ Donadio JV, Grande JP (2002). “IgA nephropathy”. N Engl J Med. 347 (10): 738–48. doi:10.1056/NEJMra020109. PMID 12213946.
    2. ↑ Suzuki H, Kiryluk K, Novak J, Moldoveanu Z, Herr AB, Renfrow MB; et al. (2011). “The pathophysiology of IgA nephropathy”. J Am Soc Nephrol. 22 (10): 1795–803. doi:10.1681/ASN.2011050464. PMID 21949093.
    3. ↑ McCarthy PA, Maino DM (2000). “Alport syndrome: a review”. Clin Eye Vis Care. 12 (3–4): 139–150. PMID 11137428.
    4. ↑ Bodziak KA, Hammond WS, Molitoris BA (1994). “Inherited diseases of the glomerular basement membrane”. Am J Kidney Dis. 23 (4): 605–18. PMID 8154501.
    5. ↑ Yoshizawa N, Yamakami K, Fujino M, Oda T, Tamura K, Matsumoto K, Sugisaki T, Boyle MD (July 2004). “Nephritis-associated plasmin receptor and acute poststreptococcal glomerulonephritis: characterization of the antigen and associated immune response”. J. Am. Soc. Nephrol. 15 (7): 1785–93. PMID 15213266.
    6. ↑ Oda T, Yoshizawa N, Yamakami K, Tamura K, Kuroki A, Sugisaki T, Sawanobori E, Higashida K, Ohtomo Y, Hotta O, Kumagai H, Miura S (September 2010). “Localization of nephritis-associated plasmin receptor in acute poststreptococcal glomerulonephritis”. Hum. Pathol. 41 (9): 1276–85. doi:10.1016/j.humpath.2010.02.006. PMID 20708459.
    7. ↑ Kwoh C, Shannon MB, Miner JH, Shaw A (2006). “Pathogenesis of nonimmune glomerulopathies”. Annu Rev Pathol. 1: 349–74. doi:10.1146/annurev.pathol.1.110304.100119. PMID 18039119.
    8. ↑ Reidy K, Kaskel FJ (March 2007). “Pathophysiology of focal segmental glomerulosclerosis”. Pediatr. Nephrol. 22 (3): 350–4. doi:10.1007/s00467-006-0357-2. PMC 1794138. PMID 17216262.
    9. ↑ D’Agati VD, Fogo AB, Bruijn JA, Jennette JC (2004). “Pathologic classification of focal segmental glomerulosclerosis: a working proposal”. Am J Kidney Dis. 43 (2): 368–82. PMID 14750104.
    10. ↑ Couser WG (1998). “Pathogenesis of glomerular damage in glomerulonephritis”. Nephrol Dial Transplant. 13 Suppl 1: 10–5. PMID 9507491.
    11. ↑ Atkins RC, Nikolic-Paterson DJ, Song Q, Lan HY (1996). “Modulators of crescentic glomerulonephritis”. J Am Soc Nephrol. 7 (11): 2271–8. PMID 8959617.
    12. ↑ Jennette JC (March 2003). “Rapidly progressive crescentic glomerulonephritis”. Kidney Int. 63 (3): 1164–77. doi:10.1046/j.1523-1755.2003.00843.x. PMID 12631105.
    13. ↑ Schwartz N, Goilav B, Putterman C (September 2014). “The pathogenesis, diagnosis and treatment of lupus nephritis”. Curr Opin Rheumatol. 26 (5): 502–9. doi:10.1097/BOR.0000000000000089. PMC 4221732. PMID 25014039.
    14. ↑ Giannico G, Fogo AB (2013). “Lupus nephritis: is the kidney biopsy currently necessary in the management of lupus nephritis?”. Clin J Am Soc Nephrol. 8 (1): 138–45. doi:10.2215/CJN.03400412. PMID 22977215.
    15. ↑ Baker, R. J.; Pusey, C. D. (2004). “The changing profile of acute tubulointerstitial nephritis”. Nephrology Dialysis Transplantation. 19 (1): 8–11. doi:10.1093/ndt/gfg464. ISSN 0931-0509.
    16. ↑ Kelly C, Tomaszewski J, Neilson E. Immunopathogenic mechanisms of tubulointerstitial injury. In: Tisher C, Brenner B, eds, Renal Pathology: With Clinical and Functional Correlations, 2nd Edn., Vol. 1. J. B. Lippincott & Co, Philadelphia, PA, 1994; 699–722
    17. ↑ Dharmarajan TS, Yoo J, Russell RO, Boateng YA. Acute post streptococcal interstitial nephritis in an adult and review of the literature. Int Urol Nephrol 1999; 31:145
    18. ↑ Hochreiter W, Knoll T, Hess B (February 2003). “[Pathophysiology, diagnosis and conservative therapy of non-calcium kidney calculi]”. Ther Umsch (in German). 60 (2): 89–97. doi:10.1024/0040-5930.60.2.89. PMID 12649987.
    19. ↑ Trinchieri A (February 2013). “Diet and renal stone formation”. Minerva Med. 104 (1): 41–54. PMID 23392537.
    20. ↑ Cohen HT, McGovern FJ (2005). “Renal-cell carcinoma”. N Engl J Med. 353 (23): 2477–90. doi:10.1056/NEJMra043172. PMID 16339096.
    21. ↑ Leveridge MJ, Bostrom PJ, Koulouris G, Finelli A, Lawrentschuk N (June 2010). “Imaging renal cell carcinoma with ultrasonography, CT and MRI”. Nat Rev Urol. 7 (6): 311–25. doi:10.1038/nrurol.2010.63. PMID 20479778.
    22. ↑ Jolly RD, Stellwagen E, Babul J, Vodkaĭlo LV, Titov VL, Moldomusaev DM, Maianskiĭ AN (November 1975). “Mannosidosis of Angus Cattle: a prototype control program for some genetic diseases”. Adv Vet Sci Comp Med. 19 (23): 1–21. PMID 1978.
    23. ↑ Stefanowicz J, Sierota D, Balcerska A, Stoba C (2004). “[Wilms’ tumour of unfavorable histology–results of treatment with the SIOP 93-01 protocol at the Gdańsk centre. Preliminary report]”. Med Wieku Rozwoj (in Polish). 8 (2 Pt 1): 197–200. PMID 15738594.
    24. ↑ Hartman DS, Sanders RC (April 1982). “Wilms’ tumor versus neuroblastoma: usefulness of ultrasound in differentiation”. J Ultrasound Med. 1 (3): 117–22. PMID 6152936.
    25. ↑ De Campo JF (1986). “Ultrasound of Wilms’ tumor”. Pediatr Radiol. 16 (1): 21–4. PMID 3003660.
    26. ↑ Cahan LD (1985). “Failure of encephalo-duro-arterio-synangiosis procedure in moyamoya disease”. Pediatr Neurosci. 12 (1): 58–62. PMID 4080660.
    27. ↑ Pons F, Orsola A, Morote J, Bellmunt J (2011). “Variant forms of bladder cancer: basic considerations on treatment approaches”. Curr Oncol Rep. 13 (3): 216–21. doi:10.1007/s11912-011-0161-4. PMID 21360040.
    28. ↑ Metts MC, Metts JC, Milito SJ, Thomas CR (June 2000). “Bladder cancer: a review of diagnosis and management”. J Natl Med Assoc. 92 (6): 285–94. PMC 2640522. PMID 10918764.
    29. ↑ Rom M, Kuehhas FE, Djavan B (2007). “New findings in bladder and prostate cancer: highlights of the 22nd annual congress of the European association of urology, march 21-24, 2007, berlin, Germany”. Rev Urol. 9 (4): 214–9. PMC 2199502. PMID 18231618.
    30. ↑ Chung SD, Liu SP, Lin HC (2013). “Association between prostate cancer and urinary calculi: a population-based study”. PLoS ONE. 8 (2): e57743. doi:10.1371/journal.pone.0057743. PMC 3581486. PMID 23451265.
    31. ↑ Rom M, Kuehhas FE, Djavan B (2007). “New findings in bladder and prostate cancer: highlights of the 22nd annual congress of the European association of urology, march 21-24, 2007, berlin, Germany”. Rev Urol. 9 (4): 214–9. PMC 2199502. PMID 18231618.
    32. ↑ Gabow PA (July 1993). “Autosomal dominant polycystic kidney disease”. N. Engl. J. Med. 329 (5): 332–42. doi:10.1056/NEJM199307293290508. PMID 8321262.
    33. ↑ Adeva M, El-Youssef M, Rossetti S, Kamath PS, Kubly V, Consugar MB, Milliner DM, King BF, Torres VE, Harris PC (January 2006). “Clinical and molecular characterization defines a broadened spectrum of autosomal recessive polycystic kidney disease (ARPKD)”. Medicine (Baltimore). 85 (1): 1–21. doi:10.1097/01.md.0000200165.90373.9a. PMID 16523049.
    34. ↑ U. Kuhlmann, J. Steurer, A. Bollinger, G. Pouliadis, J. Briner & W. Siegenthaler (1981). “[Incidence and clinical significance of thromboses and thrombo-embolic complications in nephrotic syndrome patients]”. Schweizerische medizinische Wochenschrift. 111 (27–28): 1034–1040. PMID 7268357. Unknown parameter |month= ignored (help)
    35. ↑ F. Llach, S. Papper & S. G. Massry (1980). “The clinical spectrum of renal vein thrombosis: acute and chronic”. The American journal of medicine. 69 (6): 819–827. PMID 7446547. Unknown parameter |month= ignored (help)
    36. ↑ Pagnoux C (2016). “Updates in ANCA-associated vasculitis”. Eur J Rheumatol. 3 (3): 122–133. doi:10.5152/eurjrheum.2015.0043. PMID 27733943.
    37. ↑ Lee KS, Kim TS, Fujimoto K, Moriya H, Watanabe H, Tateishi U, Ashizawa K, Johkoh T, Kim EA, Kwon OJ (2003). “Thoracic manifestation of Wegener’s granulomatosis: CT findings in 30 patients”. Eur Radiol. 13 (1): 43–51. doi:10.1007/s00330-002-1422-2. PMID 12541109.
    38. ↑ Kallenberg CG, Heeringa P, Stegeman CA (2006). “Mechanisms of Disease: pathogenesis and treatment of ANCA-associated vasculitides”. Nat Clin Pract Rheumatol. 2 (12): 661–70. doi:10.1038/ncprheum0355. PMID 17133251.
    39. ↑ Jennette JC, Falk RJ (November 1997). “Small-vessel vasculitis”. N. Engl. J. Med. 337 (21): 1512–23. doi:10.1056/NEJM199711203372106. PMID 9366584.
    40. ↑ Jennette JC, Falk RJ (November 1997). “Small-vessel vasculitis”. N. Engl. J. Med. 337 (21): 1512–23. doi:10.1056/NEJM199711203372106. PMID 9366584.
    41. ↑ Chen JY, Mao JH (February 2015). “Henoch-Schönlein purpura nephritis in children: incidence, pathogenesis and management”. World J Pediatr. 11 (1): 29–34. doi:10.1007/s12519-014-0534-5. PMID 25557596.
    42. ↑ Hochreiter W, Knoll T, Hess B (February 2003). “[Pathophysiology, diagnosis and conservative therapy of non-calcium kidney calculi]”. Ther Umsch (in German). 60 (2): 89–97. doi:10.1024/0040-5930.60.2.89. PMID 12649987.
    43. ↑ Flannigan R, Choy WH, Chew B, Lange D (June 2014). “Renal struvite stones–pathogenesis, microbiology, and management strategies”. Nat Rev Urol. 11 (6): 333–41. doi:10.1038/nrurol.2014.99. PMID 24818849.
    44. ↑ Pereira DJ, Schoolwerth AC, Pais VM (March 2015). “Cystinuria: current concepts and future directions”. Clin. Nephrol. 83 (3): 138–46. PMID 25685869.
    45. ↑ Pereira DJ, Schoolwerth AC, Pais VM (March 2015). “Cystinuria: current concepts and future directions”. Clin. Nephrol. 83 (3): 138–46. PMID 25685869.
    46. ↑ Rosen DA, Hooton TM, Stamm WE, Humphrey PA, Hultgren SJ (2007). “Detection of intracellular bacterial communities in human urinary tract infection”. PLoS Med. 4 (12): e329. doi:10.1371/journal.pmed.0040329. PMC 2140087. PMID 18092884.
    47. ↑ Franco AV (2005). “Recurrent urinary tract infections”. Best Pract Res Clin Obstet Gynaecol. 19 (6): 861–73. doi:10.1016/j.bpobgyn.2005.08.003. PMID 16298166.
    48. ↑ Franco AV (2005). “Recurrent urinary tract infections”. Best Pract Res Clin Obstet Gynaecol. 19 (6): 861–73. doi:10.1016/j.bpobgyn.2005.08.003. PMID 16298166.
    49. ↑ John N. Krieger, Ulrich Dobrindt, Donald E. Riley & Eric Oswald (2011). “Acute Escherichia coli prostatitis in previously health young men: bacterial virulence factors, antimicrobial resistance, and clinical outcomes”. Urology. 77 (6): 1420–1425. doi:10.1016/j.urology.2010.12.059. PMID 21459419. Unknown parameter |month= ignored (help)
    50. ↑ Sharp VJ, Takacs EB, Powell CR (2010). “Prostatitis: diagnosis and treatment”. Am Fam Physician. 82 (4): 397–406. PMID 20704171.
    51. ↑ McNagny SE, Parker RM, Zenilman JM, Lewis JS (1992). “Urinary leukocyte esterase test: a screening method for the detection of asymptomatic chlamydial and gonococcal infections in men”. J. Infect. Dis. 165 (3): 573–6. PMID 1538163.
    52. ↑ Brill JR (2010). “Diagnosis and treatment of urethritis in men”. Am Fam Physician. 81 (7): 873–8. PMID 20353145.

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    Epidemiology and Demographics

    Epidemiology and Demographics

    Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Steven C. Campbell, M.D., Ph.D.; Associate Editor(s)-in-Chief: Rim Halaby, M.D. [2] Farima Kahe M.D. [3] Shanshan Cen, M.D. [4]

    Overview

    The prevalence of bladder cancer is approximately 130.5 per 100,000 individuals in the United States. The incidence of bladder cancer is approximately 20.3 per 100,000 individuals in the United States. The incidence of bladder cancer increases with age; the median age at diagnosis is 73 years. Males are more commonly affected with bladder cancer than females. Bladder cancer usually affects individuals of the white race. African American, Asian, and Hispanic individuals are less likely to develop bladder cancer.

    Epidemiology and Demographics

    Prevalence

    • In the United States, the age-adjusted prevalence of bladder cancer is 130.5 per 100,000 persons in 2011.[1][2]

    Incidence

    • The incidence of bladder cancer is approximately 20.3 per 100,000 individuals in the United States, based on 2008-2012 data.[3][4]
    • The delay-adjusted incidence of bladder cancer in 2011 was estimated to be 20.74 per 100,000 persons in the United States.[1][5]
    • In 2011, the age-adjusted incidence of bladder cancer was 20.13 per 100,000 persons in the United States.[1]

    Age

    • While the overall age-adjusted incidence of bladder cancer in the United States between 2007 and 2011 is 20.5 per 100,000, the age-adjusted incidence of bladder cancer by age category is:[1][6]
      • Under 65 years: 5.4 per 100,000
      • 65 and over: 124.7 per 100,000
    • The incidence of bladder cancer increases with age; the median age at diagnosis is 73 years.[3]

    Gender

    • In the United States, the age-adjusted prevalence of bladder cancer by gender in 2011 is:[1][7]
      • In males: 228.9 per 100,000
      • In females: 56.6 per 100,000
    • In the United States, the delay-adjusted incidence of bladder cancer by gender in 2011 is:[1][8]
      • In males: 36.24 per 100,000 persons
      • In females: 8.98 per 100,000 persons
    • In the United States, the age-adjusted incidence of bladder cancer by gender on 2011 is:[1][9]
      • In males: 35.18 per 100,000 persons
      • In females: 8.72 per 100,000 persons
    • Shown below is an image depicting the delay-adjusted incidence and observed incidence of bladder cancer by gender and race in the United States between 1975 and 2011. These graphs are adapted from SEER: The Surveillance, Epidemiology, and End Results Program of the National Cancer Institute.[1]

    <figure-inline class=”mw-default-size”></figure-inline>

    Race

    • Shown below is a table depicting the age-adjusted prevalence of bladder cancer by race in 2011 in the United States.[1]
    All Races White Black Asian/Pacific Islander Hispanic
    Age-adjusted prevalence 130.5 per 100,000 148.2 per 100,000 62.9 per 100,000 58.7 per 100,000 64.4 per 100,000
    • Shown below is an image depicting the incidence of bladder cancer by race in the United States between 1975 and 2011.[1]

    <figure-inline class=”mw-default-size”></figure-inline>

    API: Asian/Pacific Islander; AI/AN: American Indian/ Alaska Native

    Developed Countries

    • The incidence of bladder cancer is higher in Western countries as compared to developing countries.[10]

    Developing Countries

    • In the late 1980’s and early 1990’s, approximately one third of cancer cases in Egypt were cases of bladder cancer. Given the improved treatment of schistosomiasis in Egypt, the incidence of bladder cancer has been decreasing.[14]

    References

    1. ↑ 1.00 1.01 1.02 1.03 1.04 1.05 1.06 1.07 1.08 1.09 Howlader N, Noone AM, Krapcho M, Garshell J, Miller D, Altekruse SF, Kosary CL, Yu M, Ruhl J, Tatalovich Z,Mariotto A, Lewis DR, Chen HS, Feuer EJ, Cronin KA (eds). SEER Cancer Statistics Review, 1975-2011, National Cancer Institute. Bethesda, MD, http://seer.cancer.gov/csr/1975_2011/, based on November 2013 SEER data submission, posted to the SEER web site, April 2014.
    2. ↑ Malats N, Real FX (April 2015). “Epidemiology of bladder cancer”. Hematol. Oncol. Clin. North Am. 29 (2): 177–89, vii. doi:10.1016/j.hoc.2014.10.001. PMID 25836927.
    3. ↑ 3.0 3.1 Bladder Cancer.Surveillance, Epidemiology, and End Results Program 2015.http://seer.cancer.gov/statfacts/html/urinb.html
    4. ↑ Antoni S, Ferlay J, Soerjomataram I, Znaor A, Jemal A, Bray F (January 2017). “Bladder Cancer Incidence and Mortality: A Global Overview and Recent Trends”. Eur. Urol. 71 (1): 96–108. doi:10.1016/j.eururo.2016.06.010. PMID 27370177.
    5. ↑ Chavan S, Bray F, Lortet-Tieulent J, Goodman M, Jemal A (July 2014). “International variations in bladder cancer incidence and mortality”. Eur. Urol. 66 (1): 59–73. doi:10.1016/j.eururo.2013.10.001. PMID 24451595.
    6. ↑ Zhang Y, Zhu C, Curado MP, Zheng T, Boyle P (January 2012). “Changing patterns of bladder cancer in the USA: evidence of heterogeneous disease”. BJU Int. 109 (1): 52–6. doi:10.1111/j.1464-410X.2011.10283.x. PMC 3218244. PMID 21592300.
    7. ↑ Dobruch J, Daneshmand S, Fisch M, Lotan Y, Noon AP, Resnick MJ, Shariat SF, Zlotta AR, Boorjian SA (February 2016). “Gender and Bladder Cancer: A Collaborative Review of Etiology, Biology, and Outcomes”. Eur. Urol. 69 (2): 300–10. doi:10.1016/j.eururo.2015.08.037. PMID 26346676.
    8. ↑ Fajkovic H, Halpern JA, Cha EK, Bahadori A, Chromecki TF, Karakiewicz PI, Breinl E, Merseburger AS, Shariat SF (August 2011). “Impact of gender on bladder cancer incidence, staging, and prognosis”. World J Urol. 29 (4): 457–63. doi:10.1007/s00345-011-0709-9. PMID 21656173.
    9. ↑ Horstmann M, Witthuhn R, Falk M, Stenzl A (December 2008). “Gender-specific differences in bladder cancer: a retrospective analysis”. Gend Med. 5 (4): 385–94. doi:10.1016/j.genm.2008.11.002. PMID 19108811.
    10. ↑ Burger M, Catto JW, Dalbagni G, Grossman HB, Herr H, Karakiewicz P; et al. (2013). “Epidemiology and risk factors of urothelial bladder cancer”. Eur Urol. 63 (2): 234–41. doi:10.1016/j.eururo.2012.07.033. PMID 22877502.
    11. ↑ 11.0 11.1 Shokeir AA (2004). “Squamous cell carcinoma of the bladder: pathology, diagnosis and treatment”. BJU Int. 93 (2): 216–20. PMID 14690486.
    12. ↑ el-Mawla NG, el-Bolkainy MN, Khaled HM (2001). “Bladder cancer in Africa: update”. Semin Oncol. 28 (2): 174–8. PMID 11301380.
    13. ↑ Ploeg M, Aben KK, Kiemeney LA (June 2009). “The present and future burden of urinary bladder cancer in the world”. World J Urol. 27 (3): 289–93. doi:10.1007/s00345-009-0383-3. PMC 2694323. PMID 19219610.
    14. ↑ Zaghloul MS (2012). “Bladder cancer and schistosomiasis”. J Egypt Natl Canc Inst. 24 (4): 151–9. doi:10.1016/j.jnci.2012.08.002. PMID 23159285.

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    Risk Factors

    Risk Factors

    Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Steven C. Campbell, M.D., Ph.D.; Associate Editor(s)-in-Chief: Farima Kahe M.D. [2] Shanshan Cen, M.D. [3]

    Overview

    Common risk factors in the development of bladder cancer are smoking, occupational exposure to chemicals, chronic bladder irritation, chemotherapy, radiation therapy, arsenic, personal history of cancer in the urinary tract, congenital bladder anomalies, and aristolochic acids.

    Common Risk Factors

    Less Common Risk Factors

    • Less common risk factors in the development of bladder cancer include:[7][8][9][10]

    References

    1. ↑ Janković S, Radosavljević V (2007). “Risk factors for bladder cancer”. Tumori. 93 (1): 4–12. PMID 17455864.
    2. ↑ Letašiová S, Medve’ová A, Šovčíková A, Dušinská M, Volkovová K, Mosoiu C, Bartonová A (June 2012). “Bladder cancer, a review of the environmental risk factors”. Environ Health. 11 Suppl 1: S11. doi:10.1186/1476-069X-11-S1-S11. PMC 3388449. PMID 22759493.
    3. ↑ Ugnat AM, Luo W, Semenciw R, Mao Y (2004). “Occupational exposure to chemical and petrochemical industries and bladder cancer risk in four western Canadian provinces”. Chronic Dis Can. 25 (2): 7–15. PMID 15554606.
    4. ↑ Bhatt VR, Loberiza FR, Tandra P, Krishnamurthy J, Shrestha R, Wang J (January 2014). “Risk factors, therapy and survival outcomes of small cell and large cell neuroendocrine carcinoma of urinary bladder”. Rare Tumors. 6 (1): 5043. doi:10.4081/rt.2014.5043. PMC 3977167. PMID 24711904.
    5. ↑ Vermeulen SH, Hanum N, Grotenhuis AJ, Castaño-Vinyals G, van der Heijden AG, Aben KK, Mysorekar IU, Kiemeney LA (February 2015). “Recurrent urinary tract infection and risk of bladder cancer in the Nijmegen bladder cancer study”. Br. J. Cancer. 112 (3): 594–600. doi:10.1038/bjc.2014.601. PMC 4453642. PMID 25429525.
    6. ↑ Hess MJ, Zhan EH, Foo DK, Yalla SV (2003). “Bladder cancer in patients with spinal cord injury”. J Spinal Cord Med. 26 (4): 335–8. PMID 14992333.
    7. ↑ Gu J, Wu X (May 2011). “Genetic susceptibility to bladder cancer risk and outcome”. Per Med. 8 (3): 365–374. doi:10.2217/PME.11.15. PMC 3172962. PMID 21927616.
    8. ↑ Zhang X, Zhang Y (September 2015). “Bladder Cancer and Genetic Mutations”. Cell Biochem. Biophys. 73 (1): 65–9. doi:10.1007/s12013-015-0574-z. PMID 27352265.
    9. ↑ Castaño-Vinyals G, Cantor KP, Malats N, Tardon A, Garcia-Closas R, Serra C, Carrato A, Rothman N, Vermeulen R, Silverman D, Dosemeci M, Kogevinas M (January 2008). “Air pollution and risk of urinary bladder cancer in a case-control study in Spain”. Occup Environ Med. 65 (1): 56–60. doi:10.1136/oem.2007.034348. PMID 17634245.
    10. ↑ Fortuny J, Kogevinas M, Zens MS, Schned A, Andrew AS, Heaney J, Kelsey KT, Karagas MR (August 2007). “Analgesic and anti-inflammatory drug use and risk of bladder cancer: a population based case control study”. BMC Urol. 7: 13. doi:10.1186/1471-2490-7-13. PMC 2018698. PMID 17692123.

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    Screening

    Screening

    Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Farima Kahe M.D. [2]

    Overview

    There is insufficient evidence to recommend routine screening for bladder cancer.

    Screening

    There is insufficient evidence to recommend routine screening for bladder cancer.

    References

    Natural History, Complications and Prognosis

    Natural History, Complications and Prognosis

    Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Farima Kahe M.D. [2] Rim Halaby, M.D. [3] Shanshan Cen, M.D. [4]

    Overview

    Common complications of bladder cancer include metastasis, anemia, hydronephrosis, urethral stricture, and urinary incontinence. Prognosis is generally good, and the 5-year survival rate is approximately 77.4%. The prognosis varies with the stages of tumor; carcinoma in situ have the most favorable prognosis.

    Natural History, Complications, and Prognosis

    Natural History

    • The symptoms of bladder cancer usually develop in the 6th and 7th decade of life, and start with symptoms such as hematuria, difficulty urinating and dysuria.[1][2]

    Complications

    Prognosis

    • Based on data from 2005-2011, the 5-year survival rate of patients with bladder cancer is approximately 77.4%.[7]
    • Between 2004 and 2010, the 5-year relative survival of patients with bladder cancer was 79.1%.[8]
    • When stratified by age, the 5-year relative survival of patients with bladder cancer was 83.8% and 74.1% for patients <65 and ≥ 65 years of age respectively.[8]
    • The survival of patients with bladder cancer varies with the stage of the disease. Shown below is a table depicting the 5-year relative survival by the stage of bladder cancer:[8]
    Stage 5-year relative survival (%), (2004-2010)
    All stages 77.4%
    In situ 96.2%
    Localized 69.2%
    Regional 33.7%
    Distant 5.5%
    Unstaged 48.7%
    • Shown below is an image depicting the 5-year conditional relative survival (probability of surviving in the next 5-years given the cohort has already survived 0, 1, 3 years) between 2004 and 2010 of bladder cancer by stage at diagnosis according to SEER. These graphs are adapted from SEER: The Surveillance, Epidemiology, and End Results Program of the National Cancer Institute.[8]

    5-year conditional relative survival (probability of surviving in the next 5-years given the cohort has already survived 0, 1, 3 years) between 2004 and 2010 of bladder cancer by stage at diagnosis according to SEER.

    References

    1. ↑ Aliramaji A, Kaseean A, Yousefnia Pasha YR, Shafi H, Kamali S, Safari M, Moudi E (2015). “Age distribution types of bladder cancers and their relationship with opium consumption and smoking”. Caspian J Intern Med. 6 (2): 82–6. PMC 4478456. PMID 26221505.
    2. ↑ Gupta P, Jain M, Kapoor R, Muruganandham K, Srivastava A, Mandhani A (April 2009). “Impact of age and gender on the clinicopathological characteristics of bladder cancer”. Indian J Urol. 25 (2): 207–10. doi:10.4103/0970-1591.52916. PMC 2710066. PMID 19672348.
    3. ↑ Pagliaro LC, Sharma P (March 2006). “Review of metastatic bladder cancer”. Minerva Urol Nefrol. 58 (1): 53–71. PMID 16760884.
    4. ↑ Anderson TS, Regine WF, Kryscio R, Patchell RA (May 2003). “Neurologic complications of bladder carcinoma: a review of 359 cases”. Cancer. 97 (9): 2267–72. doi:10.1002/cncr.11354. PMID 12712482.
    5. ↑ Taylor JA, Kuchel GA (March 2009). “Bladder cancer in the elderly: clinical outcomes, basic mechanisms, and future research direction”. Nat Clin Pract Urol. 6 (3): 135–44. doi:10.1038/ncpuro1315. PMC 2957872. PMID 19265855.
    6. ↑ Shinagare AB, Ramaiya NH, Jagannathan JP, Fennessy FM, Taplin ME, Van den Abbeele AD (January 2011). “Metastatic pattern of bladder cancer: correlation with the characteristics of the primary tumor”. AJR Am J Roentgenol. 196 (1): 117–22. doi:10.2214/AJR.10.5036. PMID 21178055.
    7. ↑ Bladder Cancer. Surveillance, Epidemiology, and End Results Program 2015.http://seer.cancer.gov/statfacts/html/urinb.html
    8. ↑ 8.0 8.1 8.2 8.3 Howlader N, Noone AM, Krapcho M, Garshell J, Miller D, Altekruse SF, Kosary CL, Yu M, Ruhl J, Tatalovich Z,Mariotto A, Lewis DR, Chen HS, Feuer EJ, Cronin KA (eds). SEER Cancer Statistics Review, 1975-2011, National Cancer Institute. Bethesda, MD, http://seer.cancer.gov/csr/1975_2011/, based on November 2013 SEER data submission, posted to the SEER web site, April 2014.

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    Diagnosis

    Diagnosis

    Staging | History and Symptoms | Physical Examination | Laboratory Findings | X Ray | CT | MRI | Ultrasound | Other Imaging Findings | Other Diagnostic Studies | Biopsy

    Treatment

    Treatment

    Medical Therapy | Surgery | Primary prevention | Secondary Prevention | Cost-Effectiveness of Therapy | Future or Investigational Therapies

    Steven C. Campbell, M.D., Ph.D.

    Treatment

    The treatment of bladder cancer depends on how deep the tumor invades into the bladder wall. Superficial tumors (those not entering the muscle layer) can be “shaved off” using an electrocautery device attached to a cystoscope. Immunotherapy in the form ofBCG instillation is also used to treat and prevent the recurrence of superficial tumors.[1] BCG immunotherapy is effective in up to 2/3 of the cases at this stage. Instillations of chemotherapy into the bladder can also be used to treat superficial disease.

    Untreated, superficial tumors may gradually begin to infiltrate the muscular wall of the bladder. Tumors that infiltrate the bladder require more radical surgery where part or all of the bladder is removed (a cystectomy) and the urinary stream is diverted. In some cases, skilled surgeons can create a substitute bladder (a neobladder) from a segment of intestinal tissue, but this largely depends upon patient preference, age of patient, renal function, and the site of the disease.

    A combination of radiation and chemotherapy can also be used to treat invasive disease. It has not yet been determined how the effectiveness of this form of treatment compares to that of radical ablative surgery.

    There is weak observational evidence from one very small study (84) to suggest that the concurrent use of statins is associated with failure of BCG immunotherapy.[2]

    References

    1. ↑ “BCG immunotherapy of bladder cancer: 20 years on”. 353 (9165). 1999: 1689&ndash, 94.
    2. ↑ “Use of statins and outcome of BCG treatment for bladder cancer”. 355 (25). 2006: 2705&ndash, 7.

    Template:Tumors

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    Case Studies

    Case Studies

    Case #1

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