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Computed tomography and ultrasound appearance of bladder malacoplakia
CT: THE JOURNAL OF COMPUTED TOMOGRAPHY 1985; 9:119-123
119
COMPUTED TOMOGRAPHY AND ULTRASOUND APPEARANCE OF BLADDER MALACOPLAKIA WENZEL VAS, MD, B. CATRAL, MD, B. CARLIN, P. TANG-BARTON, MD, AND Z. SALIMI, MD The computed tomography and ultrasound findings of two patients with malacoplakia of the bladder, both at the time of initial diagnosis and following response to treatment, are presented. Because bladder wall involvement is demonstrated by these modalities in female patients with repeated episodes of urinary tract infection, this entity should be entertained in the differential diagnosis. KEY WORDS: Bladder, malacoplakia; Computed tomography; Ultrasound
Malacoplakia, an uncommon entity that usually affects the bladder, was originally described by Michaelis and Gutmann in 1902 (1). It is characterized by multiple, soft plaque-like lesions that are seen on histologic examination to be composed of histiocytes and lymphocytes. Characteristic spheroidal bodies of calcium, the calcospheroids or MichaelisGutmann [M-G) bodies, are seen within the histiocytes and are pathognomonic for this condition. These M-G bodies are believed to represent calcification around incompletely digested bacteria. The computed tomography (CT) and ultrasound findings in two patients with malacoplakia of the bladder are described.
From the Department of Diagnostic Radiology, St. Louis City Hospital, St. Louis University School of Medicine, St. Louis,
Missouri. Address reprint requests to: Wenzel Vas, MD, Director, Department of Radiology, St. Louis City Hospital, 1515 Layfayette Avenue, St. Louis, Missouri 63104. Received February 1984. 0 1985 by Elsevier Science Publishing Co., Inc. 52 Vanderbilt Ave., New York, NY 10017 0149-936X/85/$3.30
MD,
CASE REPORTS Case 1 A 44-yeaf-old black female was admitted with a 2day history of urinary retention. There was no history of dysuria or hematuria. Past medical history included recurrent episodes of urinary tract infections. Physical examination on admission was unremarkable. A straight catheter was introduced into the bladder and 500 mL of dark-colored urine was obtained, which showed numerous erythrocytes and leukocytes and which subsequently grew Escherichia coli on culture. Laboratory values included a serum creatinine value of 6.5 mg/dL and a blood urea nitrogen value of 55 mg/dL. Following insertion of an indwelling Foley catheter, the serum creatinine level fell to normal over the course of the next 4 days. An ultrasound examination at the time of admission revealed bilateral hydronephrosis and hydroureter up to the ureterovesical junction. The bladder wall was thickened uniformly (Figure 1). A CT scan performed immediately after the sonogram confirmed the ultrasound findings and showed the bladder wall to be lobulated and thickened throughout [Figure 2). An enlarged uterus was noted behind the bladder. A cystogram was performed on the following day and this once again confirmed diffuse bladder wall involvement by multiple lobulations (Figure 3). At cystoscopy, the bladder wall was noted to be hyperemic with well-circumscribed, pinkish-tan nodules throughout that were most marked in the region of the trigone. Adequate distention of the bladder was unobtainable. An attempt was made to perform retrograde pyelography, but this was unsuccessful as the ureters could not be cannulated. Multiple biopsies were obtained from various parts of the bladder. Histologic examination revealed
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VAS ET AL.
FIGURE 1. Transverse section through the bladder region. Bilateral dilatation of the ureters is seen, more pronounced on the right than the left (black arrows). There is diffuse involvement of the bladder wall (white arrows).
many histiocytes containing M-G bodies, consistent with bladder malacoplakia. The patient was placed on a regimen of bethanechol chloride and trimethoprim-sulfamethoxazole with resulting rapid improvement, and was asymp-
FIGURE 3. Anteroposterior view of the contrast mediumfilled bladder reveals multiple lobulated filling defects involving the bladder wall.
CT: THE JOURNAL OF COMPUTED TOMOGRAPHY VOL. 9 NO. 1
FIGURE 2. A CT scan through the pelvis shows the bladder wall to be thickened circumferentially (white arrows). Dilatation of both ureters is once again identified (black arrows).
tomatic on discharge. A repeat CT scan and ultrasound examination 2 months later revealed the bladder wall to be of normal thickness [Figures 4 and 5).
FIGURE 4. Repeat ultrasound examination 2 months later reveals resolution of both the bladder wall thickening and obstruction of the ureters.
APRIL 1985
Case 2
CT OF BLADDER MALACOPLAKIA
121
The second patient, a %-year-old black female, was admitted with a l-day history of left lower quadrant pain, fever, and hematuria. There was no history of frequency or dysuria. Her past medical history included recurrent urinary tract infections and a hysterectomy. Physical examination on admission was
unremarkable. Laboratory values included a serum creatinine value of 1.2 mg/dL and a blood urea nitrogen value of 13 mg/dL. Urinalysis showed numerous white and red cells, and E. coli was grown on culture. An excretory urogram showed bilateral hydronephrosis and hydroureter up to the ureterovesical
FIGURE 6. (A) Delayed image on excretory urogram (case 2) reveals bilateral hydroureter with bladder wall thickening and contraction of the bladder. (B) Repeat ex-
cretory urogram 1 month later following treatment reveals resolution of the obstruction. There is still some bladder wall irregularity.
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junctions, along with a contracted urinary bladder (Figure 6A). The same day the patient had an ultrasound examination that showed irregular thickening of the bladder wall (Figure 7). The next day a CT scan of the pelvis confirmed the sonographic findings (Figure 8). The bladder wall was again noted to be thickened throughout. At cystoscopy, the bladder wall was seen to be reddish, soft, and friable. The ureteral orifices could not be cannulated because of poor visualization, A cystometrogram confirmed the bladder to be of small capacity. Histologic examination of multiple biopsy specimens showed findings consistent with bladder malacoplakia. The patient was treated with the appropriate antibiotics and discharged. A month later she was readmitted with a repeat episode of hematuria. A repeat urogram showed no obstruction but the bladder wall was irregular (Figure 6B). Cystoscopy was performed and this revealed inflammation of the bladder wall. Biopsy on the second occasion revealed evidence of cystitis only.
CT: THE JOURNAL OF COMPUTED TOMOGRAPHY VOL. 9 NO. 2
FIGURE 7. Longitudinal scan through the bladder reveals bladder wall thickening with slight suggestion of vesicles in the heaped up areas.
DISCUSSION Malacoplakia is an unusual inflammatory disease that was originally described in the bladder but has subsequently been found in other genitourinary sites and rarely in other organs such as the stomach, colon, appendix, prostate, and bone (l-3). The disease is more common in females than males in a ratio of 4 : 1, with the greatest incidence in the fifth decade. It is essentially a granulomatous process. Macroscopically, the plaques of malacoplakia appear as discrete, slightly elevated, pinkish-brown nodules, ranging in size from 1 mm to as large as 3 cm. These may show central ulceration and circumferential hyperemia. The lesions are composed primarily of histiocytes called Hansemann cells and of collections of lymphocytes. The large phagocytic cells frequently contain concentrically laminated concretions of calcium known as calcospherites or inclusion bodies of Michaelis-Gutmann, which are pathognomic for this entity. Little is known about the pathogenesis of this disorder. Because of a frequent association with urinary tract infections, an infectious agent has long been suspected. It has been postulated that malacoplakia represents a morphologic manifestation of altered host macrophage response to E coli (4, 5). More recently, several patients with this condition were found to have abnormal monocyte function (6, 7). Urinary tract malacoplakia is generally consid-
ered a self-limited inflammatory disease. Patients often present with symptoms related to the lower urinary tract such as dysuria or retention. These symptoms usually resolve following treatment with trimethoprim-sulfamethoxazole or bethanechol chloride (6, 7). Both the CT and ultrasound examinations in our patients revealed circumferential bladder wall thickening with multiple lobules. These lobulations represent the nodular plaques of malacoplakia. The extent of involvement was enough to cause bilateral hydronephrosis and hydroureter. FIGURE 8. A CT scan through the pelvis confirms the diffuse bladder wall thickening.
CT OF BLADDER MALACOPLAKIA
APRIL 1985
To date, the CT appearance of only one other case has been described (8). In that case, CT revealed a large solid mass within the left side of the bladder with extension to the adjacent side wall of the pelvis. Some interval reduction in size followed treatment. The CT appearance in both these patients cannot be differentiated from other more serious entities such as bladder carcinoma, secondary involvement of the bladder by malignancies of adjacent structures, or endometriosis. However, these findings on a CT or ultrasound study in females with a history of repeated urinary tract infections should suggest the possibility of malacoplakia. The extent of involvement can be accurately gauged and response to conservative therapy can also be evaluated in a noninvasive manner. The authors would like to thank Ulysses Johnson and Connie Cornell for technical assistance and Jennifer Ferrell for secretarial help.
123
REFERENCES 1. Michaelis L, Gutmann C: Uber einschlusse in Blassentumoren. 2 Klin Med 1902;47:208-15. 2. Smith BH: Malackoplakia of the urinary tract: A study of twenty-four cases. Am J Clin Path01 1965;43:409-17. 3. Yunis EJ, Estevez JM, Pinzon GJ, et al.: Malackoplakia: Discussion of pathogenesis and report of three cases including one of fatal gastric and colonic involvement. Arch Path01 1967;83:180-7. 4. Lou TY, Teplitz C: Malackoplakia: Pathogenesis and ultrastructural morphogenesis. A problem of altered macrophage (phagolysosomal) response. Hum Path01 1974;5:191-207. 5. Lewin KJ, Fair WR, Steigbigel RT, et al.: Clinical and laboratory studies into the pathogenesis of malackoplakia. J Clin Pathol 1976;29:354-63. 6. Abdou NI, NaPombejara C, Sagawa A, et al.: Malackoplakia: Evidence for monocytic lysosomal abnormality correctable by cholinergic agonist in vitro and in vivo. N Engl J Med 1977;297:14-139, 7. Maderazo EG, Berlin BB, Morhardt C: Treatment of malackotrimethoprimsulfamethoxazole. Urology plakia with 1979;13:703. 8. Epstein BM, Pate1 V, Porteous PH: Case Report-CT appearance of bladder malackoplakia. J Comput Assist Tomogr 1983:7:541-3.
119
COMPUTED TOMOGRAPHY AND ULTRASOUND APPEARANCE OF BLADDER MALACOPLAKIA WENZEL VAS, MD, B. CATRAL, MD, B. CARLIN, P. TANG-BARTON, MD, AND Z. SALIMI, MD The computed tomography and ultrasound findings of two patients with malacoplakia of the bladder, both at the time of initial diagnosis and following response to treatment, are presented. Because bladder wall involvement is demonstrated by these modalities in female patients with repeated episodes of urinary tract infection, this entity should be entertained in the differential diagnosis. KEY WORDS: Bladder, malacoplakia; Computed tomography; Ultrasound
Malacoplakia, an uncommon entity that usually affects the bladder, was originally described by Michaelis and Gutmann in 1902 (1). It is characterized by multiple, soft plaque-like lesions that are seen on histologic examination to be composed of histiocytes and lymphocytes. Characteristic spheroidal bodies of calcium, the calcospheroids or MichaelisGutmann [M-G) bodies, are seen within the histiocytes and are pathognomonic for this condition. These M-G bodies are believed to represent calcification around incompletely digested bacteria. The computed tomography (CT) and ultrasound findings in two patients with malacoplakia of the bladder are described.
From the Department of Diagnostic Radiology, St. Louis City Hospital, St. Louis University School of Medicine, St. Louis,
Missouri. Address reprint requests to: Wenzel Vas, MD, Director, Department of Radiology, St. Louis City Hospital, 1515 Layfayette Avenue, St. Louis, Missouri 63104. Received February 1984. 0 1985 by Elsevier Science Publishing Co., Inc. 52 Vanderbilt Ave., New York, NY 10017 0149-936X/85/$3.30
MD,
CASE REPORTS Case 1 A 44-yeaf-old black female was admitted with a 2day history of urinary retention. There was no history of dysuria or hematuria. Past medical history included recurrent episodes of urinary tract infections. Physical examination on admission was unremarkable. A straight catheter was introduced into the bladder and 500 mL of dark-colored urine was obtained, which showed numerous erythrocytes and leukocytes and which subsequently grew Escherichia coli on culture. Laboratory values included a serum creatinine value of 6.5 mg/dL and a blood urea nitrogen value of 55 mg/dL. Following insertion of an indwelling Foley catheter, the serum creatinine level fell to normal over the course of the next 4 days. An ultrasound examination at the time of admission revealed bilateral hydronephrosis and hydroureter up to the ureterovesical junction. The bladder wall was thickened uniformly (Figure 1). A CT scan performed immediately after the sonogram confirmed the ultrasound findings and showed the bladder wall to be lobulated and thickened throughout [Figure 2). An enlarged uterus was noted behind the bladder. A cystogram was performed on the following day and this once again confirmed diffuse bladder wall involvement by multiple lobulations (Figure 3). At cystoscopy, the bladder wall was noted to be hyperemic with well-circumscribed, pinkish-tan nodules throughout that were most marked in the region of the trigone. Adequate distention of the bladder was unobtainable. An attempt was made to perform retrograde pyelography, but this was unsuccessful as the ureters could not be cannulated. Multiple biopsies were obtained from various parts of the bladder. Histologic examination revealed
120
VAS ET AL.
FIGURE 1. Transverse section through the bladder region. Bilateral dilatation of the ureters is seen, more pronounced on the right than the left (black arrows). There is diffuse involvement of the bladder wall (white arrows).
many histiocytes containing M-G bodies, consistent with bladder malacoplakia. The patient was placed on a regimen of bethanechol chloride and trimethoprim-sulfamethoxazole with resulting rapid improvement, and was asymp-
FIGURE 3. Anteroposterior view of the contrast mediumfilled bladder reveals multiple lobulated filling defects involving the bladder wall.
CT: THE JOURNAL OF COMPUTED TOMOGRAPHY VOL. 9 NO. 1
FIGURE 2. A CT scan through the pelvis shows the bladder wall to be thickened circumferentially (white arrows). Dilatation of both ureters is once again identified (black arrows).
tomatic on discharge. A repeat CT scan and ultrasound examination 2 months later revealed the bladder wall to be of normal thickness [Figures 4 and 5).
FIGURE 4. Repeat ultrasound examination 2 months later reveals resolution of both the bladder wall thickening and obstruction of the ureters.
APRIL 1985
Case 2
CT OF BLADDER MALACOPLAKIA
121
The second patient, a %-year-old black female, was admitted with a l-day history of left lower quadrant pain, fever, and hematuria. There was no history of frequency or dysuria. Her past medical history included recurrent urinary tract infections and a hysterectomy. Physical examination on admission was
unremarkable. Laboratory values included a serum creatinine value of 1.2 mg/dL and a blood urea nitrogen value of 13 mg/dL. Urinalysis showed numerous white and red cells, and E. coli was grown on culture. An excretory urogram showed bilateral hydronephrosis and hydroureter up to the ureterovesical
FIGURE 6. (A) Delayed image on excretory urogram (case 2) reveals bilateral hydroureter with bladder wall thickening and contraction of the bladder. (B) Repeat ex-
cretory urogram 1 month later following treatment reveals resolution of the obstruction. There is still some bladder wall irregularity.
122
VAS ET AL.
junctions, along with a contracted urinary bladder (Figure 6A). The same day the patient had an ultrasound examination that showed irregular thickening of the bladder wall (Figure 7). The next day a CT scan of the pelvis confirmed the sonographic findings (Figure 8). The bladder wall was again noted to be thickened throughout. At cystoscopy, the bladder wall was seen to be reddish, soft, and friable. The ureteral orifices could not be cannulated because of poor visualization, A cystometrogram confirmed the bladder to be of small capacity. Histologic examination of multiple biopsy specimens showed findings consistent with bladder malacoplakia. The patient was treated with the appropriate antibiotics and discharged. A month later she was readmitted with a repeat episode of hematuria. A repeat urogram showed no obstruction but the bladder wall was irregular (Figure 6B). Cystoscopy was performed and this revealed inflammation of the bladder wall. Biopsy on the second occasion revealed evidence of cystitis only.
CT: THE JOURNAL OF COMPUTED TOMOGRAPHY VOL. 9 NO. 2
FIGURE 7. Longitudinal scan through the bladder reveals bladder wall thickening with slight suggestion of vesicles in the heaped up areas.
DISCUSSION Malacoplakia is an unusual inflammatory disease that was originally described in the bladder but has subsequently been found in other genitourinary sites and rarely in other organs such as the stomach, colon, appendix, prostate, and bone (l-3). The disease is more common in females than males in a ratio of 4 : 1, with the greatest incidence in the fifth decade. It is essentially a granulomatous process. Macroscopically, the plaques of malacoplakia appear as discrete, slightly elevated, pinkish-brown nodules, ranging in size from 1 mm to as large as 3 cm. These may show central ulceration and circumferential hyperemia. The lesions are composed primarily of histiocytes called Hansemann cells and of collections of lymphocytes. The large phagocytic cells frequently contain concentrically laminated concretions of calcium known as calcospherites or inclusion bodies of Michaelis-Gutmann, which are pathognomic for this entity. Little is known about the pathogenesis of this disorder. Because of a frequent association with urinary tract infections, an infectious agent has long been suspected. It has been postulated that malacoplakia represents a morphologic manifestation of altered host macrophage response to E coli (4, 5). More recently, several patients with this condition were found to have abnormal monocyte function (6, 7). Urinary tract malacoplakia is generally consid-
ered a self-limited inflammatory disease. Patients often present with symptoms related to the lower urinary tract such as dysuria or retention. These symptoms usually resolve following treatment with trimethoprim-sulfamethoxazole or bethanechol chloride (6, 7). Both the CT and ultrasound examinations in our patients revealed circumferential bladder wall thickening with multiple lobules. These lobulations represent the nodular plaques of malacoplakia. The extent of involvement was enough to cause bilateral hydronephrosis and hydroureter. FIGURE 8. A CT scan through the pelvis confirms the diffuse bladder wall thickening.
CT OF BLADDER MALACOPLAKIA
APRIL 1985
To date, the CT appearance of only one other case has been described (8). In that case, CT revealed a large solid mass within the left side of the bladder with extension to the adjacent side wall of the pelvis. Some interval reduction in size followed treatment. The CT appearance in both these patients cannot be differentiated from other more serious entities such as bladder carcinoma, secondary involvement of the bladder by malignancies of adjacent structures, or endometriosis. However, these findings on a CT or ultrasound study in females with a history of repeated urinary tract infections should suggest the possibility of malacoplakia. The extent of involvement can be accurately gauged and response to conservative therapy can also be evaluated in a noninvasive manner. The authors would like to thank Ulysses Johnson and Connie Cornell for technical assistance and Jennifer Ferrell for secretarial help.
123
REFERENCES 1. Michaelis L, Gutmann C: Uber einschlusse in Blassentumoren. 2 Klin Med 1902;47:208-15. 2. Smith BH: Malackoplakia of the urinary tract: A study of twenty-four cases. Am J Clin Path01 1965;43:409-17. 3. Yunis EJ, Estevez JM, Pinzon GJ, et al.: Malackoplakia: Discussion of pathogenesis and report of three cases including one of fatal gastric and colonic involvement. Arch Path01 1967;83:180-7. 4. Lou TY, Teplitz C: Malackoplakia: Pathogenesis and ultrastructural morphogenesis. A problem of altered macrophage (phagolysosomal) response. Hum Path01 1974;5:191-207. 5. Lewin KJ, Fair WR, Steigbigel RT, et al.: Clinical and laboratory studies into the pathogenesis of malackoplakia. J Clin Pathol 1976;29:354-63. 6. Abdou NI, NaPombejara C, Sagawa A, et al.: Malackoplakia: Evidence for monocytic lysosomal abnormality correctable by cholinergic agonist in vitro and in vivo. N Engl J Med 1977;297:14-139, 7. Maderazo EG, Berlin BB, Morhardt C: Treatment of malackotrimethoprimsulfamethoxazole. Urology plakia with 1979;13:703. 8. Epstein BM, Pate1 V, Porteous PH: Case Report-CT appearance of bladder malackoplakia. J Comput Assist Tomogr 1983:7:541-3.