CYSTITIS GLANDULARIS G. DAVIES,
B.Sc.,
J. E. CASTRO,
M.B.,
PH.D.,
B.S.
M.S.,
F.R.C.S.
From the Urology and Transplantation Unit, Royal Postgraduate Medical School, Hammersmith Hospital, London, England
- We present 12 cases of cystitis glandular-is which fall into two distinct groups, one characterized by hematuria and the other by urinary tract infection. We can produce no clinical evidence that this disease is premalignant, but emphasize the necessity of histology to exclude malignancy since, macroscopically, the condition is indistinguishable from mitotic changes. We also describe the association of cystitis glandularis and pelvic lipomatosis. ABSTRACT
Cystitis glandularis was first described by Morgagni in 1761’ who reported 2 patients with cysts in the urinary tract. Giani’ introduced capsules containing tubercle bacilli into the bladders of rabbits by a suprapubic cystostomy and produced changes similar to cystitis glandularis; he concluded that chronic irritation was an im-;_ portant etiologic factor. More recentl$Nesb@* considered the association between cystitis glandularis and urothelial malignancy. The object of this study was to review 12 cases to see how their modes of presentation and subsequent clinical course correspond to the current theories relating to cystitis glandularis. Material
and Methods
We present 12 patients with histologically confirmed cystitis glandularis treated at this hospital between 1965 and 1975. Of these, 9 were male and 3 female; their ages ranged between forty-two and eighty-two years, the highest incidence being in the fifth decade. The symptoms with which patients presented are shown in Table I, their mode of presentation falling into two distinct groups. Group 1 consisted of 7 males with recurrent painless hematuria; 2 of whom had coexisting transitional cell bladder neoplasm, 2 had associated pelvic lipomatosis, including 1 who presented with
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right hydroureter and hydronephrosis with ureteric calculus. Group 2 represented 5 patients, including the 3 females, presenting with recurrent urinary tract infections. The organisms causing the infection were Escherichia coli in 2 cases, Klebsiella in 1, and Proteus in 2. urography in Group 1 revealed - . Intravenous .._. --_ definite- bladder pathology in all cases. In 5 patients there was a space-occupying lesion in the bladder, and in the other 2 there was dilatation of the upper tracts due to ureteric obstruction, including 1 case of pelvic lipomatosis. In Group 2 the only pathologic abnormality was a small pyelonephritic kidney in 1 case. Cystoscopic examination of Group 1 patients revealed only 1 patient with the classic cobblestone appearance of cystitis glandularis. The remaining 6 patients had changes suggestive of TABLE I.
Presenting features (12 patients)
Presenting Feature
Number
Infected urine Bladder tumor Renal calculi Pelvic lipomatosis Pelvic lipomatosis plus hydronephrosis Hydronephrosis Outflow tract obstruction plus urinary tract infection
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neoplasm, but this was confirmed in only 2 cases despite multiple biopsies and follow-up. In Group 2, 1 patient had typical changes, whereas 4 had raised inflammatory areas. In all cases, the area of the bladder involved was divided equally between the trigone and the areas adjacent to the left and right ureteric orifices. There was no relationship between sites and mode of presentation. Follow-up included cystoscopy, urography, and biopsy and has varied between one month and nine years. In Group 1, 2 patients with coexisting malignancy died within nine months, 1 from malignancy and 1 from other causes. The
FIGURE 1. Histologic changes of cystitis glandular-is showing von Bmnn’s nests and changes suggestive of colonic epithelium. (Hematoxylin and eosin stain, original magnifkation X 60.)
other 5 patients
continued to have positive findings at biopsy and continuing episodes of painless hematuria, but no evidence of ensuing malignant change; they have not been treated. In Group 2, treatment of urinary tract infection resulted in complete cessation of symptoms and a return to normal, both cystoscopically and histologically. Comment Cystitis glandularis is considered to be a rare condition, but in association with other diseases it is seen so often that it is rarely reported by pathologists. Many factors have been considered in the etiology, including avitaminosis, allergy, toxic products of metabolism, hormonal imbalance, and specific inducing enzymes.4 However, it is now generally accepted that
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lithiasis, chronic irritation, infection, and outflow tract obstruction are predominantly responsible. Many interesting theories advancing an embryologic origin have been considered indicating that cystitis glandularis may develop in rests displaced in separation of the rectum from the urogenital tract or from the embryonal inclusion of germinal cells of the lower gastrointestinal tract. This theory is unsatisfactory since cystitis glandularis also occurs in ureter and renal pelvis. The histologic changes are shown in Figure 1. Histologically, cysts develop in the mucosa of bladder, ureter, or renal pelvis. There is a progressive metaplasia from transitional cells to goblet cells. A downward projection of epithelial cell rests produces the changes described by von Brunn.5 The multiple cysts are lined by flattened epithelium which project into the trigone and secrete mucin. Cystitis cystica is a condition in which Brunn’s nests predominate but which do not secrete mucin. These nests may also contain Kulchitsky cells and small bowel epithelium. Another interesting association is between cystitis glandularis and pelvic lipomatosis.6 Pelvic lipomatosis is a rare condition originally described by Engles7 in which there is abnormal deposition of fat around the bladder, rectum, and prostate. This occurred in 2 of our cases. There are many reports of proliferative change occurring in association with bladder tumor, but there is no definite satisfactory evidence to suggest that this is a premalignant condition despite the fact that the two conditions often coexist. London W12 OHS, England (DR. CASTRO)
References 1. Morgagni JB: The Seats and Causes of Diseases Investigated by Anatomy. Translated by B. Alexander, London, Miller, 1769. 2. Giani R: Enstelehung der Cystitis Cysitica, Zentralbl. Allg. Pathol. 17: 906 (1966). 3. Nesbit RM: Is cystitis cystica an innocent or a malefic lesion? Br. J. Urol. 75: 443 (1956). 4. Parker C: Cystitis cystica and glandularis: a study of 40 cases, Proc. Roy. Sot. Med. 63: 239 (1970). 5. von Brunn A: Uber drusenahnliche Bildungen in der Schleinhaut des Mierenbeckens des Ureters und der Hamblase bein Menschen, Arch. Mikroskopische Anat. 41: 303 (1893). 6. Yalla SV, Ivker M, Burros HM, and Dorey F: Cystitis glandularis with perivesical Iipomatosis, Urology 5: 383 (1975). 7. Engles EP: Lymphoid colon and urinary bladder in high fixation, Radiology 72: 419 (1959).
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