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Purple urine bag syndrome
American Journal of Emergency Medicine (2005) 23, 521 – 524
www.elsevier.com/locate/ajem
Purple urine bag syndrome Federico Vallejo-Manzur MDa, Eduardo Mireles-Cabodevila MDb, Joseph Varon MDc,* a
University of Massachusetts, Worcester, MA 01605, USA Maryland General Hospital, Baltimore, MD 21201, USA c The University of Texas Health Science Center, St. Lukes Episcopal Hospital, Houston, TX 77030, USA b
Received 15 October 2004; accepted 15 October 2004
Abstract The purple urine bag syndrome (PUBS) is a rare condition associated with chronic urinary catheterization. It is characterized by the purple discoloration of the urine, collecting bag, and tubing. A number of factors are involved, but not always present, in its development including female sex, urinary tract infection, constipation, indicanuria, and alkaline urine. Despite multiple theories that involve the complex tryptophan metabolism to the tubing dye, the cause remains elusive. The syndrome resolves usually after treatment of urinary tract infection or changing of the collecting bag. We present a case of a patient with purple urine bag syndrome and a pertinent literature review. D 2005 Elsevier Inc. All rights reserved.
1. Introduction
2. Case report
The purple urine bag syndrome (PUBS) is a term that has been used to describe the purple discoloration of the collecting bag and tubing. The PUBS occurs predominantly in elderly women who are bedridden, chronically catheterized, and constipated and has also been described in patients with ileal diversions [1-3]. This condition appears hours or days after catheterization and has been related to indicanuria and urinary tract infection caused by indican (indoxyl sulfate) degrading bacteria [1-8]. Many hypotheses as to the etiology of this phenomenon have been formulated; most of them have not been proven to apply to all the patients reported in the literature [9-12]. We report a case of PUBS with absence of some of the typical features previously described.
We report on a 72-year-old gentleman who is bedridden, chronically debilitated, and a nursing home resident with a past medical history of chronic renal failure, cerebral vascular accident, hypertension, advanced Parkinson’s disease, and the requirement for a chronic indwelling urinary catheter. The patient was brought from a nursing home to the emergency department because he was found to be lethargic and had recent purple discoloration of his urine. A review of his medications failed to disclose any pharmacological agent that could cause urine discoloration but included an alkalinizing agent, sodium citrate and citric acid (Bicitra), to manage his chronic renal tubular acidosis. Upon arrival to the emergency department, purple discoloration of the urine bag and tubing was found (Fig. 1). On physical examination, the patient was found to be hypotensive with a blood pressure of 70/50 mm Hg, afebrile, and lethargic and the urinary bladder was found
T Corresponding author. Tel.: +1 713 669 1670; fax: +1 713 839 1467. E-mail address: [email protected] (J. Varon). 0735-6757/$ – see front matter D 2005 Elsevier Inc. All rights reserved. doi:10.1016/j.ajem.2004.10.006
522
Fig. 1 Purple discoloration of the urinary catheter plastic tubing and bag.
to be distended above the umbilicus despite the presence of a urinary catheter. His urinary analysis revealed a pH of 9.0, too-numerousto-count white blood cells per high power field, positive leukocyte esterase, negative nitrites, red blood cells 20 to 25 per high power field, and marked bacteria. His urine culture grew more of 100 000 colonies of Escherichia coli. Urine indican and serum tryptophan were tested and there was no indicanuria (not detected in qualitative method), and the serum tryptophan level was 23 lmol/L (20-95 lmol/L). Ultrasound of the urinary bladder and kidneys revealed findings suggesting chronic bladder outlet obstruction, with presence of echogenic sediment in a distended urinary bladder and hydronephrosis. After changing the bladder catheter, frank pus drained from the bladder. The second collecting bag also turned purple. A diagnosis of severe sepsis secondary to pneumonia and urinary tract infection was made; the patient was treated with piperacillin/tazobactam for the first 3 days and with levofloxacin for 14 days. After receiving antibiotic treatment, his urine bag did not become purple again. The patient improved clinically, returning to his baseline mental status, and was transferred back to the nursing home after 8 days of hospitalization (Fig. 2).
F. Vallejo-Manzur et al. (indican) and is then excreted to the urine, which, if exposed to the air, becomes oxidized into indigo blue. Months later, Sammons et al [2] and Payne and Grant [3] recognized the basis for the long-standing theory that has prevailed. They described that this phenomenon is infrequent but not entirely unobserved and found this phenomenon in 5 elderly female patients with indwelling catheters of whom one was incontinent and the rest were constipated and all had indigo blue in the urine. Indicanuria was again suggested and the presence of blue discoloration happened with the addition of an oxidizing agent such as sodium hypochlorite. These authors also considered that alkaline urine favors the deposition of indigo; chronic urinary tract infection with Pseudomonas aeuruginosa and/or Proteus spp was present in all the patients [2,3]. The PUBS was associated with the blue diaper syndrome described by Drummond et al [13] in 1964 and has been frequently cited as an explanation of the metabolism and intestinal transport of tryptophan as the cause of indicanuria that was correlated with blue discoloration of the diaper [2,5-9]. Hildreth and Cass [5] described 5 cases of asymptomatic discoloration of blue collecting bags in children with ileal diversion, all related with urinary tract infections (only mentioned E coli in one patient), of whom only 2 were tested and had indicanuria. Hinberg et al [6] described the process by which the purple discoloration of the urine was secondary to highly alkaline urine in contact with the plastic in the bags, after which the dye used to eliminate the yellow tint of the bag discolors the urine. In a similar observation, Pankau [7] placed indoxyl sulfate (indican) in a plastic tubing for 72 hours, after which it became oxidized and discolored the tubing to purple and the solution became colorless. Years later, Wagner and Joyner [8] described the process by which tryptophan is converted to indole by mixing enteric indole-producing bacteria with an enriched tryptophan media in the presence of liver enzyme extracts obtaining indigo blue pigment.
3. Discussion The purplish or bluish discoloration of urine collecting bags was first described by Barlow and Dickson [1] in 1978 when they reported the classic discoloration of the disposable bags of children with spina bifida and urinary diversions. These authors assumed that the discoloration was secondary to the presence of indigo blue as identified by spectrophotometric analysis [1]. Their article described the presence of indigo to the metabolism of tryptophan in the setting of intestinal obstruction and constipation that undergoes bacterial decomposition to indoxyl sulfate
Fig. 2
Foley catheter and tubing after removal.
Purple urine bag syndrome Table 1 PUBS
523
Bacteria isolated in urine of some patients with
Alcaligenes spp Bacteroides spp Citrobacter diversus Citrobacter freundi Citrobacter koseri Enterobacter aerogenes Enterobacter agglomerans Enterobacter cloacae Enterococcus avium Enterococcus faecalis Escherichia coli Klebsiella oxytoca
Klebsiella ozaenae Klebsiella pneumoniae Morganella morganii Proteus mirabilisi Proteus vulgaris Providencia rettgeri Providencia stuartii Pseudomonas aeuruginosa Pseudomonas spp Serratia marcescens Staphylococcus epidermidis Streptococcus agalactiae
More recently, Stott et al [9] described 3 elderly female patients with PUBS, all of whom had alkaline urine, concluding that the bacterial pathogens had no relation with the PUBS, that indicanuria is not a prerequisite, and that the blue diaper syndrome has possibly a different etiology than PUBS. Moreover, these investigators proposed that the structure of the dye suggests a steroidal or bile acid conjugate. The PUBS has been associated with Providencia stuartii, Klebsiella pneumoniae, and Enterobacter agglomerans, bacteria with the ability to produce indigo [10,11]. Nobukuni et al [12] described that indicanuria is not a requirement for PUBS. Other investigators have shown that the activity of bacterial indoxyl sulfatase, which catalyzes the conversion of indican into indigo blue, was present only in strong alkaline urine [13-15]. Nakayama and Kanmatsuse [16] reported lower serum levels of tryptophan and valine in patients with PUBS, suggesting abnormal absorption of amino acids secondary to colonic dismotility and intestinal bacterial overgrowth. As noted before, multiple bacteria have been isolated in the urine in several case reports of PUBS, some with known sulfatase and phosphatase activities but the rest without it. The presence of alkaline urine is a common characteristic in most cases [3,5,8,9,17-24] (Table 1). It is interesting to note that PUBS usually occurs in patients in geriatric wards and that in most of these patients, common occurrences include alkaline urine and female predominance. No specific cause has been found. The PUBS has not been observed in short-term care facilities and has been associated with bhospital infectionQ transmitted by staff. There is no causative relationship between PUBS and bacteria strains, but bacterial counts are significantly higher in PUBS patients. Indican is present in the urine of healthy people, and the measurement can be hindered by sampling errors [24,25]. Of interest is the presence of this syndrome in patients with ileal diversion and urostomies having, in different degrees, the presence of hyperchloremic metabolic acidosis secondary to loss of bicarbonate through the ileal or sigmoid pouch. This evidently increases the urinary pH, which will
increase even more if an infectious process is added [26,27]. In our patient, the renal loss of bicarbonate in addition to the infectious process created highly alkaline urine. Since its description, the cause of PUBS has not been consistently proven, it remains to be elusive. Ultimately, the PUBS appears to be a benign condition. It has not been demonstrated to have any implication other than the possibility of a urinary tract infection and has not been proven to change the prognosis of patients. Clinicians dealing with patients who have indwelling bladder catheters need to be aware of this condition.
Acknowledgment The authors wish to acknowledge Mabrook Shehata, MD for his help in data gathering.
References [1] Barlow GB, Dickson JAS. Purple urine bags. Lancet 1978;28:220 - 1. [2] Sammons HG, Skinner C, Fields J. Purple urine bags. Lancet 1978;1:502. [3] Payne B, Grant A. Purple urine bags. Lancet 1978;1:502. [4] Fain-Ghironu N, Le Gondiec P, Schaeffer M. Purple urine bag syndrome. Presse Med 2003;32:985 - 7. [5] Hildreth TA, Cass AS. Blue collection bag after ileal diversion. Urology 1978;11:168 - 9. [6] Hinberg I, Katz L, Weber F, Dodge P. Purple urine? Nursing 1982;1:124. [7] Pankau EF. Purple urine bags. J Urol 1983;130:372. [8] Wagner GE, Joyner PA. Investigating the indigo drainage bag. Am J Nurs 1984;84:180. [9] Stott A, Khan M, Roberts C, Galpin IJ. Purple urine bag syndrome. Ann Clin Biochem 1987;24:185 - 8. [10] Dealler SF, Belfield PW, Bedford M, Whitley AJ, Mulley GP. Purple urine bags. J Urol 1989;142:769 - 70. [11] Dealler SF, Hawkey PM, Millar M. Enzymatic degradation of urinary indoxyl sulfate by Providencia stuartii and Klebsiella pneumoniae causes the purple urine bag syndrome. J Clin Microbiol 1988; 26:2152 - 6. [12] Nobukuni K, Kawahara S, Nagare H, Fujita Y. Study on purple pigmentation in five cases with purple urine bag syndrome. Kansenshogaku Zasshi 1995;69:1269 - 71. [13] Drummond K, Alfred AF, Ulstrom RA, Good RA. The blue diaper syndrome: familial hypercalcemia with nephrocalcinosis and indicanuria. Am J Med 1964;37:928 - 48. [14] Umeki S. Purple urine bag syndrome (PUBS) associated with strong alkaline urine. Kansenshogaku Zasshi 1993;67:1172 - 7. [15] Arnold WA. King George III’s urine and indigo blue. Lancet 1996;347:1811 - 3. [16] Nakayama T, Kanmatsuse K. Serum levels of amino acid in patients with purple urine bag syndrome. Nippon Jinzo Gakkai Shi 1997;39:470 - 3. [17] Al-Jubouri MA, Vardhan MS. A case of purple urine bag syndrome associated with Providencia rettgeri. J Clin Pathol 2001;54:412. [18] Ishida T, Ogura S, Kawakami Y. Five cases of purple urine bag syndrome in a geriatric ward. Nippon Ronen Igakkai Zasshi 1999;36:826 - 9. [19] Matsuo H, Ishibashi T, Araki C, Sakamaki H, Mazume H, Ueki Y, et al. Report of three cases of purple urine bag syndrome which occurred with a combination of both E coli and M morganii. Kansenshogaku Zasshi 1993;67:487 - 90.
524 [20] Coquard A, Martin E, Jego A, Capet C, Chassagne PH, Doucet J, et al. Purple urine bags: a geriatric presentation of lower urinary tract infection. J Am Geriatr Soc 1999;47:1481 - 2. [21] Lin H-H, Li S-J, Su K-B, Wu L-S. Purple urine bag syndrome: a case report and review of the literature. J Intern Med Taiwan 2002; 13:209 - 12. [22] Ihama Y, Hokama A. Purple urine bag syndrome. Urology 2002; 60:910. [23] Fain-Ghironi N, Le Giondaec P, Schaeffer M. Purple urine bag syndrome. Presse Med 2003;32:985 - 7.
F. Vallejo-Manzur et al. [24] Mantani N, Ochiai H, Imanishi N, Kogure T, Terasawa K, Tamura J. A case-control study of purple urine bag syndrome in geriatric wards. J Infect Chemother 2003;9:53 - 7. [25] Kirkland JL, Vargas E, Lye M. Indican excretion in the elderly. Postgrad Med J 1983;59:717 - 9. [26] Lueng AKH, Tan IKS. Critical care and the urologic patient. Crit Care Clin 2003;19:1 - 10. [27] Ollapallil J, Irukulla S, Gunawardena I. Purple urine bag syndrome. ANZ J Surg 2002;72:309 - 10.
www.elsevier.com/locate/ajem
Purple urine bag syndrome Federico Vallejo-Manzur MDa, Eduardo Mireles-Cabodevila MDb, Joseph Varon MDc,* a
University of Massachusetts, Worcester, MA 01605, USA Maryland General Hospital, Baltimore, MD 21201, USA c The University of Texas Health Science Center, St. Lukes Episcopal Hospital, Houston, TX 77030, USA b
Received 15 October 2004; accepted 15 October 2004
Abstract The purple urine bag syndrome (PUBS) is a rare condition associated with chronic urinary catheterization. It is characterized by the purple discoloration of the urine, collecting bag, and tubing. A number of factors are involved, but not always present, in its development including female sex, urinary tract infection, constipation, indicanuria, and alkaline urine. Despite multiple theories that involve the complex tryptophan metabolism to the tubing dye, the cause remains elusive. The syndrome resolves usually after treatment of urinary tract infection or changing of the collecting bag. We present a case of a patient with purple urine bag syndrome and a pertinent literature review. D 2005 Elsevier Inc. All rights reserved.
1. Introduction
2. Case report
The purple urine bag syndrome (PUBS) is a term that has been used to describe the purple discoloration of the collecting bag and tubing. The PUBS occurs predominantly in elderly women who are bedridden, chronically catheterized, and constipated and has also been described in patients with ileal diversions [1-3]. This condition appears hours or days after catheterization and has been related to indicanuria and urinary tract infection caused by indican (indoxyl sulfate) degrading bacteria [1-8]. Many hypotheses as to the etiology of this phenomenon have been formulated; most of them have not been proven to apply to all the patients reported in the literature [9-12]. We report a case of PUBS with absence of some of the typical features previously described.
We report on a 72-year-old gentleman who is bedridden, chronically debilitated, and a nursing home resident with a past medical history of chronic renal failure, cerebral vascular accident, hypertension, advanced Parkinson’s disease, and the requirement for a chronic indwelling urinary catheter. The patient was brought from a nursing home to the emergency department because he was found to be lethargic and had recent purple discoloration of his urine. A review of his medications failed to disclose any pharmacological agent that could cause urine discoloration but included an alkalinizing agent, sodium citrate and citric acid (Bicitra), to manage his chronic renal tubular acidosis. Upon arrival to the emergency department, purple discoloration of the urine bag and tubing was found (Fig. 1). On physical examination, the patient was found to be hypotensive with a blood pressure of 70/50 mm Hg, afebrile, and lethargic and the urinary bladder was found
T Corresponding author. Tel.: +1 713 669 1670; fax: +1 713 839 1467. E-mail address: [email protected] (J. Varon). 0735-6757/$ – see front matter D 2005 Elsevier Inc. All rights reserved. doi:10.1016/j.ajem.2004.10.006
522
Fig. 1 Purple discoloration of the urinary catheter plastic tubing and bag.
to be distended above the umbilicus despite the presence of a urinary catheter. His urinary analysis revealed a pH of 9.0, too-numerousto-count white blood cells per high power field, positive leukocyte esterase, negative nitrites, red blood cells 20 to 25 per high power field, and marked bacteria. His urine culture grew more of 100 000 colonies of Escherichia coli. Urine indican and serum tryptophan were tested and there was no indicanuria (not detected in qualitative method), and the serum tryptophan level was 23 lmol/L (20-95 lmol/L). Ultrasound of the urinary bladder and kidneys revealed findings suggesting chronic bladder outlet obstruction, with presence of echogenic sediment in a distended urinary bladder and hydronephrosis. After changing the bladder catheter, frank pus drained from the bladder. The second collecting bag also turned purple. A diagnosis of severe sepsis secondary to pneumonia and urinary tract infection was made; the patient was treated with piperacillin/tazobactam for the first 3 days and with levofloxacin for 14 days. After receiving antibiotic treatment, his urine bag did not become purple again. The patient improved clinically, returning to his baseline mental status, and was transferred back to the nursing home after 8 days of hospitalization (Fig. 2).
F. Vallejo-Manzur et al. (indican) and is then excreted to the urine, which, if exposed to the air, becomes oxidized into indigo blue. Months later, Sammons et al [2] and Payne and Grant [3] recognized the basis for the long-standing theory that has prevailed. They described that this phenomenon is infrequent but not entirely unobserved and found this phenomenon in 5 elderly female patients with indwelling catheters of whom one was incontinent and the rest were constipated and all had indigo blue in the urine. Indicanuria was again suggested and the presence of blue discoloration happened with the addition of an oxidizing agent such as sodium hypochlorite. These authors also considered that alkaline urine favors the deposition of indigo; chronic urinary tract infection with Pseudomonas aeuruginosa and/or Proteus spp was present in all the patients [2,3]. The PUBS was associated with the blue diaper syndrome described by Drummond et al [13] in 1964 and has been frequently cited as an explanation of the metabolism and intestinal transport of tryptophan as the cause of indicanuria that was correlated with blue discoloration of the diaper [2,5-9]. Hildreth and Cass [5] described 5 cases of asymptomatic discoloration of blue collecting bags in children with ileal diversion, all related with urinary tract infections (only mentioned E coli in one patient), of whom only 2 were tested and had indicanuria. Hinberg et al [6] described the process by which the purple discoloration of the urine was secondary to highly alkaline urine in contact with the plastic in the bags, after which the dye used to eliminate the yellow tint of the bag discolors the urine. In a similar observation, Pankau [7] placed indoxyl sulfate (indican) in a plastic tubing for 72 hours, after which it became oxidized and discolored the tubing to purple and the solution became colorless. Years later, Wagner and Joyner [8] described the process by which tryptophan is converted to indole by mixing enteric indole-producing bacteria with an enriched tryptophan media in the presence of liver enzyme extracts obtaining indigo blue pigment.
3. Discussion The purplish or bluish discoloration of urine collecting bags was first described by Barlow and Dickson [1] in 1978 when they reported the classic discoloration of the disposable bags of children with spina bifida and urinary diversions. These authors assumed that the discoloration was secondary to the presence of indigo blue as identified by spectrophotometric analysis [1]. Their article described the presence of indigo to the metabolism of tryptophan in the setting of intestinal obstruction and constipation that undergoes bacterial decomposition to indoxyl sulfate
Fig. 2
Foley catheter and tubing after removal.
Purple urine bag syndrome Table 1 PUBS
523
Bacteria isolated in urine of some patients with
Alcaligenes spp Bacteroides spp Citrobacter diversus Citrobacter freundi Citrobacter koseri Enterobacter aerogenes Enterobacter agglomerans Enterobacter cloacae Enterococcus avium Enterococcus faecalis Escherichia coli Klebsiella oxytoca
Klebsiella ozaenae Klebsiella pneumoniae Morganella morganii Proteus mirabilisi Proteus vulgaris Providencia rettgeri Providencia stuartii Pseudomonas aeuruginosa Pseudomonas spp Serratia marcescens Staphylococcus epidermidis Streptococcus agalactiae
More recently, Stott et al [9] described 3 elderly female patients with PUBS, all of whom had alkaline urine, concluding that the bacterial pathogens had no relation with the PUBS, that indicanuria is not a prerequisite, and that the blue diaper syndrome has possibly a different etiology than PUBS. Moreover, these investigators proposed that the structure of the dye suggests a steroidal or bile acid conjugate. The PUBS has been associated with Providencia stuartii, Klebsiella pneumoniae, and Enterobacter agglomerans, bacteria with the ability to produce indigo [10,11]. Nobukuni et al [12] described that indicanuria is not a requirement for PUBS. Other investigators have shown that the activity of bacterial indoxyl sulfatase, which catalyzes the conversion of indican into indigo blue, was present only in strong alkaline urine [13-15]. Nakayama and Kanmatsuse [16] reported lower serum levels of tryptophan and valine in patients with PUBS, suggesting abnormal absorption of amino acids secondary to colonic dismotility and intestinal bacterial overgrowth. As noted before, multiple bacteria have been isolated in the urine in several case reports of PUBS, some with known sulfatase and phosphatase activities but the rest without it. The presence of alkaline urine is a common characteristic in most cases [3,5,8,9,17-24] (Table 1). It is interesting to note that PUBS usually occurs in patients in geriatric wards and that in most of these patients, common occurrences include alkaline urine and female predominance. No specific cause has been found. The PUBS has not been observed in short-term care facilities and has been associated with bhospital infectionQ transmitted by staff. There is no causative relationship between PUBS and bacteria strains, but bacterial counts are significantly higher in PUBS patients. Indican is present in the urine of healthy people, and the measurement can be hindered by sampling errors [24,25]. Of interest is the presence of this syndrome in patients with ileal diversion and urostomies having, in different degrees, the presence of hyperchloremic metabolic acidosis secondary to loss of bicarbonate through the ileal or sigmoid pouch. This evidently increases the urinary pH, which will
increase even more if an infectious process is added [26,27]. In our patient, the renal loss of bicarbonate in addition to the infectious process created highly alkaline urine. Since its description, the cause of PUBS has not been consistently proven, it remains to be elusive. Ultimately, the PUBS appears to be a benign condition. It has not been demonstrated to have any implication other than the possibility of a urinary tract infection and has not been proven to change the prognosis of patients. Clinicians dealing with patients who have indwelling bladder catheters need to be aware of this condition.
Acknowledgment The authors wish to acknowledge Mabrook Shehata, MD for his help in data gathering.
References [1] Barlow GB, Dickson JAS. Purple urine bags. Lancet 1978;28:220 - 1. [2] Sammons HG, Skinner C, Fields J. Purple urine bags. Lancet 1978;1:502. [3] Payne B, Grant A. Purple urine bags. Lancet 1978;1:502. [4] Fain-Ghironu N, Le Gondiec P, Schaeffer M. Purple urine bag syndrome. Presse Med 2003;32:985 - 7. [5] Hildreth TA, Cass AS. Blue collection bag after ileal diversion. Urology 1978;11:168 - 9. [6] Hinberg I, Katz L, Weber F, Dodge P. Purple urine? Nursing 1982;1:124. [7] Pankau EF. Purple urine bags. J Urol 1983;130:372. [8] Wagner GE, Joyner PA. Investigating the indigo drainage bag. Am J Nurs 1984;84:180. [9] Stott A, Khan M, Roberts C, Galpin IJ. Purple urine bag syndrome. Ann Clin Biochem 1987;24:185 - 8. [10] Dealler SF, Belfield PW, Bedford M, Whitley AJ, Mulley GP. Purple urine bags. J Urol 1989;142:769 - 70. [11] Dealler SF, Hawkey PM, Millar M. Enzymatic degradation of urinary indoxyl sulfate by Providencia stuartii and Klebsiella pneumoniae causes the purple urine bag syndrome. J Clin Microbiol 1988; 26:2152 - 6. [12] Nobukuni K, Kawahara S, Nagare H, Fujita Y. Study on purple pigmentation in five cases with purple urine bag syndrome. Kansenshogaku Zasshi 1995;69:1269 - 71. [13] Drummond K, Alfred AF, Ulstrom RA, Good RA. The blue diaper syndrome: familial hypercalcemia with nephrocalcinosis and indicanuria. Am J Med 1964;37:928 - 48. [14] Umeki S. Purple urine bag syndrome (PUBS) associated with strong alkaline urine. Kansenshogaku Zasshi 1993;67:1172 - 7. [15] Arnold WA. King George III’s urine and indigo blue. Lancet 1996;347:1811 - 3. [16] Nakayama T, Kanmatsuse K. Serum levels of amino acid in patients with purple urine bag syndrome. Nippon Jinzo Gakkai Shi 1997;39:470 - 3. [17] Al-Jubouri MA, Vardhan MS. A case of purple urine bag syndrome associated with Providencia rettgeri. J Clin Pathol 2001;54:412. [18] Ishida T, Ogura S, Kawakami Y. Five cases of purple urine bag syndrome in a geriatric ward. Nippon Ronen Igakkai Zasshi 1999;36:826 - 9. [19] Matsuo H, Ishibashi T, Araki C, Sakamaki H, Mazume H, Ueki Y, et al. Report of three cases of purple urine bag syndrome which occurred with a combination of both E coli and M morganii. Kansenshogaku Zasshi 1993;67:487 - 90.
524 [20] Coquard A, Martin E, Jego A, Capet C, Chassagne PH, Doucet J, et al. Purple urine bags: a geriatric presentation of lower urinary tract infection. J Am Geriatr Soc 1999;47:1481 - 2. [21] Lin H-H, Li S-J, Su K-B, Wu L-S. Purple urine bag syndrome: a case report and review of the literature. J Intern Med Taiwan 2002; 13:209 - 12. [22] Ihama Y, Hokama A. Purple urine bag syndrome. Urology 2002; 60:910. [23] Fain-Ghironi N, Le Giondaec P, Schaeffer M. Purple urine bag syndrome. Presse Med 2003;32:985 - 7.
F. Vallejo-Manzur et al. [24] Mantani N, Ochiai H, Imanishi N, Kogure T, Terasawa K, Tamura J. A case-control study of purple urine bag syndrome in geriatric wards. J Infect Chemother 2003;9:53 - 7. [25] Kirkland JL, Vargas E, Lye M. Indican excretion in the elderly. Postgrad Med J 1983;59:717 - 9. [26] Lueng AKH, Tan IKS. Critical care and the urologic patient. Crit Care Clin 2003;19:1 - 10. [27] Ollapallil J, Irukulla S, Gunawardena I. Purple urine bag syndrome. ANZ J Surg 2002;72:309 - 10.