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Intestinal pseudotumorous gouty nodulosis: a colonic tophus without manifestation of gouty arthritis
CASE STUDIES
(compared with bone marrow transplantation). Typically, FCH represents a unique course of HBV or HCV infection (re)occurring after (liver) engrafting. In contrast, in this patient chronic HBV infection was documented long before renal transplantation and must have permutated into a FCH due to immunosuppression. Because our patient succumbed to 3 different severe and potentially fatal viral infections (FCH B, focal necrotizing adenoviral hepatitis, and necrotizing enteroviral enteritis), we suggest that he suffered from a severe breakdown of resistance to viral infections. This is unlikely to be due to the standard immunosuppression for kidney transplant patients alone, and may further reside on an additional preexisting or acquired immune insufficiency. REFERENCES 1. Lee HK, Yoon GS, Min KS, et al: Fibrosing cholestatic hepatitis: A report of three cases. J Korean Med Sci 15:111-114, 2000 2. Lam PW, Wachs ME, Somberg KA, et al: Fibrosing cholestatic hepatitis in renal transplant recipients. Transplantation 61:378-381, 1996 3. Munoz de Bustillo E, Ibarrola C, Andres A, et al: Hepatitis B virus– related fibrosing cholestatic hepatitis after renal transplantation with acute graft failure following interferon-alpha therapy. Nephrol Dial Transplant 13: 1574-1576, 1998 4. Chen CH, Chen PJ, Chu JS, et al: Fibrosing cholestatic hepatitis in a
hepatitis B surface antigen carrier after renal transplantation. Gastroenterology 107:1514-1518, 1994 5. Davies SE, Portmann BC, O’Grady JG, et al: Hepatic histological findings after transplantation for chronic hepatitis B virus infection, including a unique pattern of fibrosing cholestatic hepatitis. Hepatology 13:150-157, 1991 6. Hale GA, Heslop HE, Krance RA, et al: Adenovirus infection after pediatric bone marrow transplantation. Bone Marrow Transplant 23:277-282, 1999 7. Piedra PA, Kasel JA, Norton HJ, et al: Description of an adenovirus type 8 outbreak in hospitalized neonates born prematurely. Pediatr Infect Dis J 11:460-465, 1992 8. Hierholzer JC: Adenoviruses in the immunocompromised host. Clin Microbiol Rev 5:262-274, 1992 9. Johnson PR, Yin JA, Morris DJ, et al: Fulminant hepatic necrosis caused by adenovirus type 5 following bone marrow transplantation. Bone Marrow Transplant 5:345-347, 1990 10. Krilov LR, Rubin LG, Frogel M, et al: Disseminated adenovirus infection with hepatic necrosis in patients with human immunodeficiency virus infection and other immunodeficiency states. Rev Infect Dis 12:303-307, 1990 11. Abzug MJ: Prognosis for neonates with enterovirus hepatitis and coagulopathy. Pediatr Infect Dis J 20:758-763, 2001 12. Chen CA, Tsao PN, Chou HC, et al: Severe echovirus 30 infection in twin neonates. J Formos Med Assoc 102:59-61, 2003 13. Carmichael GP Jr, Zahradnik JM, Moyer GH, et al: Adenovirus hepatitis in an immunosuppressed adult patient. Am J Clin Pathol 71:352-355, 1979 14. Saad RS, Demetris AJ, Lee RG, et al: Adenovirus hepatitis in the adult allograft liver. Transplantation 64:1483-1485, 1997 15. Chakrabarti S, Collingham KE, Fegan CD, et al: Fulminant adenovirus hepatitis following unrelated bone marrow transplantation: Failure of intravenous ribavirin therapy. Bone Marrow Transplant 231:1209-1211, 1999
INTESTINAL PSEUDOTUMOROUS GOUTY NODULOSIS: A COLONIC TOPHUS WITHOUT MANIFESTATION OF GOUTY ARTHRITIS HUIQING WU, MD, MICHAEL J. KLEIN, MD, ROSALYN E. STAHL, MD,
AND
A 37-year-old black woman with nephritis secondary to systemic lupus erythematosus, steroid-induced diabetes mellitus, and hypertension presented with fever, nausea, vomiting, and right upper quadrant abdominal pain with distension. Abdominal computed tomography (CT) scan revealed a colonic mass, and CT- guided fineneedle aspiration demonstrated birefringent crystalline material. After several weeks of antibiotic therapy, the patient underwent laparoscopic examination followed by extended right hemicolectomy for a large mass in the subserosa of the transverse colon. Pathological
examination of this mass revealed it to be a gouty tophus. To our knowledge, no case of tophaceous gout presenting as an intestinal mass has previously been reported. HUM PATHOL 35:897-899. © 2004 Elsevier Inc. All rights reserved. Key words: gout, gouty nodulosis, intestinal tophus, colonic tophus, uric acid crystals. Abbreviations: BUN, blood urea nitrogen; CT, computed tomography; SLE, systemic lupus erythematosus.
Gout is a clinical syndrome resulting from the tissue deposition of monosodium urate monohydrate.1 It encompasses a group of disorders including hyperuricemia, gouty arthritis, tophaceous deposition, uric acid urolithiasis, and
gouty nephropathy. Although the typical sequence involves progression through asymptomatic hyperuricemia, acute gouty arthritis, interval or intercritical gout, and chronic or tophaceous gout, the manifestations can occur in any combination or alone.1,2 Extra-articular uric acid deposits, also called tophi, can occur in the absence of gouty arthritis in the connective tissue of ears, breast, kidney, elbows, wrists, fingers, finger pulp, legs, knees, ankles, feet, and toes.3-7 We report the case of 36-year-old woman with a large urate tophus in the colonic wall resembling a tumor in the absence of gouty arthritis.
From the Department of Pathology, Mount Sinai School of Medicine, New York, NY and Department of Pathology and Laboratory Medicine, Englewood Hospital and Medical Center, Englewood, NJ. Accepted for publication March 25, 2004. Huiqing Wu is currently at the Department of Pathology, Brigham and Women’s Hospital, Harvard Medical School, Boston, MA. Michael J. Klein is currently at the Department of Pathology, University of Alabama at Birmingham School of Medicine, Birmingham, AL. Address correspondence and reprint requests to Dr. Miguel A. Sanchez, Department of Pathology and Laboratory Medicine, Englewood Hospital and Medical Center, 350 Engle St., Englewood, NJ 07631. 0046-8177/$—see front matter © 2004 Elsevier Inc. All rights reserved. doi:10.1016/j.humpath.2004.04.003
MIGUEL A. SANCHEZ, MD
CASE REPORT The patient is a 36-year-old black woman with a past medical history significant for systemic lupus erythematosus (SLE) diagnosed 6 years ago, nephritis secondary to lupus vasculitis, steroid-induced diabetes mellitus, hypertension, pancreatitis, and nongouty arthritis. On February 12, 2001, she presented to the Englewood Hospital and Medical Center with a 2-day history of nausea, vomiting, diffuse right upperquadrant pain precipitated by food intake, and shortness of
897
HUMAN PATHOLOGY
Volume 35, No. 7 (July 2004)
FIGURE 1. CT scan shows a mass in the transverse colon with no obstruction.
FIGURE 2. A cross-section of the transverse colon shows a cystic lesion in the subserosal wall of colon. The cyst with trabeculation is filled with white-yellow fibrous chalky material.
FIGURE 3. (A) The cyst wall shows chronic reactive changes. The cyst content is acellular and eosinophilic (hematoxylin and eosin). (B) Polarized light microscopy reveals strongly negative birefringence in the needle-shaped urate crystals (eosin-absolute alcohol stain15). The arrow points to the axis of compensator slow ray.
breath. She had a temperature of 101.3°F and a heart rate of 118 beats/minute. On physical examination, her lungs were clear and her abdomen was distended. Laboratory testing revealed a slightly elevated white blood cell count, blood urea nitrogen (BUN) of 34 mg/dL, creatinine level of 3.1 mg/dL, and amylase, lipase, liver function tests, and electrolytes values within normal limits. Abdominal X-rays were negative for obstruction and free air. Abdominal computed tomography (CT) scan revealed a colonic mass (Fig 1), and subsequent CT-guided fine-needle aspiration demonstrated “acellular debris containing abundant birefringent crystalline material with very few foci of benign fibrous tissue.” The patient was treated for a presumed infection with imipenem and metronidazole. She was discharged when she was asymptomatic and her laboratory values returned to baseline. On May 3, 2001, the patient’s abdominal pain recurred. She returned to the Englewood Hospital and Medical Center 2 weeks after this episode, where an elective laparoscopic exploration of her abdominal mass revealed a ⬎5 cm colonic mass appearing to extend through the wall of the colon. An extended right hemicolectomy with functional end-to-end anastomosis was performed. The operation and postoperative period were uneventful. The patient’s BUN and creatinine values were labile, with maximal levels of 24 mg/dL and 1.5 mg/dL, respectively. Her serum uric acid level was 8.9 mg/dL. Her current medications included prednisone, hydrochlorothiazide, amlodipine, enalapril, and omeprazole. She denied tobacco, ethanol, or illicit
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CASE STUDIES
drug use. Her father had a history of hypertension and her mother had a history of cancer, not specified. PATHOLOGICAL FINDINGS An extended right hemicolectomy specimen was received consisting of tissue from the terminal ileum, cecum, appendix, and ascending and transverse colon. A 9 ⫻ 6 ⫻ 4 cm cystic mass was found in the transverse colon, located in the subserosal colonic wall (Fig 2). The cyst was filled with white-yellow chalky material and exhibited peripheral fibrosis. The cyst wall was smooth with focal trabeculation. The mucosa and serosa of the transverse colon was smooth with focal hemorrhages. No fibrinous exudates were seen. No obstruction was found. The specimen was otherwise unremarkable. Histologically, the colonic mucosa and serosa were unremarkable. The cyst wall was composed of subserosa exhibiting fibrosis, occasional multinucleated giant cells, and chronic inflammatory changes (Fig 3A). The cyst content was acellular and eosinophilic, and consisted of needle-shaped crystals. These crystals demonstrated strong negative birefringence consistent with monosodium urate when examined under compensated, polarized microscopy (Fig 3B). DISCUSSION It is well accepted that visible tophaceous deposits of monosodium urate occur after several years of gouty arthritis, especially in the absence of treatment to control hyperuricemia.8,9 Urate tophi rarely occur as the initial or sole manifestation of gout in such locations as the ears, breast, kidney, elbows, wrists, hands, knees, ankles, and feet and have been termed gouty nodulosis.3-7 To our knowledge, no intestinal tophus has ever been reported in a patient with or without gouty arthritis. This patient has a history of hypertension, renal insufficiency, SLE, and elevated serum uric acid level. She takes multiple antihypertensive drugs, including diuretics, as well as steroids for SLE. Associations of gout with hypertension, diuretic use, and renal insufficiency are well established;1 25% to 50% of patients with gout are hypertensive.10,11 Approximately 33% of hypertensive patients are hyperuricemic, a proportion that rises to nearly 67% in patients with treated hypertension and patients with renal disease.12 Tophaceous deposits may be more prevalent in women with renal insufficiency and in the geriatric population.3
Acute gouty arthritis is very infrequently associated with inflammatory connective tissue disorders, such as rheumatoid arthritis and SLE.13 Hyperuricemia and crystal deposition may indeed occur in such situations, although an acute inflammatory response might not be elicited, due in part to synovial hypocomplementemia in rheumatoid arthritis and SLE.7,14 It is possible that this patient’s long-term steroid use caused suppression of acute gouty arthritis and permitted the silent accumulation of urate deposits with indolent tissue reactions in the colonic wall for a long period. Acknowledgment. The authors thank Dr. Mark Shapiro for providing the CT image; Joseph Samet, Robert Kim, and Glenn Spiro for the photographic assistance; and Dr. Cary Johnson for advice. REFERENCES 1. Becker MA: Clinical aspects of monosodium urate monohydrate crystal deposition disease (gout). Rheum Dis Clin of North Am 14:377-393, 1988 2. Wortmann RL: Gout and other disorders of purine metabolism, in Fauci AS, Braunwald E, Isselbacher KJ, et al (eds): Harrison’s Principles of Internal Medicine, ed 14. New York, McGraw-Hill, 1998, pp 21-61 3. Iglesias GA, Londono JC, Saaibi DL, et al: Gout nodulosis: Widespread subcutaneous deposits without gout. Arthritis Care Res 9:74-77, 1996 4. Shmerling RH, Stern SH, Gravallese EM, et al: Tophaceous deposition in the finger pads without gouty arthritis. Arch Intern Med 148:1830-1832, 1988 5. Vukmir RB, Weiss L, Verdile VP: Polyarticular symmetric tophaceous joint inflammation as the initial presentation of gout. Am J Emerg Med 8:43-45, 1990 6. Wernick R, Winkler C, Campbell S: Tophi as the initial manifestation of gout: Report of six cases and review of the literature. Arch Intern Med 152:873-876, 1992 7. Scott JT, Hollingworth P, Burry HC: Urate deposits without gouty arthritis. Adv Exp Med Biol 165:133-136, 1984 8. Yu RG, Gutman AB: Principles of current management of primary gout. Am J Med Sci 254:893-907, 1967 9. Lawry GV II, Fan PT, Bluestone R: Polyarticular versus monoarticular gout: A prospective, comparative analysis of clinical features. Medicine (Baltimore) 67:335-343, 1988 10. Berger L, Yu FT: Renal function in gout. IV. An analysis of 524 gouty subjects including long-term follow-up studies. Am J Med 59:605-613, 1975 11. Grahame R, Scott JT: Clinical survey of 354 patients with gout. Ann Rheum Dis 29:461-468, 1970 12. Cannon PJ, Stason WB, Demartini FE, et al: Hyperuricemia in primary and renal hypertension. N Engl J Med 275:457-464, 1966 13. Wall BA, Agudelo CA, Weinblatt ME, et al: Acute gout and systemic lupus erythematosus: Report of 2 cases and literature review. J Rheumatol 9:305-307, 1982 14. Hasselbacher P: Immunoelectrophoretic assay for synovial fluid C3 with correction for synovial fluid globulin. Arthritis Rheum 22:243-250, 1979 15. Shidham VB, Galindo LM, Gupta D, et al: Urate crystals in tissue: A novel staining method for formalin-fixed, paraffin-embedded sections. Lab Med 29:109-113, 1998
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(compared with bone marrow transplantation). Typically, FCH represents a unique course of HBV or HCV infection (re)occurring after (liver) engrafting. In contrast, in this patient chronic HBV infection was documented long before renal transplantation and must have permutated into a FCH due to immunosuppression. Because our patient succumbed to 3 different severe and potentially fatal viral infections (FCH B, focal necrotizing adenoviral hepatitis, and necrotizing enteroviral enteritis), we suggest that he suffered from a severe breakdown of resistance to viral infections. This is unlikely to be due to the standard immunosuppression for kidney transplant patients alone, and may further reside on an additional preexisting or acquired immune insufficiency. REFERENCES 1. Lee HK, Yoon GS, Min KS, et al: Fibrosing cholestatic hepatitis: A report of three cases. J Korean Med Sci 15:111-114, 2000 2. Lam PW, Wachs ME, Somberg KA, et al: Fibrosing cholestatic hepatitis in renal transplant recipients. Transplantation 61:378-381, 1996 3. Munoz de Bustillo E, Ibarrola C, Andres A, et al: Hepatitis B virus– related fibrosing cholestatic hepatitis after renal transplantation with acute graft failure following interferon-alpha therapy. Nephrol Dial Transplant 13: 1574-1576, 1998 4. Chen CH, Chen PJ, Chu JS, et al: Fibrosing cholestatic hepatitis in a
hepatitis B surface antigen carrier after renal transplantation. Gastroenterology 107:1514-1518, 1994 5. Davies SE, Portmann BC, O’Grady JG, et al: Hepatic histological findings after transplantation for chronic hepatitis B virus infection, including a unique pattern of fibrosing cholestatic hepatitis. Hepatology 13:150-157, 1991 6. Hale GA, Heslop HE, Krance RA, et al: Adenovirus infection after pediatric bone marrow transplantation. Bone Marrow Transplant 23:277-282, 1999 7. Piedra PA, Kasel JA, Norton HJ, et al: Description of an adenovirus type 8 outbreak in hospitalized neonates born prematurely. Pediatr Infect Dis J 11:460-465, 1992 8. Hierholzer JC: Adenoviruses in the immunocompromised host. Clin Microbiol Rev 5:262-274, 1992 9. Johnson PR, Yin JA, Morris DJ, et al: Fulminant hepatic necrosis caused by adenovirus type 5 following bone marrow transplantation. Bone Marrow Transplant 5:345-347, 1990 10. Krilov LR, Rubin LG, Frogel M, et al: Disseminated adenovirus infection with hepatic necrosis in patients with human immunodeficiency virus infection and other immunodeficiency states. Rev Infect Dis 12:303-307, 1990 11. Abzug MJ: Prognosis for neonates with enterovirus hepatitis and coagulopathy. Pediatr Infect Dis J 20:758-763, 2001 12. Chen CA, Tsao PN, Chou HC, et al: Severe echovirus 30 infection in twin neonates. J Formos Med Assoc 102:59-61, 2003 13. Carmichael GP Jr, Zahradnik JM, Moyer GH, et al: Adenovirus hepatitis in an immunosuppressed adult patient. Am J Clin Pathol 71:352-355, 1979 14. Saad RS, Demetris AJ, Lee RG, et al: Adenovirus hepatitis in the adult allograft liver. Transplantation 64:1483-1485, 1997 15. Chakrabarti S, Collingham KE, Fegan CD, et al: Fulminant adenovirus hepatitis following unrelated bone marrow transplantation: Failure of intravenous ribavirin therapy. Bone Marrow Transplant 231:1209-1211, 1999
INTESTINAL PSEUDOTUMOROUS GOUTY NODULOSIS: A COLONIC TOPHUS WITHOUT MANIFESTATION OF GOUTY ARTHRITIS HUIQING WU, MD, MICHAEL J. KLEIN, MD, ROSALYN E. STAHL, MD,
AND
A 37-year-old black woman with nephritis secondary to systemic lupus erythematosus, steroid-induced diabetes mellitus, and hypertension presented with fever, nausea, vomiting, and right upper quadrant abdominal pain with distension. Abdominal computed tomography (CT) scan revealed a colonic mass, and CT- guided fineneedle aspiration demonstrated birefringent crystalline material. After several weeks of antibiotic therapy, the patient underwent laparoscopic examination followed by extended right hemicolectomy for a large mass in the subserosa of the transverse colon. Pathological
examination of this mass revealed it to be a gouty tophus. To our knowledge, no case of tophaceous gout presenting as an intestinal mass has previously been reported. HUM PATHOL 35:897-899. © 2004 Elsevier Inc. All rights reserved. Key words: gout, gouty nodulosis, intestinal tophus, colonic tophus, uric acid crystals. Abbreviations: BUN, blood urea nitrogen; CT, computed tomography; SLE, systemic lupus erythematosus.
Gout is a clinical syndrome resulting from the tissue deposition of monosodium urate monohydrate.1 It encompasses a group of disorders including hyperuricemia, gouty arthritis, tophaceous deposition, uric acid urolithiasis, and
gouty nephropathy. Although the typical sequence involves progression through asymptomatic hyperuricemia, acute gouty arthritis, interval or intercritical gout, and chronic or tophaceous gout, the manifestations can occur in any combination or alone.1,2 Extra-articular uric acid deposits, also called tophi, can occur in the absence of gouty arthritis in the connective tissue of ears, breast, kidney, elbows, wrists, fingers, finger pulp, legs, knees, ankles, feet, and toes.3-7 We report the case of 36-year-old woman with a large urate tophus in the colonic wall resembling a tumor in the absence of gouty arthritis.
From the Department of Pathology, Mount Sinai School of Medicine, New York, NY and Department of Pathology and Laboratory Medicine, Englewood Hospital and Medical Center, Englewood, NJ. Accepted for publication March 25, 2004. Huiqing Wu is currently at the Department of Pathology, Brigham and Women’s Hospital, Harvard Medical School, Boston, MA. Michael J. Klein is currently at the Department of Pathology, University of Alabama at Birmingham School of Medicine, Birmingham, AL. Address correspondence and reprint requests to Dr. Miguel A. Sanchez, Department of Pathology and Laboratory Medicine, Englewood Hospital and Medical Center, 350 Engle St., Englewood, NJ 07631. 0046-8177/$—see front matter © 2004 Elsevier Inc. All rights reserved. doi:10.1016/j.humpath.2004.04.003
MIGUEL A. SANCHEZ, MD
CASE REPORT The patient is a 36-year-old black woman with a past medical history significant for systemic lupus erythematosus (SLE) diagnosed 6 years ago, nephritis secondary to lupus vasculitis, steroid-induced diabetes mellitus, hypertension, pancreatitis, and nongouty arthritis. On February 12, 2001, she presented to the Englewood Hospital and Medical Center with a 2-day history of nausea, vomiting, diffuse right upperquadrant pain precipitated by food intake, and shortness of
897
HUMAN PATHOLOGY
Volume 35, No. 7 (July 2004)
FIGURE 1. CT scan shows a mass in the transverse colon with no obstruction.
FIGURE 2. A cross-section of the transverse colon shows a cystic lesion in the subserosal wall of colon. The cyst with trabeculation is filled with white-yellow fibrous chalky material.
FIGURE 3. (A) The cyst wall shows chronic reactive changes. The cyst content is acellular and eosinophilic (hematoxylin and eosin). (B) Polarized light microscopy reveals strongly negative birefringence in the needle-shaped urate crystals (eosin-absolute alcohol stain15). The arrow points to the axis of compensator slow ray.
breath. She had a temperature of 101.3°F and a heart rate of 118 beats/minute. On physical examination, her lungs were clear and her abdomen was distended. Laboratory testing revealed a slightly elevated white blood cell count, blood urea nitrogen (BUN) of 34 mg/dL, creatinine level of 3.1 mg/dL, and amylase, lipase, liver function tests, and electrolytes values within normal limits. Abdominal X-rays were negative for obstruction and free air. Abdominal computed tomography (CT) scan revealed a colonic mass (Fig 1), and subsequent CT-guided fine-needle aspiration demonstrated “acellular debris containing abundant birefringent crystalline material with very few foci of benign fibrous tissue.” The patient was treated for a presumed infection with imipenem and metronidazole. She was discharged when she was asymptomatic and her laboratory values returned to baseline. On May 3, 2001, the patient’s abdominal pain recurred. She returned to the Englewood Hospital and Medical Center 2 weeks after this episode, where an elective laparoscopic exploration of her abdominal mass revealed a ⬎5 cm colonic mass appearing to extend through the wall of the colon. An extended right hemicolectomy with functional end-to-end anastomosis was performed. The operation and postoperative period were uneventful. The patient’s BUN and creatinine values were labile, with maximal levels of 24 mg/dL and 1.5 mg/dL, respectively. Her serum uric acid level was 8.9 mg/dL. Her current medications included prednisone, hydrochlorothiazide, amlodipine, enalapril, and omeprazole. She denied tobacco, ethanol, or illicit
898
CASE STUDIES
drug use. Her father had a history of hypertension and her mother had a history of cancer, not specified. PATHOLOGICAL FINDINGS An extended right hemicolectomy specimen was received consisting of tissue from the terminal ileum, cecum, appendix, and ascending and transverse colon. A 9 ⫻ 6 ⫻ 4 cm cystic mass was found in the transverse colon, located in the subserosal colonic wall (Fig 2). The cyst was filled with white-yellow chalky material and exhibited peripheral fibrosis. The cyst wall was smooth with focal trabeculation. The mucosa and serosa of the transverse colon was smooth with focal hemorrhages. No fibrinous exudates were seen. No obstruction was found. The specimen was otherwise unremarkable. Histologically, the colonic mucosa and serosa were unremarkable. The cyst wall was composed of subserosa exhibiting fibrosis, occasional multinucleated giant cells, and chronic inflammatory changes (Fig 3A). The cyst content was acellular and eosinophilic, and consisted of needle-shaped crystals. These crystals demonstrated strong negative birefringence consistent with monosodium urate when examined under compensated, polarized microscopy (Fig 3B). DISCUSSION It is well accepted that visible tophaceous deposits of monosodium urate occur after several years of gouty arthritis, especially in the absence of treatment to control hyperuricemia.8,9 Urate tophi rarely occur as the initial or sole manifestation of gout in such locations as the ears, breast, kidney, elbows, wrists, hands, knees, ankles, and feet and have been termed gouty nodulosis.3-7 To our knowledge, no intestinal tophus has ever been reported in a patient with or without gouty arthritis. This patient has a history of hypertension, renal insufficiency, SLE, and elevated serum uric acid level. She takes multiple antihypertensive drugs, including diuretics, as well as steroids for SLE. Associations of gout with hypertension, diuretic use, and renal insufficiency are well established;1 25% to 50% of patients with gout are hypertensive.10,11 Approximately 33% of hypertensive patients are hyperuricemic, a proportion that rises to nearly 67% in patients with treated hypertension and patients with renal disease.12 Tophaceous deposits may be more prevalent in women with renal insufficiency and in the geriatric population.3
Acute gouty arthritis is very infrequently associated with inflammatory connective tissue disorders, such as rheumatoid arthritis and SLE.13 Hyperuricemia and crystal deposition may indeed occur in such situations, although an acute inflammatory response might not be elicited, due in part to synovial hypocomplementemia in rheumatoid arthritis and SLE.7,14 It is possible that this patient’s long-term steroid use caused suppression of acute gouty arthritis and permitted the silent accumulation of urate deposits with indolent tissue reactions in the colonic wall for a long period. Acknowledgment. The authors thank Dr. Mark Shapiro for providing the CT image; Joseph Samet, Robert Kim, and Glenn Spiro for the photographic assistance; and Dr. Cary Johnson for advice. REFERENCES 1. Becker MA: Clinical aspects of monosodium urate monohydrate crystal deposition disease (gout). Rheum Dis Clin of North Am 14:377-393, 1988 2. Wortmann RL: Gout and other disorders of purine metabolism, in Fauci AS, Braunwald E, Isselbacher KJ, et al (eds): Harrison’s Principles of Internal Medicine, ed 14. New York, McGraw-Hill, 1998, pp 21-61 3. Iglesias GA, Londono JC, Saaibi DL, et al: Gout nodulosis: Widespread subcutaneous deposits without gout. Arthritis Care Res 9:74-77, 1996 4. Shmerling RH, Stern SH, Gravallese EM, et al: Tophaceous deposition in the finger pads without gouty arthritis. Arch Intern Med 148:1830-1832, 1988 5. Vukmir RB, Weiss L, Verdile VP: Polyarticular symmetric tophaceous joint inflammation as the initial presentation of gout. Am J Emerg Med 8:43-45, 1990 6. Wernick R, Winkler C, Campbell S: Tophi as the initial manifestation of gout: Report of six cases and review of the literature. Arch Intern Med 152:873-876, 1992 7. Scott JT, Hollingworth P, Burry HC: Urate deposits without gouty arthritis. Adv Exp Med Biol 165:133-136, 1984 8. Yu RG, Gutman AB: Principles of current management of primary gout. Am J Med Sci 254:893-907, 1967 9. Lawry GV II, Fan PT, Bluestone R: Polyarticular versus monoarticular gout: A prospective, comparative analysis of clinical features. Medicine (Baltimore) 67:335-343, 1988 10. Berger L, Yu FT: Renal function in gout. IV. An analysis of 524 gouty subjects including long-term follow-up studies. Am J Med 59:605-613, 1975 11. Grahame R, Scott JT: Clinical survey of 354 patients with gout. Ann Rheum Dis 29:461-468, 1970 12. Cannon PJ, Stason WB, Demartini FE, et al: Hyperuricemia in primary and renal hypertension. N Engl J Med 275:457-464, 1966 13. Wall BA, Agudelo CA, Weinblatt ME, et al: Acute gout and systemic lupus erythematosus: Report of 2 cases and literature review. J Rheumatol 9:305-307, 1982 14. Hasselbacher P: Immunoelectrophoretic assay for synovial fluid C3 with correction for synovial fluid globulin. Arthritis Rheum 22:243-250, 1979 15. Shidham VB, Galindo LM, Gupta D, et al: Urate crystals in tissue: A novel staining method for formalin-fixed, paraffin-embedded sections. Lab Med 29:109-113, 1998
899