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Table. Clinical and Laboratory Data of 7 Patients with Salmonella Paratyphi A Bacteremia Clinical Features Patient No. (Age, in years/ Sex) Family
Positive White Blood C-Reactive Diarrhea Culture Blood Cell Protein* AST/ALT Widal Reaction† (/mm3) (date) (date) (mg/dL) (U/L) (date)
5 (16/F) 6 (16/M)
Antibiotic Treatment (days)
1:20 (9/15, 10/8) Ceftriaxone (5), ciprofloxacin (10) 1:20 (9/3, 9/17, Ofloxacin (5), 10/12) amoxicillin (9) 1:20 (9/3) Amoxicillin (14) 1:100 (10/8) 1:80 (12/1) 1:200 (9/4) Amoxicillin (14) 1:160 (9/18) 1:20 (10/23) 1:20 (8/31) Amoxicillin (14) 1:40 (9/10) Ceftriaxone (4), 1:20 (10/8) Amoxicillin (7) 1:40 (9/4) Ciprofloxacin (12)
* Normal, ⬍0.8 mg/mL. † Salmonella paratyphi A-H (flagellar antigen b) agglutination titers. AST/ALT ⫽ aspartate aminotransferase/alanine aminotransferase; F ⫽ female; M ⫽ male; NA ⫽ not available.
blood cultures even if the patients do not have fevers or abnormal white blood cell counts. Hepatitis associated with Salmonella paratyphi A bacteremia is an emerging clinical entity and should be listed among the various manifestations and complications of paratyphoid fever. Po-Ren Hsueh, MD Jia-Horng Kao, MD, PhD Yee-Chun Chen, MD Pan-Chyr Yang, MD, PhD Kwen-Tay Luh, MD National Taiwan University Hospital National Taiwan University College of Medicine Taipei, Taiwan Tien-Kuei Wang, PhD Szu-Fong Lin, MS Center for Disease Control, Department of Health Taipei, Taiwan 1. Teoh YL, Goh KT, Neo KS, Yeo M. A national outbreak of coconut-associated paratyphi A fever in Singapore. Ann Acad Med Singapore. 1997;26:544 –548. 2. Sood S, Kapil A, Dash N, et al. Paratyphoid fever in India: an emerging problem. Emerg Infect Dis. 1999;5:483–484. 3. Kao JH, Chen W, Hsiang SC, et al. Prevalence and implication of TT virus infection: 258
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minimal role in patients with non-A-E hepatitis in Taiwan. J Med Virol. 1999;59:307– 312. Thong KL, Nair S, Chaudhry R, et al. Molecular analysis of Salmonella paratyphi A from an outbreak in New Delhi, India. Emerg Infect Dis. 1998;4:507–508. Pramoolsinsap C, Viranuvatti V. Salmonella hepatitis. J Gastroenterol Hepatol. 1998;13:745–750. Ramachandran S, Godfrey JJ, Perera MVF. Typhoid hepatitis. JAMA. 1974;230:236 – 240. Thisyakorn U, Mansuwan P, Taylor DN. Typhoid and paratyphoid fever in 192 hospitalized children in Thailand. Am J Dis Child. 1987;141:862–865. Phadke AY, Desai HG. Hepatitis E virus and Salmonella paratyphi A coinfection. Indian J Gastroenterol. 1997;16:115–116.
NEPHROTIC SYNDROME PRESENTING AS DURAL SINUS THROMBOSIS To the Editor: Venous thromboembolic complications of nephrotic syndrome have an overall incidence of 10% to 40% (1). Dural sinus thrombosis is encountered infrequently, and most reports describe patients who were di-
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agnosed with glomerular disease before the thrombotic episode (2– 6). We describe a man with nephrotic syndrome who did not have a previous history of renal disease but who presented with extensive dural sinus thrombosis. A previously healthy 46-year-old man presented with a 2-week history of worsening headache that was followed by horizontal diplopia. The physical examination was normal except for a left sixth nerve palsy. A cerebral venogram revealed thrombosis throughout the dural sinus system (Figure, left). He had no personal or family history of thrombosis or bleeding disorders. Electrolyte panel and complete blood count were normal. Laboratory examination revealed the following values: serum albumin, 1.4 g/dL; serum urea nitrogen, 15 mg/dL; serum creatinine, 1.1 mg/dL; total cholesterol, 361 mg/dL; triglycerides, 165 mg/dL; high-density lipoprotein cholesterol, 92 mg/dL; and low-density lipoprotein cholesterol, 255 mg/dL. These values were normal about 2 years before. A 24-hour urine collection contained 3.7 g of protein. A
Letters to the Editor
Figure. Superior sagittal sinus venogram via microcatheter demonstrating occlusion of the superior sagittal sinus before tissue plasminogen activator (tPA) infusion (left). Repeat venogram after 46 hours of tPA infusion demonstrating patency of the superior sagittal sinus (right).
work-up for hypercoagulable states was normal except for an antithrombin III (AT-III) level of 70% (normal, 84% to 141%) and plasminogen activity of 70% (normal, 84% to 140%). Hospital course included anticoagulation with intravenous heparin. Magnetic resonance imaging 3 days after admission showed further extension of dural thrombus. The patient underwent microcatheter placement into the superior sagittal sinus, with 46 hours of continuous tissue plasminogen activator (tPA) infusion (0.5 mg/h). We administered an 8-mg bolus of tPA, followed by two 4-mg boluses, during interval venograms to monitor clot dissolution. A final venogram performed on day 5 documented patency of the dural sinuses, with no cortical venous collateral filling (Figure, right). Corticosteroid and warfarin therapy was initiated, and he was discharged without residual neurologic symptoms. Five weeks later, the patient was taking prednisone (10 mg/d), and a 24-hour urine collection revealed 195 mg of protein. Serum albumin and cholesterol levels were normal. Repeat AT-III level was 154% and plas-
minogen activity was 71%. Prednisone therapy was tapered off, but treatment with warfarin was continued. The hemostatic system is activated in nephrotic syndrome, with an increased tendency toward thrombosis (1). Contributing factors include altered levels of coagulation factors, defects in the fibrinolytic system, and platelet dysfunction (1). Abnormalities of the coagulation system result from a complex interplay between increased hepatic synthesis and intravascular consumption of coagulation factors, urinary loss of proteins such as AT-III and plasminogen, and accelerated thrombin generation (1,7). The levels of these hemostatic factors normalize after clinical remission of the nephrotic syndrome (3). Anticoagulation may be difficult in patients with nephrotic syndrome, as thrombin antagonism by heparin may be insufficient in the presence of low AT-III levels (8,9). Our patient’s thrombosis progressed while he was receiving intravenous heparin. Antithrombin III concentrate has been found to be beneficial in the prevention of venous thrombosis (8), and August 15, 2002
extremely low levels of AT-III may warrant the use of AT-III concentrate or fresh frozen plasma to ensure adequate anticoagulation with heparin. Microcatheter infusion of thrombolytic agents via interventional techniques can dissolve thrombus rapidly and restore venous flow in patients with dural sinus thrombosis (10). A review of endovascular treatment of cerebral venous thrombosis found an overall improvement of 94% with a mortality of 2% (10), and a low risk of hemorrhage that was attributed to low arterial concentration of thrombolytic agents. Heparin prevents vessel reocclusion when used after tPA fibrinolysis, probably by inhibiting thrombin released by the dissolving clot (8). Our patient had no signs of peripheral edema, yet he lost 8 lbs after remission was induced, suggesting that the disease process was detected early and that severe thrombotic complications can occur during this period. It is remarkable that complications of dural sinus thrombosis were his first clinical manifestation of nephrotic syndrome. It is likely that he had min-
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imal change nephropathy because of the rapid resolution of nephrotic syndrome in response to corticosteroid therapy. In children with minimal change nephropathy, it is common to forego a renal biopsy and to treat empirically with corticosteroids, with a rapid remission assumed to confirm the diagnosis. Susannah P. Friemel, MD Daniel W. Mackey, MD Andrew Z. Fenves, MD Joseph H. Hise, MD Edson H. Cheung, MD Marvin J. Stone, MD Baylor University Medical Center Dallas, Texas 1. Sagripanti A, Barsotti G. Hypercoagulability, intraglomerular coagulation, and thromboembolism in nephrotic syndrome. Nephron. 1995;70:271–281. 2. Tullu MS, Deshmukh CT, Save SU, et al. Superior sagittal sinus thrombosis: a rare complication of nephrotic syndrome. J Postgrad Med. 1999;45:120 –122. 3. Sung S, Jeng J, Yip P, Huang K. Cerebral venous thrombosis in patients with nephrotic syndrome: case reports. Angiology. 1999;50:427–432. 4. Burns A, Wilson E, Harber M, et al. Cerebral venous sinus thrombosis in minimal change nephrotic syndrome. Nephrol Dial Transplant. 1995;10:30 –34. 5. Urch C, Pusey CD. Sagittal sinus thrombosis in adult minimal change nephrotic syndrome. Clin Nephrol. 1996;45:131–132. 6. Lau SO, Bock GH, Edson JR, Michael AF. Sagittal sinus thrombosis in the nephrotic syndrome. J Pediatr. 1980;97:948 –950. 7. Lau SO, Tkachuck JY, Hasegawa DK, Edson JR. Plasminogen and antithrombin III deficiencies in the childhood nephrotic syndrome associated with plasminogenuria and antithrombinuria. J Pediatr. 1980;96:390 –392. 8. Lam K, Lui C. Successful treatment of acute inferior vena cava and unilateral renal vein thrombosis by local infusion of recombinant tissue plasminogen activator. Am J Kidney Dis. 1998;32:1075–1079. 9. Peces R, Pobes A, Rodriguez M, Navascues R. Multiple venous thrombosis and massive pulmonary artery thrombus as the presenting features of steroid-responsive nephrotic syndrome. Nephrol Dial Transplant. 1999;14:1306 –1309. 10. Philips MF, Bagley LJ, Sinson GP, et al. Endovascular thrombolysis for symptomatic cerebral venous thrombosis. J Neurosurg. 1999;90:65–71. 260
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THE ABSENCE OF RHABDOMYOLYSISINDUCED RENAL FAILURE FOLLOWING THE WORLD TRADE CENTER COLLAPSE To the Editor: We wish to report the relative absence of rhabdomyolysis-induced acute renal failure following the collapse of the World Trade Center on September 11, 2001. Nephrologists in New York City were prepared to dialyze large numbers of people with acute renal failure in the days following the terrorist attack. To our knowledge, there was only one case of acute renal failure attributable to rhabdomyolysis following the event. This involved a 38-yearold policeman who had been trapped under debris for 24 hours before he was rescued and who had severe crush injuries to both legs. On admission to Bellevue Hospital on September 12, he was anuric. He received hemodialysis on admission, later that evening, and then daily for 5 days. His creatine kinase level peaked at 37,000 U/L on September 13. He underwent hemodialysis for almost 1 month before full recovery of his renal function. His serum creatinine level was 0.7 mg/dL when he was discharged. There were 2 other patients with rhabdomyolysis seen at Bellevue Hospital: one with a creatine kinase level of 66,800 U/L and a serum creatinine level of 1.6 mg/dL, and the other with a creatine kinase peak of 20,700 U/L and a serum creatinine concentration of 0.6 mg/dL. In the former patient, renal function recovered completely by September 13, with a serum creatinine concentration of 0.8 to 1.0 mg/dL. Both patients were treated with intravenous normal saline, sodium bicarbonate, and mannitol. We also learned of another 2 patients who were seen elsewhere in New York, but no other patients required dialysis. There were no other cases of rhabdomyolysis-induced acute renal failure in New York City. We spoke with nephrologists at most large teaching hospitals in Manhattan, including St.
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Vincent’s Hospital and New York University Downtown Hospital, which, together with Bellevue, were the closest to the scene and had the largest number of emergency department visits following the disaster. Acute renal failure is relatively common after the collapse of buildings, and nephrologists often go to the scene to perform dialysis. New York City’s nephrologists prepared on September 11 by stockpiling supplies, preparing staff to work extra shifts, and arranging for patients with chronic renal failure to be dialyzed elsewhere or at other times. We appreciated receiving telephone calls and e-mails from nephrologists in the United States and from elsewhere in the world who offered supplies and assistance. All of us were disappointed not to have had more of an opportunity to serve the injured by performing hemodialysis, because the unexpected absence of patients with acute renal failure reflected the lethality of the event. David S. Goldfarb, MD Nephrology Section New York VA Medical Center New York University School of Medicine New York, New York Susie Chung, MD Bellevue Hospital New York University School of Medicine New York, New York
VISCERAL INVOLVEMENT DUE TO LEISHMANIA MEXICANA IN A PATIENT WITH ACQUIRED IMMUNODEFICIENCY SYNDROME To the Editor: A 44-year-old Argentinian man who had human immunodeficiency virus (HIV) infection and a history of intravenous drug use was admitted because of rectal pain. He reported progressive anal pain, tenesmus, and wasting during the previous month. He had spent 2 years in Barcelona and