Letters to the Editor
in asymptomatic pancreatic hyperenzymemia. Pancreas 2009;38:396–400. 5. Sarner M, Cotton PB. Classification of pancreatitis. Gut 1984;25:756–9. 6. Sainani NI, Conwell DL. Secretin-enhanced MRCP: proceed with cautious optimism. Am J Gastroenterol 2009;104:1787–9. 7. Schmitz-Moormann HP, Hein J. Altersveränderungen des pankreasgangsystems und ihre rückwirkungen auf das parenchym. Virchows Arch [Pathol Anat] 1976;371:145–52. 8. Lankisch PG. Erhöhte Pankreasenzyme ohne erkennbare pankreaserkrankung. Dtsch Med Wochenschr 2009;134:2232–5. 9. Imrie CW, King J, Henderson AR. Macroamylasemia—survey of prevalence in a mixed population. N Engl J Med 1972;287:931. 10. Bode C, Riederer J, Brauner B et al. Macrolipasemia: a rare cause of persistently elevated serum lipase. Am J Gastroenterol 1990;85: 412–6. 1
Reiherstieg 23, D-21337 Lüneburg, Germany. Correspondence: Paul Georg Lankisch, MD, FRCP, FACG, Reiherstieg 23, D-21337 Lüneburg, Germany. E-mail:
[email protected]
per min), P < 0.001. Urinary excretion of calcium was significantly lower in group I (mean 16.4±7.6 mg) compared with group II (mean 39.2±7.8 mg), P < 0.001. Our study demonstrated that lowerbody-weight individuals develop high serum phosphate levels for prolonged periods of time after ingesting sodium phosphate, even under the idealized condition of continuous monitoring of fluids and weight. This suggests that adequate hydration in lower-bodyweight individuals does not protect against the secondary effects of hyperphosphatemia, as others have proposed (4,5). Individuals of lower body weight are a newly described group at risk for APN when they use colonos copy preparations containing sodium phosphate. CONFLICT OF INTEREST
Calcium Phosphate Nephropathy From Colonoscopy Preparations: Effect of Body Weight Deepak Parakkal, MD1 and Eli D. Ehrenpreis, MD2,3 doi:10.1038/ajg 2009.677
To the Editor: We read with interest the article by Mackey et al. (1) highlighting the risk of acute phosphate nephropathy (APN) from sodium phosphate tablets. In a pharmacokinetic analysis performed by our group (2,3), 45 ml of Fleet Phospho-Soda containing 30 g of sodium phosphate was administered to 13 normal volunteers. They were divided into two groups: group I having a median weight of 60 kg and group II, a median weight of 119.2 kg. Serum and urine electrolytes were measured for 12 h. Hydration was maintained by monitoring the weight, fluid intake, and total body water. Markedly elevated serum phosphate levels were observed in group I compared with group II. The normalized area under the phosphate vs. time curve was much higher in group I (1120±190 mg/dl per min) than in group II (685±136 mg/dl © 2010 by the American College of Gastroenterology
Guarantor of the article: Deepak Parakkal, MD. Specific author contributions: Deepak Parakkal and Eli D. Ehrenpreis participated actively in conceiving, initiating, and writing up the research project. Financial support: None. Potential competing interests: None. REFERENCES 1. Mackey AC, Green L, Amand KS et al. Sodium phosphate tablets and acute phosphate nephropathy. Am J Gastroenterol 2009;104: 1903–6. 2. Ehrenpreis ED. Increased serum phosphate levels and calcium fluxes are seen in smaller individuals after a single dose of sodium phosphate colon cleansing solution: a pharmacokinetic analysis. Aliment Pharmacol Ther 2009;29: 1202–11. 3. Ehrenpreis ED, Varala K, Hammon B. Lower weight is a risk factor for calcium phosphate nephropathy with sodium phosphate colonoscopy preparation: a simulation study. Am J Gastroenterol 2008;103:S408–55. 4. Pelham R, Dobre A, Van Diest K et al. Oral sodium phosphate bowel preparations: How much hydration is enough? Gastrointest Endosc 2007;65:AB314. 5. Patel V, Emmett M, Santa Ana CA et al. Pathogenesis of nephrocalcinosis after sodium phosphate catharsis to prepare for colonoscopy: intestinal phosphate absorption and its effect on urine mineral and electrolyte excretion. Hum Pathol 2007;38:193–4. 1 Department of Gastroenterology, NorthShore University Hospital, Evanston, Illinois, USA; 2 Gastroenterology and Endoscopy, Highland Park Hospital, NorthShore University Health System, Chicago, Illinois, USA; 3Department of Medicine,
University of Chicago, Chicago, Illinois, USA. Correspondence: D. Parakkal, MD, Department of Gastroenterology, NorthShore University Hospital, Evanston, Illinois, USA. E-mail:
[email protected]
Antibiotics Prophylaxis in Acute Necrotizing Pancreatitis: An Update Yu Bai, MD1,2,3, Jun Gao, MD1,2, Duo-Wu Zou, MD1,2 and Zhao-Shen Li, MD1,2,3 doi:10.1038/ajg.2009.676
To the Editor: Previously we investigated the role of prophylactic antibiotics in the treatment of acute necrotizing pancreatitis (ANP) in a meta-analysis involving seven randomized controlled trials (RCTs) (1). The study suggested that infected pancreatic necrosis and mortality rates were not significantly different between the antibiotics group and the control group. However, this estimate was largely based on studies mainly from Western countries, where the predominant etiology was alcohol, and it is unclear whether this conclusion could be applied to other populations in which biliary disease is the predominant etiology of acute pancreatitis (2). Therefore, we updated the meta-analysis (1) by computing the summary risk ratios (RRs) and 95% confidence intervals (CIs) for patients receiving antibiotics, by applying the same methods as in the previous meta-analysis (1). Briefly, we performed a Pubmed search of the literature from 2007 to October 2009, using the MeSH term “pancreatitis” and limitation of the publication type of “randomized controlled trials”. We also cross-checked the reference lists of the publications retrieved. We used a random-effects model to pool the data regardless of whether statistical heterogeneity was present. After a comprehensive literature search, it is found that since the publication of our study (1), two more RCTs were The American Journal of GASTROENTEROLOGY
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