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ABSTRACT: A 36-year-old woman presented with erythematous confluent macules on her whole body with fever and chills associated with jaundice after 8 months of dapsone therapy. Her symptoms had developed progressively, and a physical examination revealed bilateral cervical lymphadenopathy and splenomegaly. Excisional biopsy of a cervical lymph node showed effacement of the normal architecture with atypical lymphoid hyperplasia and proliferation of high endothelial venules compatible with angioimmunoblastic T-cell lymphoma. However, it was assumed that the cervical lymphadenopathy was a clinical manifestation of a systemic hypersensitivity reaction because her clinical course was reminiscent of dapsone-induced hypersensitivity syndrome. A liver biopsy revealed drug-induced hepatitis with no evidence of lymphomatous involvement. Intravenous glucocorticoid was immediately initiated and her symptoms and clinical disease dramatically improved. The authors present an unusual case of cervical lymphadenopathy mimicking angioimmunoblastic T-cell lymphoma as an adverse reaction to dapsone.
The Korean Journal of Pathology 12/2012; 46(6):606-10. · 0.16 Impact Factor
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ABSTRACT: Mucosa-associated lymphoid tissue (MALT) lymphoma is a typical primary gastrointestinal lymphoma, particularly in the stomach. Although primary rectal lymphoma is rare, it may present as a subepithelial tumor. Several techniques have been proposed for a tissue diagnosis in subepithelial tumor, including endoscopic ultrasonography (EUS)-guided fine needle aspiration (EUS-FNA), EUS-guided trucut biopsy (EUS-TCB), and tacked biopsy. However the diagnostic efficacy of these techniques appears to be limited. The unroofing technique involves removal of the overlying mucosa, thereby exposing the subepithelial lesion. It was originally reported as a method for endoscopic treatment of colorectal lymphangioma. In this case, a subepithelial tumor of the rectum was diagnosed using the endoscopic unroofing technique. This is a useful modality for the diagnosis of subepithelial tumor, because it provides histologic results in a safe and rapid manner.
The Korean journal of gastroenterology = Taehan Sohwagi Hakhoe chi 06/2012; 59(6):428-32.
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ABSTRACT: The role of the angiotensin-converting enzyme (ACE) inhibitor and angiotensin receptor blocker (ARB) in the pathophysiology of contrast-induced acute kidney injury (AKI) is controversial, and the available literature is contradictory.
A retrospective propensity score-matched study to analyze the effect of ACE-inhibitor/ARB therapy on the development of contrast-induced AKI.
Using propensity score matching, 1,322 ACE-inhibitor/ARB recipients and nonrecipients were paired for analysis from 5,299 patients and fulfilled the inclusion criteria among 11,447 patients receiving coronary angiography (CAG) or percutaneous coronary intervention.
ACE-inhibitor/ARB use based on prescription and risk factors for contrast-induced AKI.
The incidence of contrast-induced AKI defined by AKI Network (AKIN) criteria: an absolute increase in serum creatinine levels ≥0.3 mg/dL or a relative increase ≥50% from baseline values within 48 hours after exposure to the contrast medium.
Baseline serum creatinine, hemoglobin, and albumin levels; volume of contrast agents; preprocedural medication; and post-CAG serum creatinine levels.
An ACE inhibitor/ARB was prescribed for 64.0% of patients receiving CAG. ACE-inhibitor/ARB users showed an increased incidence of contrast-induced AKI after propensity score matching (11.4% vs 6.3%; P < 0.001). In multivariable analysis, use of ACE inhibitors/ARBs remained an independent and significant predictor of contrast-induced AKI in an unmatched cohort (OR, 1.39; 95% CI, 1.10-1.76; P = 0.06). In the matched cohort, use of ACE inhibitors/ARBs also was associated with a higher adjusted OR of contrast-induced AKI (OR, 1.43; 95% CI, 1.06-1.94; P = 0.02).
A retrospective study at a single center.
Use of ACE inhibitors/ARBs during CAG has a possible influence to increase the incidence of contrast-induced AKI. Further randomized clinical trials are warranted to confirm the effect of ACE-inhibitor/ARB therapy on the development of contrast-induced AKI.
American Journal of Kidney Diseases 05/2012; 60(4):576-82. · 5.43 Impact Factor
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Shung Han Choi,
Dong Su Shin,
Eul Sik Jung,
Ae Jin Kim, Hyeonsu Park,
Jiyoon Sung,
Han Ro,
Jae Hyun Chang,
Hyun Hee Lee,
Wookyung Chung,
Ji Yong Jung
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ABSTRACT: Patient with end stage renal disease have characteristics in common with heart failure patients, and volume overload in heart failure is associated with poorer outcomes. Fluid removal during the hemodialysis (HD) is the cornerstone of volume management in this population. The objective of this study is to assess the long-term prognostic effect of interdialytic fluid retention (IDFR) and its relationship with cardiovascular (CV) events in incident HD patients who newly started dialysis. IDFR is defined as the difference between the predialysis weight and the weight at the end of the previous dialysis session, and it mainly reflects the consequence of salt and water intake between two consecutive dialysis sessions. We retrospectively reviewed the 172 patients who newly started and maintained HD over 6 months at Gachon University Gil Hospital between 1 January 2003 and 31 December 2008. The average data were collected for 3 months during the beginning period, including total IDFR and IDFR/dry weight (IDFR%), nutritional parameters, blood pressure, and other biochemical parameters. Patients were classified into 3 cohorts according to the tertile of IDFR%; low (T1; ≤ 3.21%), intermediate (T2; 3.21%-4.56%), and high (T3; ≥ 4.56%). The high IDFR% group showed higher prevalence of diabetes and better nutritional status. The adjusted odds ratio for CV events was 1.562 (95% confidence interval, 1.026-2.378) for high IDFR% group, compared with the low IDFR% group. In incident HD patients, greater IDFR% soon after HD initiation showed an independent association with higher risk for CV events.
The Tohoku Journal of Experimental Medicine 01/2012; 226(2):109-15. · 1.24 Impact Factor
