Corticosteroids therapy and peptic ulcer disease in nephrotic syndrome patients

Authors


Dr Jiing-Chyuan Luo, Division of Gastroenterology, Department of Medicine, Taipei Veterans General Hospital, 201 Shih-Pai Road, Section 2, Taipei 11217, Taiwan.
Tel.: + 886(2) 2875 7506
Fax: + 886(2) 2873 9318
E-mail: jcluo@vghtpe.gov.tw

Abstract

WHAT IS ALREADY KNOWN ABOUT THIS SUBJECT

• Whether corticosteroid use induces peptic ulcer disease (PUD) remains uncertain.

• Helicobacter pylori infection in steroid users has not been well evaluated in the past.

WHAT THIS STUDY ADDS

• Prednisolone 60 mg daily for 3 months caused few endoscopic ulcers (1.6%) and no ulcer complications in 60 nephrotic patients, which was comparative with the controls, with an odds ratio of 0.5.

• Corticosteroid therapy did not to increase PUD in nephrotic syndrome patients. Further larger studies are needed to clarify the role of corticosteroid in PUD.

AIMS

Whether corticosteroids induce peptic ulcer disease (PUD) remains uncertain. The study evaluated and compared the occurrence of PUD between nephrotic patients receiving oral prednisolone therapy and nephritic patients without steroid therapy.

METHODS

The prospective case control study compared 60 nephrotic syndrome patients who received 60 mg daily prednisolone therapy for 3 months with 30 age-and sex-matched nephritic patients without steroid therapy. Each patient underwent endoscopic examination and tissue and blood sampling before and after the study. Examined parameters included Helicobacter pylori (H. pylori) infection, and gastric and serum prostaglandin (PG) E2 and thromboxane (TX) B2 concentrations. The primary endpoint was the occurrence of endoscopic peptic ulcers between the two groups, while the secondary end point was the occurrence of ulcer complications.

RESULTS

The two groups were comparable in sex, age, smoking habits, alcohol drinking, past history of PUD, H. pylori infection rate and serum creatinine. There were no differences in the occurrence of endoscopic peptic ulcers (1.6% vs. 3.3%) and ulcer complications (0% vs. 0%), pre-therapy gastric PGE2, and pre- and post-therapy gastric TXB2, serum PGE2 and serum TXB2 between the two groups. However, there was significantly lower post-therapy gastric PGE2 concentrations in the prednisolone group.

CONCLUSIONS

Three-month therapy with 60 mg daily prednisolone caused few endoscopic ulcers (1.6%) and no ulcer complications in nephrotic patients. Corticosteroids therapy did not increase PUD in nephrotic syndrome patients [odds ratio 0.492 with 95% confidence interval (CI) 0.03, 8.142, P= 0.620]. Further larger studies are needed to clarify the role of corticosteroids in PUD.

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