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Sulphasalazine-induced leucopenia in a patient with renal dysfunction
1Department of Hospital Pharmacy, Faculty of Medicine, Kyushu University, 3-1-1 Higashi-ku, Maidashi, Fukuoka 812-8582, Japan. dteshima@st.hosp.kyushu-u.ac.jp
Journal of Clinical Pharmacy and Therapeutics
|June 11, 2003
Summary
Sulphasalazine-induced leucopenia in a patient with ulcerative colitis was linked to slow acetylator metabolism and reduced protein binding due to renal dysfunction. This highlights the importance of considering genetic factors and kidney function in sulphasalazine therapy.
Area of Science:
- Pharmacogenomics
- Clinical Pharmacology
- Gastroenterology
Background:
- Sulphasalazine is a key maintenance therapy for ulcerative colitis (UC).
- Serious adverse effects often limit its clinical utility.
- Leucopenia is a significant concern during sulphasalazine treatment.
Observation:
- A patient with severe renal dysfunction and UC developed leucopenia after sulphasalazine administration.
- The patient was undergoing regular hemodialysis.
- Diarrhea was the primary symptom reported.
Findings:
- The patient was identified as a slow acetylator due to NAT2*6A/*7B genotype, leading to elevated sulphapyridine levels.
- Severe renal dysfunction decreased sulphasalazine protein binding, increasing the free drug concentration.
- High serum concentrations of sulphapyridine and increased free sulphasalazine likely contributed to leucopenia.
Implications:
- Genetic variations in N-acetyltransferase 2 (NAT2) influence sulphasalazine metabolism and toxicity.
- Renal dysfunction can exacerbate sulphasalazine-induced adverse events by altering drug binding.
- Personalized medicine approaches considering pharmacogenetics and renal function are crucial for optimizing sulphasalazine therapy in UC patients.