Related Experiment Videos
Studies on dapsone induced haemolytic anaemia. I. Methaemoglobin production and G-6-PD activity in correlation with
Abstract:
The present study was undertaken on the hypothesis that methaemoglobin production and haemolytic anaemia following dapsone administration could be ascribed to an impairment of glucose-6-phosphate dehydrogenase-enzymatic activity. Analysis of the kinetic parameters of the G-6-PD (Vmax and KM) was performed in ten patients, normal with respect to G-6-PD, suffering from various dermatoses. It was concluded that haemolytic anaemia after dapsone therapy is not due to a functional impairment of the enzyme. The close relationship between dapsone dosage, methaemoglobin production and anaemia make reasonable the hypothesis that a toxic dapsone derivative (DDS-NHOH) could be responsible for the methaemoglobin formation and the haemolytic anaemia.
Insights
Dapsone-induced hemolytic anemia is not caused by impaired glucose-6-phosphate dehydrogenase (G-6-PD) activity. A toxic dapsone derivative, DDS-NHOH, is likely responsible for methaemoglobin production and anemia.
Area of Science:
- Pharmacology
- Hematology
- Biochemistry
Background:
- Dapsone is a medication used to treat various dermatoses.
- Dapsone administration can lead to methaemoglobin production and hemolytic anemia.
- The role of glucose-6-phosphate dehydrogenase (G-6-PD) in these adverse effects is unclear.
Purpose of the Study:
- To investigate the hypothesis that dapsone-induced methaemoglobin production and hemolytic anemia are due to impaired G-6-PD enzymatic activity.
- To analyze the kinetic parameters of G-6-PD in patients receiving dapsone therapy.
Main Methods:
- Kinetic analysis of G-6-PD (Vmax and KM) was performed.
- Ten patients with various dermatoses, normal for G-6-PD, were included in the study.
Main Results:
- The study found no functional impairment of G-6-PD in patients experiencing dapsone-induced adverse effects.
- A strong correlation was observed between dapsone dosage, methaemoglobin production, and anemia.
Conclusions:
- Hemolytic anemia following dapsone therapy is not attributed to a functional impairment of G-6-PD.
- A toxic dapsone derivative, DDS-NHOH, is hypothesized to be responsible for methaemoglobin formation and hemolytic anemia.