Acalypha indica -induced transient glucose-6-phosphate dehydrogenase deficiency with acute haemolysis

Background

Acalypha indica is a tropical herb found in Asia. The leaves, roots and the entire plant are believed to have many therapeutic purposes, including anthelmintic, anti-inflammatory, antibacterial, anticancer, antidiabetes, antiobesity, antivenom and is hepatoprotective and used for treatment of hypoxia and for faster wound healing.1 The adverse effects that have been reported in humans are acute haemolysis and methaemoglobinaemia.2 Most patients with acute haemolysis were confirmed to have glucose-6-phosphate dehydrogenase (G6PD) deficiency.2–6 Some patients also had methaemoglobinaemia at presentation.2 4 7 Here, we present an adult patient with acquired transient G6PD deficiency with acute haemolysis and methaemoglobinaemia after ingesting A. indica.

Case presentation

This is a case of a previously healthy middle-aged man without a history of haemolytic crisis. He also denied family history of haemolysis. The patient presented with acute dyspnoea, jaundice and dark urine for 2 days. He had a history of ingestion of boiled leaves of A. indica every day for 1 week. He denied respiratory tract symptoms and fever. He did not have chest pain or palpitation. Physical examination revealed afebrile, markedly pale and marked jaundice, without lymphadenopathy, hepatosplenomegaly, cyanosis and desaturation. No jugular venous engorgement or peripheral oedema was detected. Acute new-onset intravascular haemolysis was the provisional diagnosis.

Investigations

Complete blood count revealed haemoglobin of 65 g/L, white cell count of 13.72×10⁹/L (neutrophil 76%, lymphocyte 18%, monocyte 3%, eosinophil 1%) and platelet count of 257×10⁹/L. Peripheral smear showed polychromasia, haemoglobin-contracted cell, haemoglobin leakage cell and bite cell (figure 1). His blood test demonstrated reticulocytosis (8.09%), indirect hyperbilirubinaemia (indirect bilirubin 7.0 mg/dL), mild elevation of aspartate transaminase (86 U/L), normal alanine transaminase (11 U/L), high lactate dehydrogenase (868 U/L), haemoglobinuria (urine blood 3+ ) and methaemoglobinaemia (3.7%). G6PD assay, measured by CareStart G6PD Biosensor Analyzer (Wells Bio, Republic of Korea), demonstrated a low level of 0.2 U/g haemoglobin (reference range 4.60–13.5). Follow-up 4 months after haemolysis showed a G6PD level within normal range. The patient’s DNA was extracted from peripheral blood leucocytes. Multiplex allele-specific PCR was performed using primer sets specific to common G6PD variants in Southeast Asia. Canton (c.1376G>T, p.R459L), Union (c.1360C>T, p.R454C) and Viangchan (c.871G>A, p.V291M) allele mutations for G6PD were not detected.8

A. indica-induced transient G6PD deficiency with acute haemolysis was the definite diagnosis.

Treatment

The patient received red blood cell transfusion, hydration, oxygen therapy and folate supplement. Peripheral capillary oxygen saturation during admission was 98%–100%. He did not receive treatment for methaemoglobinaemia because he was asymptomatic and the methaemoglobin level was slightly increased.

Outcome and follow-up

After 1 week of admission, the patient gradually recovered. The degree of haemolysis improved as evidenced by the following: (1) decreased serum lactate dehydrogenase (446 U/L), (2) decreased haemoglobinuria and (3) normal level indirect bilirubin (0.7 mg/dL).

The patient was in full recovery at 4-month follow-up. Complete blood count and reticulocyte level were normal. Peripheral blood smear findings did not show haemolytic blood pictures. Liver function tests and serum lactate dehydrogenase were within normal limit. The G6PD level also returned to normal range (6.8 U/g haemoglobin).