Mr. Komal Raj Rijal,

      The U.S. National Library of Medicine National Institutes of Health provides the full-text to a research study published online on November 18th 2014 in the Malaria Journal entitled, "Glucose-6-phosphate dehydrogenase deficiency among malaria suspects attending Gambella hospital, southwest Ethiopia," authored by Arega Tsegaye, Lemu Golassa, Hassen Mamo, and Berhanu Erko.

      The background information contained within the abstract states, "Glucose-6-phosphate dehydrogenase deficiency (G6PDd) is widespread across malaria endemic regions. G6PD-deficient individuals are at risk of haemolysis when exposed, among other agents, to primaquine and tafenoquine, which are capable of blocking malaria transmission by killing Plasmodium falciparum gametocytes and preventing Plasmodium vivax relapses by targeting hypnozoites. It is evident that no measures are currently in place to ensure safe delivery of these drugs within the context of G6PDd risk. Thus, determining G6PDd prevalence in malarious areas would contribute towards avoiding possible complications in malaria elimination using the drugs. This study, therefore, was aimed at determining G6PDd prevalence in Gambella hospital, southwest Ethiopia, using CareStart™ G6PDd fluorescence spot test."

       The researchers in this study conducted G6PDd analysis using CareStart™ G6PDd screening test (Access Bio, New Jersey, USA). The sample collection and analysis portion of this publication states, "After a questionnaire and clinical examination, 5 ml venous blood was collected in ethylene diamine tetra acetic acid (EDTA) for measuring haematological parameters, malaria diagnosis and G6PDd screening. The haematological parameters - haemoglobin (Hb), haematocrit (HCT) and packed cell volume (PCV) - and red cell indices (mean corpuscular volume (MCV), mean corpuscular haemoglobin (MCH) and mean corpuscular haemoglobin concentration (MCHC) were determined using an automated system, CELL-DYN 1400 haematology analyzer (Abbott, USA). Thick and thin blood smears were prepared and stained using 10% Giemsa solution to detect malaria. The stained slides were examined under a light microscope using the oil immersion objective (100X). Two experienced laboratory technologists independently screened the slides and discrepancies were settled by a third person’s blind test. Parasite density was calculated per 200 white blood cells (WBC) assuming 8,000 WBC/μl of blood [20]. G6PDd was screened using CareStart™ G6PDd screening test (Access Bio, Inc., New Jersey, USA) following the manufacturer’s instruction. Briefly, a 2 μl whole blood was added to a sample well and then 100 μl of assay buffer to the buffer well immediately after application of blood. The result was read normal as distinct purple colour, deficient as no colour or a very faint purple colour; and invalid when there is no blood migration or incomplete blood migration in the reading window within 10 minutes. Additionally it is important to note that authors state the Limitations of the study to be that, "The study did not use quantitative or semi-quantitative screening methods such as spectrophotometric ultraviolet (UV). As a result, the WHO’s five classes (levels) of G6PD activity could not be determined among the study participants. Besides, because of the fact that a molecular method was not used, the underlying prevalent variants and specific mutations in the G6PD-deficient individuals could not be address."

      "The backround information in this study states, "Although in some studies glucose-6-phosphate dehydrogenase deficiency (G6PDd) is associated with protection from severe malaria [4, 5] deficient individuals are reported to suffer from haemolytic anaemia when treated with primaquine [6], which is the only available drug against Plasmodium falciparum gametocytes [7] and a radical cure of Plasmodium vivax."

     For your reference, I have attached the link to where you can access the entire full-text to the publication I am referring to. I hope the information provided will assist you in your on-going research. If i can be of any further assistance, please feel free to contact me. Hope that you have a wonderful weekend.

Regards,

Lars Lafferty

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4252010/

Hematologic

The severity of hemolytic anemia in patients with G-6-PD deficiency treated with primaquine is dependent upon the dose given and the patient's ethnic background. In American and African Blacks, hemolytic anemia is generally mild and self-limiting, and lower prophylactic doses of primaquine may be tolerated. In patients of Mediterranean and some Oriental origins, the hemolytic anemia may be severe. Most patients with hemolytic anemia present with dark urine, jaundice, vomiting, and headache.[Ref]

Hematologic side effects have included hemolytic anemia (if administered to patients with glucose-6-phosphate dehydrogenase deficiency [G-6-PD]) and methemoglobinemia in patients with nicotinamide adenine dinucleotide (NADH) methemoglobin reductase deficiency. Leukopenia, mild anemia, and leukocytosis have occasionally been reported.[Ref]

Gastrointestinal

Gastrointestinal side effects have included nausea, vomiting, abdominal cramps, and epigastric distress.[Ref]

Hypersensitivity

Hypersensitivity skin rashes have been reported in approximately 50% of AIDS patients being treated with primaquine and clindamycin for Pneumocystis carinii pneumonia.