A-Textbook-of-Clinical-Pharmacology-and-Therapeutics-5th-edition

366 MALARIA AND OTHER PARASITIC INFECTIONS
Table 47.3: Continued
Helminthic species Drug therapy Comment
Lymphatic filariasis
Wuchteria bancrofti
Diethylcarbamazine
Onchocerciasis
Onchocerca volvulus Ivermectin Single dose is curative
Schistosomiasis/blood flukes
Schistosoma mansoni Praziquantel Oxamiquine (S. mansoni)
Schistosoma japonicum
Schistosoma hematobium
Metriphonate (S. hematobium)
Liver flukes/fascioliasis
Fasciola hepatica, etc.
Praziquantel
Other gut nematodes
Ascariasis
Ascaris lumbricoides
Pyrantel pamoate or levamisole
Trichinosis
Trichinella spiralis
Mebendazole, albendazole or pyrantel pamoate
Case history
A 27-year-old male student goes on elective medical internship
at a rural hospital in West Africa. He is taking malaria
prophylaxis with chloroquine 250 mg weekly, and proguanil
200 mg daily. Two weeks after arriving at his destination he
complains of lethargy, breathlessness on exertion, ankle
swelling and paraesthesiae in his hands. He is seen by a
physician’s assistant who gives him some iron tablets as he
looks pale and investigations show a haemoglobin level of
6.8 g/dL with 5% reticulocytes.
Question
What is the underlying problem here that has not been
completely defined How should he be further managed
Answer
This patient has a significant haemolytic anaemia, which is
of recent onset and is thus most likely to be due to his
treatment with prophylactic antimalarial drugs. He was
tested for glucose-6-phosphate dehydrogenase (G6PD)
deficiency and found to have a low activity of this enzyme
in his red cells. The lack of this enzyme often only becomes
clinically manifest when the red cell is stressed, as in the
presence of an oxidant such as chloroquine (other common
drugs that precipitate haemolysis include primaquine, dapsone,
sulphonamides, the 4-quinolones, nalidixic acid and
ciprofloxacin, nitrofurantoin, aspirin and quinidine). The
patient’s erythrocytes cannot handle the increased oxidation
stress and cannot utilize the hexose monophosphate
shunt to synthesize NAPDH in order to reduce oxidized glutathione
(which is the only way to achieve this in red cells)
and are thus damaged by excessive redox stress. The
patient should be asked whether anyone in his family has
ever experienced a similar condition, as it is inherited as an
X-linked defect. Patients whose ethnic origins are from
Africa, Asia, southern Europe (Mediterranean) and Oceania
are more commonly affected. Stopping the chloroquine
and treating with folate and iron should improve the
anaemia and symptoms. The patient should be warned
about other drugs that can precipitate G6PD deficiencyrelated
haemolysis and advised to inform his physician that
he has this condition. He should also carry a card or
bracelet that bears this information.
FURTHER READING
Bradley DJ, Bannister B, on behalf of the Health Protection Agency
Advisory Committee on Malaria Prevention for UK Travellers.
Guidelines for malaria prevention in travellers from the United
Kingdom for 2003. Communicable Diseases and Public Health 2003; 6:
180–99.
Liu LX, Weller PF. Antiparasitic drugs. New England Journal of Medicine
1996; 334: 1178–84.
Molyneux M, Fox R. Diagnosis and treatment of malaria in Britain.
British Medical Journal 1993; 306: 1175–80.
Pasvol G. The treatment of complicated and severe malaria. British
Medical Bulletin 2006; 75: 29–47.
White NJ. The treatment of malaria. New England Journal of Medicine
1996; 335: 800–6.
Zuckerman JN. Preventing malaria in UK travellers. British Medical
Journal 2004; 329: 305–6.