Year : 2012 | Volume
: 5 | Issue : 3 | Page : 271--272
Unusual presentation of malaria in an adolescent girl
JL Baidya, J Ray, AK Rakshit, S Majumder
Department of Obstetrics and Gynecology, Agartala Government Medical College, Agartala, Tripura, India
J L Baidya
Ramnagar-6, II cross, Agartala - 799002, Tripura
We describe a rare case of idiopathic thrombocytopenic purpura triggered by Plasmodium vivax malarial infection in an adolescent girl. The patient developed thrombocytopenia and menorrhagia associated with an episode of malaria, and became dependent on corticosteroid therapy. The mechanisms by which this parasite evokes thrombocytopenia remain obscure.
|How to cite this article:|
Baidya J L, Ray J, Rakshit A K, Majumder S. Unusual presentation of malaria in an adolescent girl.Ann Trop Med Public Health 2012;5:271-272
|How to cite this URL:|
Baidya J L, Ray J, Rakshit A K, Majumder S. Unusual presentation of malaria in an adolescent girl. Ann Trop Med Public Health [serial online] 2012 [cited 2020 Sep 21 ];5:271-272
Available from: http://www.atmph.org/text.asp?2012/5/3/271/98637
A 16-year-old, Tribal adolescent girl, hailing from malaria endemic zone of interior Tripura was hospitalized at gynecology ward of Agartala Govt. Medical College, Agartala, with the chief complaints of low-grade intermittent fever for last one month and continuous bleeding P/V for last 20 days. On enquiry, it was found that she attained her menarche at the age of 13 and was having regular menstrual cycle with normal flow. She has been suffering from low-grade intermittent fever for last one month and being treated by local Traditional Village Practitioner. Following fever, she developed some rashes over body, followed by sudden onset of bleeding per vaginum which is being continued for last 20 days.
On examination, she was of average built; she was pale; her vitals were normal; no significant lymphadenopathy was observed; secondary sexual characters were well developed; and petichae lesions were observed all over the body mostly over trunk, abdominal wall, and extremities. There was no splenohepatomegaly.
She was labeled as a case of puberty menorrhagia with anemia. She was subjected to the following investigations:Complete hemogram - Hb: 6 gm%; platelets count: 35 000; Peripheral smear reveals reduced thrombocytes; presence of vivax malarial parasites; no abnormal cells; Vivax malarial parasitemia confirmed by kit test;Renal and liver functions were normal;USG rules out any organic pathology for abnormal uterine bleeding.
The specific investigation like platelet-associated Ig could not be done due to financial constrain.
The case was being reviewed with further enquiry into history and physical examinations. She had few episodes of spontaneous gum bleeding along with vaginal bleeding. There were no other causes for thrombocytopenia that could be elicited from the history. Finally, the provisional diagnosis of acute onset of thrombocytopenia leading to puberty menorrhagia and anemia was made.
On consultation with physician, she was put on full course of antiparasitic treatment for vivax malaria, tapering dose of corticosteroids. She was given three units of platelets and two units of fresh blood for correction of thrombocytopenia and anemia, respectively. Acute arrest of bleeding was done with intravenous tranexamic acid 1 500 mg/d. She was discharged once her bleeding was arrested and her hematological profile reverted back to normal. She was advised to continue tapering dose of corticosteroid and also advised preventive antimalarial for vivax parasitemia to prevent recurrence.
In India, malaria is endemic and commonly caused by Plasmodium vivax and Plasmodium falciparum. Thrombocytopenia is a common finding in falciparum infection, but is rare in P. vivax infection.  We report profound thrombocytopenia in a 16-year-old young girl patient due to P. vivax infection. Even though the reasons for acute thrombocytopenia are diverse, the plasmodia infection can trigger idiopathic thrombocytic purpura (ITP). The exact mechanism of ITP is not known, but the possible mechanisms would be--immune mechanism, oxidative stress, alteration in splenic function, direct interaction between plasmodia and platelets.  There are evidences (in searched literature) describing that thrombocytopenia and thrombocytic purpura is an early indicator for acute malarial infection, and this finding is frequent and present even before anemia and splenomegaly set in.  The profound thrombocytopenia is sometimes needed to be treated with corticosteroid. A major challenge for successful treatment of P. vivax malaria is prevention of recurrence due to activation of dormant intrahepatic parasitic forms--hypnozoites. As a result of strain variability, recurrences are unpredictable and can occur months or even years after initial infection. Prevention requires elimination of both erythrocytic and hepatic parasite forms by combined use of chloroquine and primaquine. ,
This paper is presented to highlight that P. vivax malaria though considered to be a benign entity can also have an unusually severe and complicated course which is usually associated with P. falciparum malaria.
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