Plasmodium falciparum and Plasmodium vivax malaria are endemic infections in India and are commonly associated with mild hematological abnormalities. Severe thrombocytopenia is common in isolated falciparum and mixed falciparum/vivax malaria, but is very rare in isolated P.vivax infection. We hereby report a case of severe thrombocytopenia (platelet count of 8x10 9 /L) in a case of vivax malaria. This is only the second case ever reported in the literature of such profound thrombocytopenia in a case of isolated P.vivax malaria. Key Words: Plasmodium vivax, malaria, severe thrombocytopenia. Malaria is common in most parts of India and is usually caused by P. falciparum and P. vivax. Though mild thrombocytopenia is common in both falciparum and vivax malaria, severe thrombocytopenia is reported especially in P. falciparum malaria and is very rare in isolated P. vivax infection. Both non-immunological as well as immunological destruction of platelets have been implicated in causing thrombocytopenia in such cases but the mechanisms involved are still not completely clear. Case ReportA 43-year-old male, resident of eastern India, arrived at the hospital emergency room with complaints of high grade, intermittent fever associated with chills and rigors during seven days. He also had a two-day history of mild spontaneous bleeding from the gums. There was no history of bleeding from any other site and no past or family history suggestive of bleeding diathesis. There was no history of any drug ingestion. On examination, the patient was febrile with a temperature of 40 o C. He had slight pallor and the liver and spleen were palpable 2 cm and 3 cm below the costal margin, respectively. There were no purpuric spots and the tourniquet test was negative.Routine blood investigations revealed 7.5 g/dL hemoglobin and a WBC count of 6.3x10 9 /L, with 54% neutrophils, 39% lymphocytes, 4% eosinophils and 3% monocytes. The platelet count was 8x10 9 /L. The peripheral blood smear showed numerous gametocytes of P. vivax in a background of marked thrombocytopenia. The 'OptiMAL® Rapid Malaria Dipstick Test' (DiaMed AG,Switzerland) for P. falciparum was negative but was positive for P. vivax. The bleeding time was prolonged to 9 minutes while the clotting time was 3 minutes, with a prothrombin time of 14 seconds (control 13 seconds) and activated partial thromboplastin time of 40 seconds (control 36 seconds). Glucose-6-phosphate dehydrogenase levels were normal and disseminated intravascular coagulation (DIC) was ruled out by normal levels of fibrinogen degradation products (FDP). Total serum bilirubin was 1.4 mg/dL with normal serum transaminase levels. Dengue serology (IgG and IgM) and Elisa for HIV were nonreactive. The patient was treated with antimalarials (quinine sulphate 10 mg/kg thrice daily) for 7 days and was given 6 units of platelet transfusions

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EUS had a moderate strength of agreement with histopathology for both T and N staging, and a high diagnostic accuracy for nodal staging.

Hepatitis E virus is one of the leading causes of acute viral hepatitis in India but usually manifests as a mild self-limiting illness. Viral hepatitis in the presence of glucose-6-phosphate dehydrogenase (G6PD) deficiency may be associated with complications such as severe anemia, hemolysis, renal failure, hepatic encephalopathy and even death. The incidence of G6PD deficiency in the general population of northern India is reported to be between 2.2% and 14%. Despite both hepatitis E infection and G6PD deficiency being common, their impact on patient illness has only recently been reported. The present study reports a case of severe hemolysis in a patient with G6PD deficiency and hepatitis E infection.Key words: Glucose-6-phosphate dehydrogenase; G6PD; Hemolysis; Hepatitis E Exposé de cas : Hépatite E aiguë en présence d'un déficit en glucose-6-phosphate-déshy-drogénase Le virus de l'hépatite E est l'une des principales causes d'hépatite aiguë en Inde, mais il s'agit en général d'une maladie bénigne, spontanément résolutive. Par contre, une hépatite virale en présence d'un déficit en glucose-6-phosphate-déshydrogénase (G6PD) peut donner lieu à des complications comme une anémie grave, l'hémolyse, l'insuffisance rénale, une encéphalopathie porto-cave et même la mort. L'incidence du déficit en G6PD dans la population en général dans le Nord de l'Inde varie entre 2,2 et 14 %. Même si l'hépatite E et le déficit en G6PD sont deux affections fréquentes, on ne fait état de leur influence sur l'évolution de la maladie que depuis peu. Voici un cas d'hémolyse grave chez un patient atteint à la fois d'un déficit en G6PD et d'une hépatite E.H epatitis E is an enterically transmitted virus and is one of the most common causes of acute viral hepatitis in India (1). Glucose-6-phosphate dehydrogenase (G6PD) deficiency is found in 2.2% to 14% of the general population in North India (2). The coexistence of viral hepatitis and G6PD deficiency has been reported to be associated with severe jaundice and other complications (3,4). Hepatitis E infection with G6PD deficiency has been associated with more severe illness in only one previous report (5). We report an additional case. CASE REPORTA 35-year-old man with no history of alcoholism or liver disease presented with low grade fever, upper abdominal pain, fatigue and loss of appetite for eight to 10 days. He had noticed a yellow discolouration of the eyes for three days and dark coloured urine for five to six days. On examination, he was deeply icteric. Abdominal examination revealed a soft, tender liver, palpable 4 cm below the costal margin. There was no splenomegaly and the remainder of the physical examination was normal.Laboratory investigations revealed a hemoglobin mass concentration of 126 g/L, a total leucocyte count of 12.2x10 9 /L, and a total serum bilirubin of 198 µmol/L with a conjugated fraction of 141 µmol/L. The serum aspartate aminotransferase (AST) concentration was 376 U/L and the alanine aminotransferase (ALT) concentration was 270 U/L. The prothrombin time wa...

EUS-guided FNA obtains a high proportion of adequate aspirates for LNs and solid masses, even without an on-site cytopathologist. Small proportions of inadequate samples still occur. For solid masses, a 25-G needle with at least 3 passes is more likely to provide an adequate aspirate than a 22-G needle and fewer passes. Hemorrhage did not affect the cytopathology's ability to make a diagnosis.