Clonal disorders of LGL may either be CD3+ CD56- or CD3- CD56+ phenotype and these have been designated as T-cell leukaemia (T-LGL) or natural killer cell (NK)-LGL leukaemia respectively. Clonality is usually demonstrated by clonal rearrangement of T-cell receptor gene rearrangement or identified by flowcytometry analysis. Most patients with T-LGL will have an indolent course. In this report we described an aggressiveness of disease in a patient with clonal CD3+ LGL leukaemia whose cells also co-expressed CD56 diagnosed by flowcytometry. The patient responded well to interrupt ALL standard risk protocol however succumbed to her disease while waiting for upfront stem cell transplant. This case highlights on both the classical laboratory findings of rare entity of disease as well as a review of the literature pertaining particularly on its management.

Plasma cell leukaemia (PCL) is a rare form of malignant plasma cell dyscrasia. It can occur as a primary form without prior evidence of multiple myeloma or as a secondary form which is a terminal event in multiple myeloma. It is characterised by a proliferation of plasma cells in blood and the bone marrow. The outcome of plasma cell leukemia is poor with conventional therapy. Here we illustrate a case of primary plasma cell leukemia complicated by para plegia. The patient initially responded to combination chemotherapy but succumbed to the disease two months after presentation

Hereditary thrombophilias are a group of inherited conditions that predispose to thrombosis. Most of the inherited thrombotic disorders ara associated with venous thromboembolism. Pulmonary embolism represents a major cause of morbidity and mortality. Chronic thromboembolic disease is a 'great masquerade' and often mistakenly diagnosed as coronary artery disease, asthma, pneumonia and psychogenic dyspnoea. Recurrent pulmonary embolism with pulmonary hypertension can be missed if awareness of the condition is not created. The consequences of a missed diagnosis can be deadly. We present a case of familial protein S defects leading to recurrent pulmonary thromboembolism.