Imatinib-induced pleural effusion: A case report.

Imatinib is a tyrosine kinase inhibitor and has rarely been reported to cause pleural effusion. We report the case of an 88-year-old male, known case of gastrointestinal stromal tumor on treatment with imatinib, who presented with a 2-week history of cough and dyspnea. He was diagnosed to have a right-sided pleural effusion and thoracentesis of the fluid revealed an exudate with low adenosine deaminase and negative cytology. Withdrawal of the drug lead to resolution of symptoms. We report this case to highlight the side effect profile of imatinib and warn physicians regarding this potential adverse effect which may be mistaken for metastasis or infection.

Making the most of Papua New Guinea's biodiversity: Establishment of an integrated set of programs that link botanical survey with pharmacological assessment in "The Land of the Unexpected"

An integrated and coordinated set of programs has been established to meet ICBG goals in Papua New Guinea (PNG). Here we give an overview of the PNG ICBG and focus on the key elements and major steps taken to establish a program necessary for the pharmacological assessment of botanicals and traditional medicines in PNG and, by extrapolation, in other developing countries.

Bronchiolitis obliterans and organising pneumonia caused by carbamazepine and mimicking community acquired pneumonia.

Bronchiolitis obliterans and organising pneumonia (BOOP) presents with fever, dyspnoea, and other features that may be mistaken for pneumonia. Treatment is, however, very different, requiring corticosteroids. A man was admitted as an emergency with fever, dyspnoea, and non-productive cough. The chest radiograph showed consolidation which, despite antibiotics, progressed to become bilateral. BOOP was considered, and confirmed by transbronchial biopsy. The response to oral prednisolone was rapid with complete resolution of symptoms and radiographic consolidation within three weeks. The cause of BOOP is often never found; it is believed, however, that in this instance it occurred as a result of carbamazepine therapy started seven weeks earlier.

Diaschisis with cerebral infarction.

Fifteen patients admitted to Philadelphia General Hospital with acute strokes had repeated measurements of cerebral blood flow measured by the 133Xenon inhalation method. A progressive decline in cerebral blood flow in both hemispheres was observed during the first week after infarction in twelve of these patients. This decline could be partially explained by loss of autoregulation, but could not be correlated with level of consciousness, clinical status of PCO2. This progressive decline in flow in the non-ischemic hemisphere indicates a process more complex than a simple destruction of axonal afferants to neurons as implied by the term diaschisis. The flow changes in the non-ischemic hemisphere are likely caused by a combination of the immediate effects of decreased neuronal stimulation modified by loss of autoregulation, release of vasoactive substances, cerebral edema, and other factors.