The effect of palm oil-derived tocotrienol-rich fraction in preserving normal retinal vascular diameter in streptozotocin-induced diabetic rats.

PURPOSE: Angiogenesis in diabetic retinopathy (DR) is associated with increased retinal expression of angiopoietin-2 (Ang-2) and protein kinase C (PKC). Tocotrienol-rich fraction (TRF) has been shown to reduce the expression vascular endothelial growth factor (VEGF) in several experimental models. However, its effect against other angiogenic markers such as Ang-2 and PKC in rat model of diabetes remains unknown. Therefore, we investigated the effect of TRF on the retinal vascular changes and Ang-2 and PKC expressions in rats with streptozotocin (STZ)-induced DR. METHODS: Sprague-Dawley rats were divided into normal control rats (N) which received vehicle, and diabetic rats which either received vehicle (DV) or 100 mg/kg of TRF (DT). Diabetes was induced with intraperitoneal injection of STZ (60 mg/kg body weight). Treatments were given orally, once daily, for 12 weeks after confirmation of hyperglycaemia. Fundus photographs were captured at baseline, 6- and 12-week post-STZ injection and average diameter of retinal veins and arteries were measured. At 12-week post-STZ injection, rats were euthanised, and retinae were collected for measurement of Ang-2 and PKC gene and protein expressions. RESULTS: Retinal venous and arterial diameters were significantly greater in DV compared to DT at week 12 post-STZ injection (p < 0.001 and < 0.05, respectively). The vessel diameter measurements in DT were comparable to N and this effect of TRF was associated with significantly lower Ang-2 and PKC gene and protein expressions compared to DV. CONCLUSION: Oral TRF reduces the expression of retinal angiogenic markers and preserves the retinal vascular diameter of rats with STZ-induced DR.

Visual loss after long-haul flight.

BACKGROUND: Deep cerebral venous sinus thrombosis is a reversible yet potentially serious thromboembolic event. A number of reports suggest a relationship between long-haul flights and thromboembolic events, mainly deep venous thrombosis (DVT) and pulmonary embolism (PE). It is rarely reported to cause deep cerebral venous sinus thrombosis. We report a case of a bilateral papilledema after long-haul flight secondary to deep cerebral venous sinus thrombosis with subsequent complete recovery post corticosteroid and anticoagulant therapy. CASE: A case of a 21-year-old woman with no known medical illness who presented with gradual painless bilateral visual loss is described. She had a history of travelling on a long-haul flight 3 weeks prior to presentation. Examination showed presence of bilateral papilloedema, no vitritis, choroiditis and retinitis. Blood investigations showed raised international normalised ratio (INR). Otherwise, workup for infectious causes of optic disc swelling, connective tissue disease screening were normal. Magnetic resonance imaging (MRI) and magnetic resonance venography (MRV) of the brain showed loss of flow signal in the right transverse sinus and the left sigmoid sinus. Blood workup for preexisting hypercoagulable state was normal. She was diagnosed with deep cerebral venous sinus thrombosis and showed complete recovery with oral corticosteroid and anticoagulant therapy. CONCLUSION: Deep cerebral venous sinus thrombosis is a potentially serious consequence of long-haul flights. A high index of suspicion along with radiological techniques is needed for early detection and initiation of anticoagulation for this reversible condition.