Risk factors for ischaemic stroke in young Greenlanders.

INTRODUCTION: Contrary to a widely held belief, ischaemic cerebral infarction is not a rare disease in Greenland, as shown recently by our institution. We report data on some of the known risk factors in patients below 60 years of age with ischaemic stroke. METHOD: Retrospective data collection and review of charts from Greenlandic patients from all of Greenland admitted to the central hospital, Dronning Ingrids Hospital in Nuuk, in the years 2001 and 2002. RESULTS: A total of 37 patients below 60 years of age were discharged with a diagnosis of cerebral infarction. All had a CT, which showed infarction in 32. Five were reported normal, and the diagnosis of infarction rested on the absence of haemorrhage combined with long-standing, major neurological defect. Median age of the group was 54 years. Fifteen (40%) were women, thirty (81%) were smokers. Nine (24%) had hypertension. Two had diabetes, one had atrial fibrillation, and one had dilated cardiomyopathy. Two had significant carotid atherosclerosis diagnosed by duplex ultrasound. Of the rest, fifteen had transoesophageal echocardiography done, thirteen of which showed atherosclerotic changes. The cholesterol levels showed relatively high HDL levels. CONCLUSION: Ischaemic stroke is a common disease in young Greenlanders and seems to be associated with atherosclerosis with smoking as the only outstanding risk factor--though not more common than in the general population.

Carbamazepine induced right bundle branch block in a Greenlandic patient.

A 53 year old Greenlandic male was admitted twice over a period of 4 years with a new complete right bundle branch block after ingestion of 10 g and 4 g of carbamazepine respectively. In both instances, reversion of intraventricular conduction to normal occurred within 72 hours, coinciding with clearance of carbamazepine from the blood stream. We recommend routine follow up by ECG of patients over the age of 50 treated with carbamazepine.

Malabsorption due to a ventral hernia.

A case of malabsorption due to a stagnant loop which occurred in a huge ventral hernia is presented. The clinical course was relatively indolent with symptoms of malabsorption and occasional abdominal pain. Although rare, abdominal hernia can lead to malabsorption due to bacterial overgrowth as a result of stagnant loop.

Modulation of tissue plasminogen activator biosynthesis by phosphatidylinositol liposomes in human fetal lung fibroblasts.

Phosphatidylinositol (PI) liposomes at 40 microM increased tissue plasminogen activator (t-PA) biosynthesis by human fetal lung fibroblasts IMR-90 (FLF), after 5 days of incubation by 7.4 +/- 1.4 times of the control level. Other phospholipid liposomes, such as phosphatidylserine (PS), phosphatidylcholine (PC), and phosphatidylglycerol (PG), had no effect on t-PA biosynthesis by FLF. The induction of t-PA biosynthesis by PI liposomes was inhibited by specific inhibitors of phosphoinositide pathway: gentamycin and lithium chloride. Thus, gentamycin inhibited the effect of PI liposomes on t-PA biosynthesis by 76% (P less than 0.001), while it had no effect on control FLF. Likewise, lithium chloride inhibited t-PA biosynthesis of both PI-treated and control FLF by greater than 84%. The induction of t-PA biosynthesis by PI liposomes was dependent on RNA transcription and independent of DNA biosynthesis.

Phosphatidylinositol liposomes increase calcium uptake and tissue plasminogen activator secretion by fetal human lung fibroblasts.

PtdIns liposomes, at a concentration of 40 microM, induced in FLF the synthesis of t-PA-Ag, and enhanced 45Ca2+ uptake. The induction of t-PA-Ag biosynthesis by PtdIns liposomes in FLF was inhibited by 5-15 microM verapamil, an inhibitor of Ca2+ uptake via the so-called "slow channels" by 0.5-10 microM TFP, an inhibitor of Ca2+ transport ATPase, and by 10-90 microM TMB-8, an inhibitor of intracellular Ca2+ mobilization. t-PA-Ag secretion was inhibited by decreasing the Ca2+ concentration less than 1.2 mM. On the other hand, addition of 0.08 microM of calcium ionophore A23187 increased t-PA-Ag biosynthesis after 72 hr of incubation by 247% (P less than 0.01). These data support previous results and indicate that the synthesis of t-PA in FLF is Ca2+ dependent. Thus, it is suggested that PtdIns liposomes increase t-PA biosynthesis by affecting calcium metabolism.

Tissue plasminogen activator levels in different types of polycythemia.

The plasma level of tissue plasminogen activator antigen (t-PA-Ag) was examined in 86 patients with polycythemia (29 polycythemia vera, 11 secondary polycythemia and 46 with spurious polycythemia) and 24 healthy volunteers. Tissue plasminogen activator antigen was significantly decreased in patients with polycythemia vera in comparison with healthy controls. On the other hand, in patients with spurious polycythemia and secondary polycythemia t-PA-Ag concentration was significantly increased. There was no significant difference in t-PA-Ag levels in polycythemic patients with or without thromboembolic disease. A significant correlation was detected between t-PA-Ag level and hemoglobin or hematocrit concentration in patients with polycythemia vera (p = 0.02, r = 0.43). However, in patients with secondary polycythemia and spurious polycythemia, no significant correlation between t-PA-Ag and hemoglobin level was found. Plasminogen activator inhibitor (PAI) levels in patients with polycythemia vera and healthy volunteers did not differ significantly.

Atrial natriuretic peptide in relative polycythemia and polycythemia vera.

Atrial natriuretic peptide (ANP) levels have been tested in patients with chronic relative polycythemia (RP), polycythemia vera, and in healthy subjects in order to find a possible underlying pathophysiological mechanism for relative polycythemia. No difference in statistical significance has been found between the mean atrial natriuretic peptide levels of the polycythemic patients and the control group. It is suggested that ANP probably plays no significant role in the contraction of plasma volume observed in normotensive patients with RP.

Chorea in polycythemia vera: a rare presentation of hyperviscosity.

A 65-year-old woman developed severe chorea as the presenting symptom of the hyperviscosity syndrome together with polycythemia vera and an ovarian cyst. Whole blood viscosity was 69.5 centipoise at a shear rate of 1.1 s-1 (normal 12.0-22.0 centipoise). After four phlebotomies the chorea subsided completely, and the blood viscosity became normal. Hemoglobin level was stable at normal range and then increased to 18.0 g/dl with recurrence of the faciobuccal dyskinesia that disappeared promptly following the phlebotomies. This case emphasizes that in elderly patients with neurological disorders, such as chorea, polycythemia should be strongly considered as one of the treatable causes.