No abstract

Using the dexamethasone suppression test, we studied the activity of the hypothalamicpituitary-adrenal axis within the first week after onset in 62 patients with acute ischemic stroke. Compared with two control groups (one comprising 25 elderly patients with various acute medical disorders and the other comprising 33 80-year-old volunteers), stroke patients had higher postdexamethasone cortisol levels (p=0.08 and /?=0.001, respectively). By multiple regression analysis, high postdexamethasone cortisol levels in the stroke patients were significantly associated with proximity of the lesion to the frontal pole of the brain (p=0.008) and with disorientation (p=0.03), whereas no association with major depression was seen. Many stroke patients are exposed to hypercortisolism, which may have negative consequences upon organ functions. The extent to which dexamethasone administration suppresses cortisol levels seems to be determined mainly by the site of brain lesion and cannot be used as an indicator of major depression early after stroke. (Stroke 1989;20:1685-1690

Twenty-six consecutive patients with primary biliary cirrhosis (PBC) from northern Sweden were studied regarding the occurrence and features of Sjögren's syndrome (SS). In more than 50% of the patients the rose bengal dye test showed conjunctival and/or corneal staining. In six patients keratoconjunctivitis sicca (KCS) was present with positive rose bengal and Schirmer tests. In a further three patients only the results of the Schirmer tests were abnormal. Radiological findings of sialectasia were demonstrated in six patients, five of whom had KCS. Two of the seven patients who fulfilled our criteria for Sjögren's syndrome were HLA-B8 positive. A high prevalence of increased immune globulins and rheumatic factor was found, but this did not correlate with the presence of Sjögren's syndrome. Some features of Sjögren's syndrome were found in 73% of PBC patients, and keratoconjunctivitis sicca and/or sialectasia were found in 27% of PBC patients. This constitutes a high frequency of secondary manifestations of the liver disease.

A randomized controlled clinical trial was carried out to study the effect of tranexamic acid (AMCA, Cyklokapron; AB Kabi, Stockholm, Sweden) in the prevention of early rebleeding after the rupture of an intracranial aneurysm. The incidence of vasospasm, hydrocephalus, cerebral ischemic and thromboembolic complications, morbidity, and mortality was also evaluated. The series comprises 59 patients, 30 treated with tranexamic acid and 29 controls. The treatment was stopped if there was rebleeding, operation, or discharge from the hospital. There were 6 recurrent hemorrhages in 6 patients in the tranexamic acid-treated group and 11 recurrences in 7 patients in the control group. Recurrent hemorrhages occurred later in tranexamic acid-treated patients than in controls. Five patients in each group died from rebleeding. Five additional treated patients and 2 controls died from cerebral ischemic dysfunction. The results suggest that tranexamic acid may protect patients with ruptured aneurysms from rebleeding for 1 or 2 weeks, but that it also may produce cerebral ischemic complications.

The occurrence of abdominal aortic aneurysms (AAAs) and intracranial aneurysms (IAs) in the same patient and in the same family was studied among 89 patients with AAAs and 485 patients with IAs. Among the AAA-patients two had IAs themselves and five had IAs in the family, whereas three IA-patients had AAAs themselves and eight had AAAs in the family. Moreover, one of the patients with both AAA and IA had a blood relative with AAA, and in six of the families with both types of aneurysms there were more than two subjects with aneurysms. The results indicate, that AAAs and IAs may have a common aetiologic factor.