8RF) write: Many reports document a variety of neurological complications resulting from both intravenous and intrathecal administration of methotrexate, but acute cerebral oedema is not among them. We describe a patient with acute myeloid leukaemia who developed cerebral oedema after treatment with intrathecal methotrexate. A 23 year old Jamaican woman was admitted with a diagnosis of acute pnyeloid leukaemia (M3).

Inflammatory bowel disease (Crohn's disease and ulcerative colitis) is associated with decreased bone mineral density and increased risk of osteoporosis. However, the pathogenesis of this bone loss is not yet fully understood. In the present study we measured lumbar bone mineral density (by dual photon absorptiometry), serum levels of parathyroid hormone (PTH) and vitamin D metabolites, and serum markers of bone turnover (alkaline phosphatase and osteocalcin) in 15 patients with Crohn's disease and in 4 patients with ulcerative colitis. The median duration of the disease was 4 years and the median lifetime steroid dose was 10g of prednisone. We compared our results to a control group of 19 normal persons, who were matched for age and sex to the patients. We found that lumbar bone density was reduced by 11% in patients compared with control persons (Z-score -0.6 +/- 0.6 versus -0.1 +/- 0.8; p < 0.05). In patients, the serum levels of PTH, 25-hydroxyvitamin D3, and calcitriol (1,25(OH)2D3) were significantly reduced compared with control persons. Serum alkaline phosphatase activity (AP) was significantly higher in the patients and was inversely related to lumbar bone density. Osteocalcin values were not different between patients and control persons. There was also no difference in serum levels of calcium between the two groups, whereas phosphorus levels were higher in patients. We conclude that malabsorption of calcium was not a primary cause of bone loss in our patients, because we did not find secondary hyperparathyroidism. Accordingly, we did not find a severe vitamin D deficiency, since 25-hydroxyvitamin D3 levels were within the normal range.(ABSTRACT TRUNCATED AT 250 WORDS)

Previous studies have shown a link between low serum insulin-like growth factor-I (IGF-I) and decreased bone mass of patients with osteoporosis. However, whether serum levels are representative for the growth factor concentration or activity available in human bone tissue is controversial. In the present study, IGF-I was assessed in serum and bone matrix extracts from the iliac crest in 19 eugonadal women with idiopathic osteoporosis and in 38 age-matched controls. In addition, the relationship between the skeletal levels of IGF-I and bone mineral density (BMD) or the susceptibility to osteoporotic fractures in women with osteoporosis was examined. Bone matrix extraction was performed based on a guanidine-HCL/ethylendiamine-tetraacetic acid (EDTA) method. No significant difference in both serum and bone matrix IGF-I levels between groups was observed. Serum IGF-I concentrations failed to be associated with bone matrix IGF-I levels in osteoporotic patients. However, in premenopausal women with idiopathic osteoporosis, skeletal IGF-I positively correlated with BMD at the lumbar spine (r = + 0.58, p = 0.01). In contrast, neither femoral neck BMD nor Ward's triangle BMD was associated with bone matrix IGF-I concentrations. A tendency towards lower levels of bone matrix IGF-I in subjects with vertebral fractures as compared to those without fractures was observed in age-adjusted analyses, however the difference failed to remain statistically significant after adjustment for bone mineral density. These data provide no clear evidence for low bone matrix IGF-I as a determinant factor of age-unrelated osteoporosis. However, low skeletal IGF-I concentrations may aggravate osteoporosis in these women.

Calcium ions are of irnportance for the function of every cell in the organism, and this applies also for the fat eells. In incubated slices of rabbit adipose tissue, ACTH-or epinephrine-stirnulated Iipolysis was accompanied by an increase in.tissue calcium (A/cgün and Rudman 1969). Werner and Löw (1973, 1974) investigated the effects of the hormones of calcium homeostasis, parathyroid hormone and calcitonin, upon lipolysis of incubated rat adipose tissue pieces and demonstrated that parathyroid hormone induced a 3 to 5 fold inerease in glycerol release, which was aecompanied by enhanced calcium aeeumulation in the tissue, whereas calcitonin exerted opposite effeets. As the question remained open whether these meehanisms were instrumental in the human organism, too, the influences of parathyroid hormone and of calcitonin upon incubated slices of human adipose tissue were studied.

The effects of intragastrically administered synthetic human calcitonin (H-CT) and salmon calcitonin (S-CT) on human gastric secretion have been compared with the effects of both CTs after intravenous infusion. Basal as well as pentagastrin-stimulated acid and pepsin output were lowered by about 50% in response to a single intragastric instillation of H-CT while an intravenous infusion of H-CT produced an inhibition of more than 70%. After intragastric instillation, dose-response curves of H-CT and S-CT were in a similar range when the dose was referred to the molarity of CT; however, related to the biological activity of CT (MRC units), S-CT was about 10–15 times less effective than H-CT. Conversely, after intravenous infusion, equal doses in reference to MRC units evoked similar responses while in reference to molarity S-CT was 20–30 times more effective than H-CT. Radioimmunological determinations of H-CT showed after intragastric instillation a stepwise decrease in concentration of H-CT in the gastric juice and no appearance of H-CT in the blood. In contrast, after intravenous administration of H-CT, no detectable H-CT activity was secreted into the juice in the presence of a peak increase in serum-immunoreactive H-CT. From the differences in the effects of CT observed after intragastric and intravenous administration, respectively, it is suggested that intragastrically administered CT might inhibit gastric secretion via local mechanisms on the gastric mucosa.