Low-dose oral iron absorption test in anaemic patients with and without iron deficiency determined by bone marrow iron content.

The low-dose oral iron absorption test (OIAT) was performed in 85 consecutive anaemic patients referred for bone marrow examination in order to investigate the ability of the test to predict bone marrow iron stores and to differentiate between different categories of anaemia. Eight patients were excluded for technical reasons. Test results from 77 patients are presented as Cmax (micromol/l): the maximum increase in S-iron measured during a 3 h period after administration of 10 mg oral iron sulfate. Iron deficiency was defined as the absence of stainable iron in bone marrow aspirates. Cmax was higher in 46 iron deficient patients [3 (median); 0 and 13 (1st and 3rd quartiles); 0-40 (range)] than in 31 non-iron-deficient patients (0; 0 and 2; 0-4) (P<0.01). 27 patients had primary bone marrow disease, 25 patients had absent bone marrow iron stores accompanied by inflammation, 17 patients had anaemia of chronic disease (ACD) and 8 patients had uncomplicated iron deficiency anaemia (IDA). Patients with IDA had higher Cmax (15; 13 and 28; 6-40) than patients with ACD (1; 0 and 2; 0-3), and than the 69 non-IDA patients (1; 0 and 3; 0-19) (P<0.001). Cmax values above 5 micromol/l always indicated absent bone marrow iron stores.

Low-dose oral iron absorption test: establishment of a reference interval.

The low-dose oral iron absorption test (OIAT), a possible test for iron deficiency, is based on the fact that intestinal iron absorption is higher in iron-deficient subjects than in those with normal or increased iron stores. The aims of this study were to establish a reference interval for the OIAT, to evaluate five different ways of presenting the results, and to advocate for the use of one of these methods. OIAT was performed in 122 healthy volunteers, 3 of whom were excluded as a result of technical difficulties. The volunteers were given 10 mg of oral iron sulphate at 0900 h on an empty stomach. S-iron was measured just before iron consumption, and after 1, 2 and 3 h. The maximum increase in S-iron during the test, presented as Cmax (micromol l(-1)), was higher in females (5 [median]; 3 and 7 [1st and 3rd quartiles]; 0-34 [range]) than in males (3; 1 and 5; 0-13) (p<0.001 Mann Whitney U-test). Furthermore, Cmax was significantly higher in females aged 22 44 years than in all other age groups (males and females), but did not fluctuate significantly with age in males. Cmax was higher in premenopausal than in postmenopausal females (6; 5 and 10; 0-34 and 4; 2 and 5; 0-12, respectively) (p <0.01 Mann Whitney U-test). In conclusion, iron absorption assessed by the OIAT was higher in premenopausal females than in postmenopausal females and males. We suggest reference intervals of 0-34 micromol l(-1) in premenopausal females, and 0-11 micromol l(-1) in all other persons, i.e. males and postmenopausal females.

Towards establishing comprehensive databases of cellular proteins from transformed human epithelial amnion cells (AMA) and normal peripheral blood mononuclear cells.

Databases of protein information derived from the analysis of two-dimensional gels have been established from transformed human amnion cells (AMA) and peripheral blood mononuclear cells (PBMCs). A total of 1781 [35S]methionine-labeled AMA proteins (1274 IEF, 537 NEPHGE) and a total of 1311 proteins from PBMC (948 IEF, 363 NEPHGE) were resolved and recorded using computerized (PDQ-SCAN and PDQUEST softwares) two-dimensional gel electrophoresis. AMA and PBMC proteins (total, 454: 301 IEF, 153 NEPHGE) were matched both manually and by the computer. Information entered in the AMA database (in most cases for some major proteins) includes: molecular weight, protein name, HeLa protein catalogue number, mouse protein catalogue number, nuclear proteins, phosphorylated proteins, distribution of proteins in Triton X-100 supernatants and cytoskeletons, proliferation- and transformation-sensitive proteins, cell cycle-specific proteins, mitochondrial proteins, proteins matched in normal human embryonal lung MRC-5 fibroblasts and PBMC cells, heat shock proteins, proteins affected by interferons, cytoskeletal proteins, and the presence of antibody against protein in human sera. Additional information has been entered for the cell cycle-regulated and DNA replication protein cyclin (PCNA). Information entered in the PBMC database includes molecular weight and potential markers for sorted populations of lymphocyte subtypes. For those proteins that have been matched to AMA proteins, information contained in some entries may be transferred from the AMA database.

Effect of propranolol treatment on bone mass, bone mineral content, bone remodelling, parathyroid function and vitamin D metabolism in hyperthyroidism.

The effect of propranolol 160-640 mg/day for 3 months on the accelerated loss of bone matrix and mineral in hyperthyroidism was studied in seventeen patients. A rise in serum thyroxine (P less than 0.01) during the first 3 weeks was followed by a fall (P less than 0.02). Serum triiodothyronine declined during the study (P less than 0.02). The enhanced bone mineral mobilization and collagen turnover continued during treatment and the bone mineral content decreased 3.2% (P less than 0.01). The secondary adaptive changes in serum parathyroid hormone and vitamin-D metabolites and in renal phosphate handling stayed unchanged. Iliac crest bone biopsies after tetracycline double-labelling showed initially a high bone turnover (P less than 0.01) with a reduced amount of cortical and trabecular bone (P less than 0.05). Following treatment bone formation rate decreased at both cellular and tissue level (P less than 0.01). No significant changes were observed in the amount of cortical and trabecular bone. The investigation shows that propranolol, in contrast to antithyroid medication, lacks any curative effect on the accelerated bone loss in hyperthyroidism.