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A method for the detection of total, type I, and type II intrinsic factor antibodies was devised. The technique comprises a two-site solid phase enzyme linked immunosorbent assay (ELISA), with human intrinsic factor conjugated with horseradish peroxidase as label and attached to polystyrene tubes as solid phase. One conjugation provides sufficient material to assay more than 10,000 patient samples. The label proved stable during the course of this evaluation and was still in use more than 12 months after preparation. When applied to 45 serum samples from cases of pernicious anaemia, intrinsic factor antibodies were shown in 30 (67%). Simplicity, high capacity, low cost and label stability, combined with relatively high clinical sensitivity make the method suitable for cost effective screening of large numbers of samples. Simple modifications to the basic assay reagents permitted type I and type II intrinsic factor antibodies to be differentiated. [ABSTRACT FROM PUBLISHER]

The iron kinetic model described by Ricketts et al was used to study haemopoiesis in chronic myelofibrosis. The clearance of 59Fe-labelled transferrin from the plasma was analysed to quantify total, effective, and ineffective erythropoiesis, denoted by the terms marrow iron turnover (MIT), red cell iron turnover (RCIT), and per cent ineffective iron turnover (IIT%), respectively, in 12 cases of this disease. The patterns obtained were variable: values for MIT ranged from 24.4 to 510 mumol/l blood/day; those for RCIT from 0.4 to 119 mumol/l blood/day; and those for IIT% from 67 to 98%. One noteworthy feature was the presence in two cases of functional erythroid hypoplasia; these were characterised by severely reduced values for MIT (24.4 and 28 mumol/l blood/day) and RCIT (0.4 and 8 mumol/l blood/day.) A systematic study of the erythrokinetic features of myelofibrosis may indicate that erythroid hypoplasia is a more common cause of anaemia in this disease than has been previously recognised. [ABSTRACT FROM PUBLISHER]

In 16 patients (9 on azathioprine, 7 not) the ineffective iron turnover (IIT) was much higher in the azathioprine group (62.7 +/- 6.7 vs. 23.5 +/- 3.5 mumol/l blood/day, p < 0.0001, 2-tailed t test), though the red cell iron turnover (RCIT) was similar (42.8 +/- 2.9 vs. 41 +/- 4.8). Erythropoietin improved the anaemia in all patients and raised the RCIT (4 still on azathioprine to 72.2 +/- 9.8, p < 0.003; 7 non-azathioprine patients to 62.7 +/- 5.3, p < 0.01); the IIT remained higher in the azathioprine-treated (85.5 +/- 19.3 vs. 37.1 +/- 5.4; p < 0.013). In 2 patients who discontinued azathioprine, the IIT declined markedly to normal. In summary, azathioprine exacerbates the anaemia of renal failure by augmenting ineffective erythropoiesis, while erythropoietin benefits those on azathioprine as much as other renal patients by stimulating both effective and ineffective erythropoiesis.