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SummaryWe have developed exchange transfusion methods to alter the haematocrit of tumour-bearing mice. The effects of anaemia and its correction by blood transfusion on the radiosensitivity of two mouse tumours (SCCVII/St and RIF-1) were studied using excision, in vivo/in vitroassay. An acute reduction in haematocrit caused a high degree of radioresistance equivalent to an increase in the hypoxic fractions by factors of 10 (SCCVII/St) and 30 (RIF-1). As the duration of the anaemia was prolonged, radioresistance was lost until within about 6 h normal radiosensitivity was observed even though the anaemia persisted. The restoration of the normal haematocrit by red blood cell transfusion after 24 h of anaemia caused increased radiosensitivity equivalent to a reduction in the hypoxic fraction by factors of 5 (SCCVII/St) and 10 (RIF-1), but again the effect was transient and normal radiosensitivity was re-established within 24––48 h of retransfusion. Measurements of 14C misonidazole (MISO) binding to RIF-1 tumours after these procedures indicated changes in the number of hypoxic cells which were qualitatively almost identical to those using the cell survival endpoint, leading us to believe that changes in oxygenation were responsible for the altered radiosensitivity. We feel that transfusion procedures could be used to advantage in the radiotherapy of some cancers.

A convenient and inexpensive radioimmunoassay for bloodspot 17α-hydroxyprogesterone (17-OHP) has been evaluated in the screening of newborn infants for congenital adrenal hyperplasia (CAH) and for home monitoring of CAH patients on steroid replacement therapy. In the screening study, analysis of 491 bloodspots taken for routine screening programmes for phenylketonuria and hypothyroidism established the upper limit of normal for infants aged 5-10 days as 64 nmol 17-OHP/l blood (99·9 centile). Home monitoring of patients by examination of fingerprick bloodspot 17-OHP profiles taken by parents over Saturday and Sunday on consecutive weekends showed that changes in control occurred as a result of transition from inpatient to outpatient treatment or following adjustment of steroid replacement regimens. The method was found to be valuable in the diagnosis and management of children with CAH.

OBJECTIVE
IGF-I and IGF binding protein (IGFBP)-3 levels in man are positively regulated by GH status; in contrast, evidence suggests an inverse relationship between GH status and IGFBP-2. We investigated the effects of somatropin administration on the serum concentrations of these analytes, together with serum and urinary concentrations of GH, to evaluate their potential as markers in the development of a test for detecting doping with GH in sports competitors. DESIGN
Somatropin was administered subcutaneously at a dose of 0.15 U/kg bodyweight/day at 1000 h for 3 days to eight healthy men (20-32 years old). MEASUREMENTS
Serum concentrations of GH, IGF-I, IGFBP-2 and -3 were determined in blood samples collected at 1600 h on the days prior to (day -1), during (days 0, 1 and 2), and following administration (days 3 and 7). Urine was collected continuously from days -2 to 3 and then on day 7. RESULTS
Serum and urinary concentrations of GH were only raised on the days of administration whereas, following cessation of somatropin, the increases in the serum concentrations of IGF-I and IGFBP-3 were sustained for at least 1 day (30 h). Serum IGFBP-2 decreased during the period of administration and was still suppressed on day 3. The concentration ratios of IGFBP-3 to IGFBP-2 and IGF-I to IGFBP-2 increased markedly with administration and both ratios were still significantly augmented compared with basal values 30 h after the last administration. CONCLUSION
With acute administration of somatropin to healthy men the serum concentration of IGFBP-2 decreases and the ratios of serum IGF-I/IGFBP-2 and IGFBP-3/IGFBP-2 increase. These ratios should be considered in the development of a test for detecting somatropin administration in sport.

OBJECTIVE The insulin stress test (IST) is the most commonly used test to assess the GH reserve in children and adults. It is a time-consuming, expensive and potentially dangerous test. We investigated whether measurement of urinary growth hormone excretion following exercise would prove a reliable method to diagnose adult GH deficiency.
DESIGN Healthy volunteers underwent a standard IST to confirm normal GH secretion. Using a standardized exercise protocol on a treadmill, the urinary excretion of GH was measured. Three patients confirmed as GH deficient by an IST were exercised using the same exercise protocol and their urinary excretion of GH was measured.
PATIENTS Ten healthy volunteers and three patients with hypopituitarism were evaluated.
MEASUREMENTS A standard IST was performed on both healthy volunteers and patients, with measurements of plasma GH and plasma cortisol. Urinary growth hormone and urinary GH/creatinine (GH/CR) ratios were measured before and after IST. On a separate visit, healthy volunteers and patients were exercised on the treadmill with measurements of plasma GH and cortisol. Urinary GH and GH/CR ratios were measured before and after exercise.
RESULTS There was at least a two-fold increase in urinary GH and GH/CR ratios following exercise in all healthy adults. By contrast, patients with GH deficiency showed no rise in urinary GH or urinary GH/CR ratios following exercise.
CONCLUSIONS Measurements of urinary GH following exercise can distinguish between GH-deficient adults and healthy volunteers. Urinary GH excretion can be measured over a timed interval following exercise or can be expressed as the GH/CR ratio. This can be measured on a single sample following exercise and can be used to diagnose GH deficiency. The exercise test employed for this study is arduous. We are therefore performing further studies with a less strenuous exercise protocol with a view to designing a `patient-friendly' exercise test for GH deficiency in adults.