Plasma concentrations of betamethasone, cortisol and corticosterone were measured before and after intraarticular injection of a betamethasone-depot preparation (Celestan-Depot) by radioimmuno-assay in 31 patients. Plasma concentration of betamethasone reached its maximum of between of 10 and 17 microgram/dl 30 min after injection. It had fallen to half after 2 hours, and practically to nil from the eighth day onwards. Lowest plasma levels of cortisol and corticosterone occurred after 6--24 hours, returning to the normal range after four days. In nine patients with knee-joint effusion and synovitis the plasma concentration of betamethasone was significantly higher after 24 hours, and cortisol and corticosterone values after 48 hours significantly more suppressed, than in patients without joint effusions and signs of inflammation. The results indicate that plasma concentration of betamethasone and the suppressant effect on the adrenal cortex after intra-articular injection is similar to that after intramuscular applications. Correspondingly, systemic application of the cortisol derivatives can cause significant side effects and be contra-indicated also after intra-articular injection.

Figure. Amount of either estradiol (0) or zeranol (0) added (mols x [10][11][12] that of Shutt (1969). Eight Blackface ewes were used for the study in vivo. Estrous activity was synchronised by thc use of intravaginal progesterone pessaries. On the day of pessary removal 4 ewes were injected with zeranol (4.8 mg). Injections were made daily for 5 days. Blood was sampled twice daily for LH assay (Chesworth 1977). Estrus was detected by a vasectomised ram. Restdts and DiscussionZeranol displaced estradiol from the binding protein, the curves were parallel but the required levels of zeranol were about five times greater. Korenman (1969) suggested that the relative efficacy of most estrogens in binding to uterine receptors approximates to their biological potcncy. Upon this basis zeranol appears to be relatively potent.After zeranol injection aU ewes were seen in estrus; treatment did not alter the timing or apparent intensity of this. All ewes had elevated LH levels at or near estrus but there were no differences between treatments either in the timing or size of the peak.The results indicate that although zeranol is apparently estrogenic in vitra it has little activity in viva. This discrepancy suggests that either zeranol is a compound whose activity in vitra does not parallel that in vivo or that zeranol is not a competitor but an inhibitor of estradiol binding. The dose used in vivo, over five days, was twice thc size of the normal im plant. The results therefore indicate that, as far as estrogenic activity is concerned, the use of zeranol with breeding females is not likely to lead to adverse effects.Increased alkaline phosphatase is commonly found in patients with hyperthyroidism (Cassar and Joseph 1969) and is generally associated with histological changes in the liver (3, 8). Studies by Chen et al. (2) showed that increased alkalinc phosphatase is at least in part of skeletal origin. In experiments on laying hens with hyperthyroidism Perek anti Snapir (7) demonstra ted increased activity of tissue alkaline phosphatase in epiphyseal cartilage. In the present study the possibility of a causal relationship between increased alkaline phosphatase and vitamin D deficiency was examined. MethodsTriiodothyronine (T 3 ), thyroxine (T4 ) and TSH were determined radioimmunologically. In our laboratory normal values of T 3 are between 0.8 and 1.7 ng/ml, for T 4 between 40 and 120 ng/ml. A TRH-test was performed in patients whose T 3 values were under 3.5 ng/ml or T 4 values were under 140 ng/ml. Those who showed an increase in TSH 30 minutes after injection of 200 ng of TRH were not included in the study. 25-OH-vitamin D (minimum-normal-value = 25 nmol/I) was evaluated with a protein-binding-assay (4). In addition to alkaline phosphatase (maximum norm-level = 180 um, the plasma concentrations of calcium, phosphorus, creatinine and enzyme activities of GOT, GPT and gamma-GT were determined in most patients. Patients whose hyperthyroidism was diagnosed between January 1975 and August 1976 were examined. Not included in t...

An acquired partial pituitary insufficiency of unknown origin with selective ACTH and STH deficiency was demonstrated in a 44-year-old patient. The clinical course over many years corresponds to subclinical Addison's disease with occasional acute crises. Ossification of both auricular cartilages and anhidrosis were outstanding signs. There is possibly a connection between the glucocorticoid deficiency over many years with normal mineralocorticoids and the auricular cartilage ossification.

No abstract

A modification of the infusion test with saralasin, an angiotensin II antagonist for the detection of renin-dependent high blood pressure was studied in renal hypertensive rats and in normotensive and hypertensive subjects. Infusion was started at a rate of 0.01 microgram/kg x min saralasin and the dose was increased ten-fold at 15 min intervals. A significant fall of diastolic blood pressure was observed at the dose of 0.1 microgram/kg x min in renal hypertensive rats, in healthy subjects treated with diuretics, and in patients with renovascular hypertension (saralasin responders). Plasma concentrations of angiotensin I, angiotensin II and of saralasin as well as plasma renin activity were measured. At the lowest infusion rate of 0.01 microgram/kg x min, saralasin plasma levels were 40-fold higher than plasma angiotensin II levels. The decrease in arterial blood pressure occurred at lower doses of saralasin than the increase of plasma renin due to inhibition of feedback on the renin secreting cells. It is concluded that if the saralasin test is performed by a stepwise increase of the infusion rate, potentially dangerous complications such as hypo- or hypertensive reactions can be avoided. The diagnostic reliability is improved by such a procedure since false positive and false negative responses may be prevented. The pressor effect of saralasin in non-renin dependent patients is an advantage since it causes a more marked difference of blood pressure change between saralasin responders and non-responders.