The effect of changes in the dialysate calcium concentration on calcium fractions and parathyroid hormone species in plasma during hemodialysis has been examined. C-terminal immunoreactive parathyroid hormone was suppressed when plasma calcium increased by > 25 % whereas N-terminal fragments demonstrated an increase. The significance of this is discussed in light of present knowledge of parathyroid hormone metabolism.

During her second pregnancy a 27-year-old woman had recurrent acute pancreatitis, in the course of which primary hyperparathyroidism was diagnosed. After regression of the acute signs and under conservative treatment a parathyroid tumour was removed in the 26th week of pregnancy. Comparison of surgical and conservative treatment of primary hyperparathyroidism during pregnancy has indicated that the risk of complications in the neonate is much lower after surgical removal of the adenoma than with an attempt to postpone by symptomatic drug treatment the parathyroidectomy until after delivery.

Two chronic alcoholics developed acute renal failure from alcoholic myopathy (acute alcohol-induced rhabdomyolysis). Severe muscle pain developed and was associated with transitory oligo-anuric renal failure, requiring dialysis in one patient. In addition to the typical history and clinical symptoms, excessive elevation of muscle enzymes, especially creatine-kinase, and the appearance of myoglobin in serum are characteristic. Brown discoloration of the urine and a falsely positive test for "blood" due to the presence of myoglobin in urine in the absence of red blood cells are also typical. Definite changes can be demonstrated histologically and electromyographically during the acute stage. It is likely that this condition is more frequent than the sparsity of published reports indicates.

We read with interest the case report 'Rhabdomyoly sis and acute renal failure after terbutaline overdose' by Blake and Ryan [1] in your September issue. In this context it may be of i merest to note that two other cases of [3r adrenoceptor agonist-induced rhabdomyolysis have been described [2,3]: one case after therapeutic oral doses of fenoterol for tocolysis [2], and the other case after an overdose of terbutaline [3], These cases confirm the observation made by Blake and Ryan.As pointed out by the authors cases of rhabdomyolysis following amphetamine have also been described [4], In addition, other adrenergic agents such as methamphetamine, phenmetrazine, methylenedioxyamphetamine, phenylpropanolamine, D-norpseudoephedrine, and fen fluramine [4][5][6][7][8] have been implicated in the pathogenesis of rhabdomyolysis. There is. therefore, considerable evi dence that under certain conditions adrenergic sub stances may have a myotoxic potential and cause rhab domyolysis.As to the mechanism underlying the myotoxicity of p2-adrenoceptor agonists, however, we do not think it probable that ischemia plays a major role: ischemia may partly explain the rhabdomyolysis of indirectly acting adrenergic agents like amphetamine, since these sub stances predominantly release noradrenaline and thus may favor a-adrenergically mediated vasospasm. (32-Adrenoceptor agonists like fenoterol and terbutaline, however, have predominantly vasodilator effects. Thus, we think it more likely that their myotoxic effects are, in fact, metabolic and are related to depletion of muscle energy stores induced by glycogenolysis and lipolysis, rather than by ischemia. These effects may be aggravated by tremor and agitation which are both common side effects of (T-adrenoceptor agonists. In contrast, both mechanisms -metabolic stress and ischemia -may work in intoxications through amphetamine-like substances: this may partly explain, why reports on myotoxic effects of amphetamine are rather common, whereas such re ports are rare for (32-adrenoceptor agonists.Last but not least, we would like to comment on the statement of the authors that 'serum and urine myoglobin measurements are an unreliable means of detecting rhab domyolysis': this statement -although commonly re peated in the literature -is not valid [9]. The opinion that in spite of major muscle necrosis myoglobin is not re leased in sufficient amounts into plasma and excreted into urine dates from an era in which reliable and sensi tive assay systems for myoglobin measurement did not exist and when myoglobin was measured by spectros copic or gel immunodiffusion methods. Indeed, it is difficult to conceive that a relatively low molecular weight molecule like myoglobin would not be released on major muscle damage, whereas high molecular weight enzymes like creatine kinase would be released. This assumption is also contradicted by myocardial infarction where myoglobin release has been shown to be more sensitive than creatine kinase [10]. When using sensitive RIA methods [10] myoglobin is consist...

The suggestion that the higher afternoon values of somatomedin activity resuIt from a decrease in inhibition of the somatomedin bioassay by cortisol (Van den Brande, Van Buul, Heinrich, Van Roon, Zurcher and Van Steirtegem 1975) are not supported by the findings of this study where cortisol and somatomedin both increase from 0900 hand both have high values between 1200 and 1400 h. Furthermore, as there is a single peak 01' somatomedin activity but two peaks in cortisol secretion, it would appear that increased plasma cortisol does not produce a decrease in somatomedin production. It would thus appear that the observed cireadian variation of somatomedin activity is independent of cortisol secretion.