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We have determined, in a group of patients suffering from massive pulmonary embolism, the ANF basic levels and the changes noticeable in anticoagulant treatment. The heparin therapy, in six patients studied, has produced a considerable clinic and functional better conditions as testified by the gradual improving from hypoxemia. The PaO2, in fact, increases from a basic value of 68.7 +/- 17.65 mmHg to 74.68 +/- 7.16 mmHg on the 7th day (p: n.s.) and to 83.66 +/- 12.46 mmHg on the 14th day (p < 0.05 on the basic value) of treatment. At the same time it has been possible to note a decreasing of plasmatic ANF mean concentrations with decrease from a basic value of 250 pg/ml to 190 pg/ml (p: n.s.) after 7 days to 185 pg/ml (p: n.s.) after 14 days of therapy. However the presents of the high values after 14 days, could be considered as evidence of a persisting change of pulmonary arterious circulation. On the basis of such notes we have tied to compare the amount of ANF, in basic conditions, with the degree of scintigraphic alterations. Of the three patients whose PRA had been previously valued (n. 4, 5, 6), n. 4 and n. 5 showed, in basic condition, a suppression of PRA and only n. 5, at the end of treatment, reached a normal range of PRA. In those three patients there hasn't been relevant changes of plasmatic aldosterone concentration during the study.

We have considered the behaviour of the atrial natriuretic factor (ANF) in eight patients suffering from chronic obstructive pulmonary disease (COPD), who have been treated with aminophylline for 24 hours. The mean of ANF concentration decreased from a basic value of 171.31 pg/ml to a value of 128.83 pg/ml (p: n.s.) after treatment. With the exception of patient n. 5 and 7, in the remaining group a significant inverse correlation between ANF and aldosterone was found in accordance with the powerful inhibitory action exerted by the ANF on the secretion of the mineralocorticoid hormone. The changes of the ANF, after a treatment with aminophylline, are characterized by considerable differences among the several patients. In all patients who had a very high basic value, we generally assist to a plasmatic concentration reduction of the hormone after methylxantine. It can be assumed that the reduction of the pulmonary arterial pressure owing to the direct vessel-dilating action of the methylxantine as well as to the effect of vein-dilating and diuretic action reduce the stimulus to the secretion of ANF.

A case of 17-alpha-hydroxylase deficiency in a genotypic male is described. The patient, who had grown up as a female, at the age of 18 years by chance was seen for enteritis. She presented primary amenorrhea and lack of secondary sexual characteristics combined with hypertension and mild hypokalemia due to excess of mineralcorticoids. The hormonal profile observed under basal conditions was evocative of a deficiency in 17-alpha-hydroxylase. High plasma aldosterone concentrations, in the face of suppressed PRA, were related to interference in RIA method: low plasma aldosterone values were observed when HPLC separation was applied. Eunucoid appearance and gigantism (195 cm) has rarely been observed as a fenotypic expression of this enzymatic deficit, but are justified by deficiency of both androgens and estrogens.

A patient with hypertension (female: aged 48 years) associated with primary hyperparathyroidism and left renal artery thrombosis is described. Taking into account that the patient was treated on the left side by lithotripsy about two years before the development of hypertension while assuming an oral dose of an estro-progestinic compound, a possible role of these two conditions is discussed in the genesis of renal artery thrombosis and development of renal hypertension.

A case of primary hyperparathyroidism with prevalent neuromuscular symptoms is described. Clinical, diagnostic and therapeutic implications are emphasized. Particular attention must involve a full clinical examination, electromyographic data and neuromuscular biopsy to make differentiation from primary myopathy or denervation pathology. Some similarity of electromyographic data with those observed in botulism and myastenia gravis should also be taken in mind. Hypercalcemia could play a pathological role in conditioning abnormalities of nervous impulse conduction at the level of neuromuscular junction. Another possible interference might be related to a direct effect of parathormone and hypophosphataemia on nervous impulse conduction. "Glandular hyperplasia", as observed in this case at istologic examination, rises some problems as far as the prognosis is concerned.