Diagnosis of primary hyperaldosteronism

Diagnosis of primary hyperaldosteronism, differential diagnosis of its various forms and other hypertensive conditions, mainly low-grade hypertensive disease, is not simple, requires a number of consecutive studies and functional tests.

With a pronounced and typical clinical picture, the primary diagnosis is based on low potassium levels and ARP in plasma and high aldosterone content.

At normal sodium content in the diet (120 meq / 24 h), the excretion of potassium is about 30 mmol / l. Potassium loading (up to 200 meq / 24 h) sharply increases the excretion of potassium and worsens the patient's well-being (severe muscle weakness, disturbance of the heart rhythm). Conducting the sample requires great care.

In aldosterome stimulating tests: orthostatic load (4-hour walking), a 3-day diet with a low (less than 20 meq / 24 h) sodium content or intake of active saluretics do not stimulate ARP, and the level of aldosterone may even decrease. Basal ARP is determined on an empty stomach after a night rest in the supine position, with a diet containing 120 meq / 24 h of sodium. Introduction of spironolactones at 600 mg / day for 3 days does not change the level of aldosterone secretion and does not stimulate ARP (spironolactone test). A test with captopril is of considerable diagnostic value. In patients with aldosteromics and at rest, and after a 4-hour walk, the circadian rhythm of aldosterone is maintained, which coincides with the rhythm of cortisol, which indicates the dependence on ACTH. The absence of this rhythm indicates the presence of a malignant tumor, rather than an aldosterone-producing adenoma.

With idiopathic hyperaldosteronism, the intensity of metabolic disorders is less than in the case of aldosterome, the level of aldosterone is lower, and the content of 18-hydroxy-corticosterone is significantly (many times) lower. ARP is also suppressed, but it rises, as well as the content of aldosterone, with orthostatic loading and angiotensin II injections. However, the effect of stimulation is significantly less than in healthy individuals. The introduction of spironolactones stimulates both ARP and the level of secretion of aldosterone.

At the same time, the sample with saline solution (2 liters of isotonic solution administered for 2 hours) does not suppress the level of aldosterone secretion in both aldosteromas and idiopathic primary hyperaldosteronism.

A sample with DOXA (10 mg, IM every 12 hours for 3 days) does not affect the plasma aldosterone content in patients with aldosterome and in most patients with idiopathic primary hyperaldosteronism. Suppression in the sample with DOXA is observed with indefinite primary hyperaldosteronism and hypertensive disease. In Table. 26 summarizes the main differential-diagnostic tests for primary hyperaldosteronism.

In carcinoma, the level of aldosterone in both plasma and urine can be very high. The reaction to all stimulating and inhibitory samples, including ACTH, is absent.

When conducting differential diagnostics with various hypertensive states, hypertensive disease with unstimulated ARP should first of all be excluded (in 10-20% of patients with hypertensive disease the level of potassium and aldosterone remains within the norm).

Primary hyperaldosteronism is differentiated with various diseases or conditions that cause secondary hyperaldosteronism.

1. Primary renal pathology, in which the ARP can be low, and normal, and high.
2. Malignant variant of hypertensive disease.
3. Pheochromocytoma.
4. Syndrome Barter (primary hyperenenism).
5. Hypertensive conditions in connection with the use of contraceptives, stimulating the renin-angiotensin-aldosterone system.

In cases where primary hyperaldosteronism is complicated by acute and chronic renal pathology (infection, nephrosclerosis), differential diagnosis is hampered by a decrease in renal clearance, aldosterone and (mostly) potassium.

It should also be remembered that the widespread use of diuretics in the treatment of hypertension causes hypokalemia, but ARP increases.

Patients with clinical and biochemically proven hyperaldosteronism are subjected to topical diagnosis, which allows to localize the pathological process. For this purpose, there are a number of methods.

1. Computed tomography is the most modern study with a large resolution, allowing in 90% of patients to detect even small tumors with a diameter of 0.5-1 cm.
2. Scanning with adrenal ¹³¹ 1-19-yodholesterolom or ¹³¹ 1-6b-iodomethyl-19-norholesterinom. This study is better performed with inhibition of the glucocorticoid function of dexamethasone (0.5 mg every 6 hours for 4 days preceding the study). In the presence of a tumor, there is an asymmetry (lateralization) of isotope accumulation in the adrenal glands.
3. Arterio or venography after the preliminary administration of ¹³¹ 1-19-iodine cholesterol.
4. Catheterization of adrenal veins with bilateral selective sampling of blood and determination of aldosterone levels in them. Sensitivity and informative value of this method increase after preliminary stimulation with synthetic ACTH, which sharply increases the level of aldosterone on the side of the tumor.
5. Echography of the adrenal glands.
6. Pneumoretroretoneumum supraorenorentgenography, combined with intravenous urography or without it; the method is formally obsolete, but today it has not lost its practical (diagnostic) value, for example, in carcinomas, when due to the large tumor size, radioisotope studies do not allow its visualization.

The most informative is computed tomography. Invasive angiographic studies are more complex for the patient and for the doctor, and less reliable. However, none of the modern methods gives 100% visualization. In this regard, it is desirable to simultaneously use 2-3 of them.

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