Blindness in dogs with pituitary dependent hyperadrenocorticism: relationship with glucose, cortisol and triglyceride concentration and with ophthalmic blood flow.

Pituitary dependent hyperadrenocorticism (PDH) shows a high morbidity and blindness is one of its complications. Compression of the optic chiasm (OC) by the hypophysis adenoma is one of the causes. Another cause could be due to vascular and metabolic alterations of the PDH. Out of a total of 70 dogs with confirmed diagnosis of PDH, 12/70 showed blindness. In only 2/12 the OC was compromised. Electroretinography in dogs without the OC being compromised showed altered A and B wave patterns. Ophthalmological Doppler showed an alteration of the blood flow only in blind dogs without OC compression. Cortisol concentrations (Co), triglycerides (Tg) and glycaemia (G) were greater in 10 dogs with non-compressive blindness vs. dogs with conserved vision. Loss of vision correlated with the increase in these variables. Blindness in dogs with PDH would be related to changes in retinal blood flow, associated to higher Co, Tg and G concentrations.

Parathyroid hormone secretion in chronic human endogenous hypercortisolism.

Osteoporosis is a common manifestation of Cushing's syndrome, but the mechanisms responsible for this abnormality have not been defined. With the objective of analyzing parathyroid hormone (PTH) secretion in chronic hypercortisolism (CH), we evaluated 11 healthy subjects and 8 patients with CH, 6 with Cushing's disease and 2 with adrenal adenoma. These volunteers were submitted to tests of PTH stimulation through hypocalcemia (EDTA), PTH suppression through hypercalcemia (iv and oral calcium), and evaluation of bone mineral density (BMD) by DEXA. During the test of PTH stimulation, the calcium and magnesium concentrations of the normal and CH groups were similar. Patients with CH showed an increased PTH response to the hypocalcemic stimulus compared to controls. PTH values were significantly higher in the CH group at 70 (17.5 +/- 3.5 vs 10.2 +/- 1.3 pmol/l, P = 0.04), and 120 min (26.1 +/- 5.9 vs 11.3 +/- 1.9 pmol/l, P = 0.008) of EDTA infusion. The area under the curve for PTH during EDTA infusion was also significantly higher in patients with CH than in normal subjects (1867 +/- 453 and 805 +/- 148 pmol l(-1) 2 h(-1), P = 0.02). During the test of PTH suppression, calcium, magnesium and PTH levels of the patients with hypercortisolism and controls were similar. BMD was decreased in patients with hypercortisolism in the spine (0.977 +/- 0.052 vs 1.205 +/- 0.038 g/cm2 in controls, P<0.01). In conclusion, our results show that subjects with CH present decreased bone mass mainly in trabecular bone. The use of dynamic tests permitted the detection of increased PTH secretion in response to a hypocalcemic stimulus in CH patients that may probably be involved in the occurrence of osteoporosis in this state.

[The diagnosis of Cushing's disease by the nocturnal dexamethasone administration test]. / Diagnóstico de la enfermedad de Cushing mediante la prueba de administración nocturna de dexametasona.

Prospective study performed at the General Hospital, National Medical Center, XXI Century, Endocrinology Ward, Mexico-City, to compare the diagnostic sensitivity in Cushing's disease of the oral high doses (8 mg) dexametazone suppression test in single doses with nocturnal administration (DXM-N) and the classic doses of two days (DXM-C). Fourteen patients with hypercortisolism were studied; on thirteen the hypophyseal origin was surgical confirmed. Sensitivity of high doses of oral dexametazone test was proved by using serial samples of serum cortisol; the Fisher test was used for analysis of the suppression of serum cortisol after the test was done.

Electrolyte metabolism of muscle in the salt-losing form of congenital adrenal hyperplasia.

The study of metabolism of muscle electrolyte in children with the salt-losing form of congenital adrenal hyperplasia reveals two types of alterations. After admission and during initial therapy with salt and desoxycorticosterone, the changes are typical of those seen in experimental animals with adrenalectomy and excessive replacement therapy. Discontinuation of the sodium supplement after three months of therapy resulted in a return of muscle electrolyte values to normal. During the period of poor growth common to these patients a different pattern was observed. Sodium and water accumulated without alteration in tissue potassium. The mechanism of this alteration is not clear; however, it is consistent with the known effects of excess cortisone on muscle composition. These observations permit the conclusion that at least two fractions of sodium are present in muscle fibers, that which exchanges potassium and that which is independent of potassium metabolism.