Isolated adrenocorticotropic hormone deficiency associated with growth hormone deficiency and empty sella.

A 38-year-old man had an acute onset of consciousness loss, pyrexia and hyponatremia. Plasma Adrenocorticotropic Hormone (ACTH) and cortisol levels were low. Plasma ACTH failed to respond to corticotropin-releasing hormone (CRH) and insulin-induced hypoglycemia whereas i.m. injection of ACTH-Z raised plasma cortisol. Plasma insulin-like growth factor-I (IGF-I) and urine growth hormone (GH) concentrations were also low and plasma thyroid-stimulating hormone (TSH) level was rather elevated. Plasma IGF-I and TSH levels were not completely normalized by glucocorticoid (GC) replacement alone although plasma GH responses to pharmacological stimuli were normalized. The GC replacement in combination with daily s.c. injection of recombinant human GH (rhGH) not only normalized plasma IGF-I and IGFBP-3 levels, but also further lowered the plasma TSH level, possibly due to an increased T4/T3 conversion, which resulted in a beneficial change in body composition.

[Unconsciousness due to hyponatremia in a patient with short stature with panhypopituitarism].

An unconscious woman of short stature (141 cm) was admitted to our hospital in March, 1994. She had hyponatremia (120 mEq/l) and had experienced massive bleeding during delivery. No increment of either plasma ACTH or cortisol levels was observed after insulin-induced hypoglycemia. However, urinary 17OHCS levels gradually increased after repeated intramuscular injections of ACTH. Plasma free T3 and free T4 levels were low. Neither plasma TSH nor prolactin (PRL) levels increased after an intravenous injection of TRH. Basal plasma LH, FSH and growth hormone (GH) levels were low and there were no observable responses to any of the stimulation tests. A magnetic resonance image (MRI) of her pituitary gland showed an empty sella. These results showed that she had a panhypopituitarism with primary empty sella. Replacement therapy with glucocorticoid was started and serum sodium levels normalized immediately. Levothyroxine was also administered. The possibility of pituitary dwarfism during her youth and a gradual postpartum reduction of other pituitary hormones may have caused an impairment of the hypothalamo-pituitary-adrenal axis.

Evidence for elevated levels of dopamine in the rabbit pulmonary and carotid artery.

Catecholamine levels in six arteries, two aortae, and atria of rabbits were determined by high-performance liquid chromatography (HPLC) coupled with electrochemical detection. An appreciable concentration of dopamine (DA) was found in the pulmonary and carotid arteries. The content in these two arteries was greater than 200 ng/g, although the mesenteric, celiac, renal, and femoral arteries had less than 55 ng/g. The ratio of DA to norepinephrine (NE) in the pulmonary artery was 32.2 +/- 6.3%, and that in the carotid artery was 9.0 +/- 3.8%. These values are equivalent to the ratio in the canine paw pad and kidney, which are considered to be innervated by a dopaminergic system among peripheral tissues. The presence of DA in the pulmonary artery was confirmed by gas chromatography and mass spectrometry. In addition, uptake and distribution of [3H]DA and significant enhancement of [3H]DA release by transmural stimulation in the pulmonary artery were observed. These results suggested the possibility of dopaminergic innervation in the rabbit pulmonary and, possibly, carotid arteries.