2-month-old male, normal pregnancy and delivery.
Birth weight 3270 g.
Symptomatic hypoglycemia at 24 h of life, attributed to hypoglycemic episodes.
Extended with exclusive direct breast, good lift.
As evidenced in the pediatric control, the patient was hospitalized.
There was no choluria, hypocholia or other symptoms.
She was feeding well.
On admission, the patient presented a good general appearance, with no dysmorphia; jaundice to the root of thighs, hepatomegaly without stenosis.
neurological symptoms were normal.
During the first hours of hospitalization, she presented repeated episodes of symptomatic hypoglycemia with minimum blood glucose values of 0.29 g/L and negative ketonemia.
The functional and hepatic enzymogram showed a pattern of stasis.
Urine examination and coagulation study were normal.
Abdominal ultrasound showed gallbladder, liver and bile ducts unchanged.
Infectious causes and inborn errors of metabolism were ruled out.
An endocrine cause was raised, due to counterregulatory hormone deficiency or excess insulin.
Fasting hypoglycemia with serum hormonal dosage was diagnosed.
Insulinemia was normal, cortisol and ACTH were very low.
Thyroid hormone dosage was requested and secondary hypothyroidism was diagnosed.
Growth factor-1 (IGF-1) and its transporter (IGFBP-3) were dosed, both descendants, suggesting a growth hormone (HC) deficiency.
These results demonstrated the presence of hypopituitarism.
Penile length was reevaluated; it was in the 5th percentile of the Sconfeld-Beebe7 table and between -2 and -2.5 standard deviations of the glandular pituitary magnetic resonance imaging (MRI) showed.
This association is known as "pituitary stem section syndrome".
Treatment was initiated with hydrolytic agents and levothyroxine.
The evolution was good, without hypoglycemia and with regression of stasis in 4 weeks.
