Functional hypothalamic amenorrhea: Impact on bone and neuropsychiatric outcomes.

Functional hypothalamic amenorrhea is a state of reversible hypogonadism common in adolescents and young women that can be triggered by energy deficit or emotional stress or a combination of these factors. Energy deficit may be a consequence of (i) reduced caloric intake, as seen in patients with eating disorders, such as anorexia nervosa, or (ii) excessive exercise, when caloric intake is insufficient to meet the needs of energy expenditure. In these conditions of energy deficit, suppression of the hypothalamic secretion of gonadotrophin-releasing hormone (with resulting hypoestrogenism) as well as other changes in hypothalamic-pituitary function may occur as an adaptive response to limited energy availability. Many of these adaptive changes, however, are deleterious to reproductive, skeletal, and neuropsychiatric health. Particularly, normoestrogenemia is critical for normal bone accrual during adolescence, and hypoestrogenemia during this time may lead to deficits in peak bone mass acquisition with longstanding effects on skeletal health. The adolescent years are also a time of neurological changes that impact cognitive function, and anxiety and depression present more frequently during this time. Normal estrogen status is essential for optimal cognitive function (particularly verbal memory and executive function) and may impact emotion and mood. Early recognition of women at high risk of developing hypothalamic amenorrhea and its timely management with a multidisciplinary team are crucial to prevent the severe and long-term effects of this condition.

Diabetic ketoacidosis, hyperosmolarity and hypernatremia: are high-carbohydrate drinks worsening initial presentation?

The case of five pediatric patients who presented to the Royal Children's Hospital, Melbourne with newly diagnosed diabetes mellitus between January 2001 and September 2003 is reported. Each case was complicated by hyperosmolarity and hypernatremia and required intensive therapy. Fluid intake prior to admission in each case was documented and consisted of between 5 and 12 L of carbonated carbohydrate beverages and 'isotonic' sports drinks. At presentation, biochemical results of the four cases (four males and one female), mean age 13.6 yr (range 11.7-15.1 yr) included glucose (mean 1460 mg/dL; range 864-2106), adjusted sodium (mean 176.3 mmol/L; range 165-183), serum osmolarity (mean 399 mmol/kg; range 364-424), anion gap (mean 48 mEq/L; range 42-84), and pH (mean 7.15; range 7.01-7.27). All five cases had evidence of ketonuria on presentation. Treatment in all five cases consisted of replacement of fluids over a prolonged period of 72 h and careful monitoring of electrolyte response. Three of five cases required hemofiltration in the first 48 h postadmission. All five cases made a complete recovery without neurological sequelae. Carbonated carbohydrate fluid intake may precipitate a more severe presentation of type 1 diabetes mellitus (T1DM). Fluid composition and intake should be carefully estimated at admission to help identify and manage similar cases.