Thyroid function in bulimia nervosa

  title={Thyroid function in bulimia nervosa},
  author={Margaret Altemus and Marion M. Hetherington and Bingham Kennedy and Julio Licinio and Philip W. Gold},
Decreased serum leptin in bulimia nervosa.
Results are consistent with the hypothesis that decreased leptin function may be associated with alterations in eating patterns, metabolic rate, and neuroendocrine regulation in bulimia nervosa.
Aetiopathogenesis and Pathophysiology of Bulimia Nervosa
Data in the literature suggest that levels of noradrenaline and serotonin are lower in individuals with bulimia nervosa than in healthy controls, and alterations in the levels of neuropeptide Y, peptide YY, β-endorphin, corticotrophin-releasing hormone, somatostatin, cholecystokinin and vasopressin have been found, with a return to levels seen in controls after remission.
Endocrine and metabolic disorders in bulimic women and effects of antiandrogenic treatment
An antiandrogenic OC treatment reduced meal-related hunger and gastric distention in women with bulimia nervosa and improved bulimic behavior in relation to reduced testosterone levels.
Plasma Leptin Concentrations in Relation to Sick Euthyroid Syndrome in Elderly Patients with Nonthyroidal Illnesses
The concurrence of modifications in plasma leptin and thyroid hormones concentrations found in elderly NTI patients with a sick euthyroid syndrome could reflect a particular neuroendocrine status, leading to a reduction in the catabolic processes in the course of chronic diseases.
Bone mineral density in bulimic women--influence of endocrine factors and previous anorexia.
Low bone mass in bulimics may be explained by previous anorexia nervosa, whereas endocrine variables related to BMD seem to be secondary determinants that are dependent on previous anoresis nervosa and BMI.
Neuroendocrine aspects of anorexia nervosa and bulimia nervosa.
Some peptides of hypothalamic origin, as well as those secreted by the adipose tissue and gastrointestinal tract including pancreatic hormones, are involved in the control of appetite and satiety and play also an important role in the mechanism of hormonal secretion.


Hypothalamic-pituitary-thyroidal axis alterations in bulimic patients.
The results suggest that normal-weight patients with bulimia have abnormalities in the hypothalamic-pituitary-thyroidal axis.
Pituitary response to TRH in bulimia
Serum thyroid hormones and thyrotropin in anorexia nervosa.
Sixteen patients with typical signs and symptoms of anorexia nervosa were studied with measurement of serum thyroxine (T4), triiodothyronine (T3) and thyrotropin (TSH), both baseline and stimulated
Low serum triiodothyronine in patients with anorexia nervosa.
The extremely low serum levels of T3 in these patients with anorexia nervosa suggest that peripheral conversion of T4 to T3 is impaired during chronic starvation.
Low serum triiodothyronine (T3) and hypothyroidism in anorexia nervosa.
The TRH and TIR data suggest a central inhibition of thyroid function, possibly by impairment of hypothalamic TRH release, in the absence of a space-occupying pituitary lesion and a probable decrease of peripheral T4 to T3 conversion leads to low serum T3 concentrations.
Nocturnal serum thyrotropin (TSH) surge and the TSH response to TSH-releasing hormone: dissociated behavior in untreated depressives.
Major endogenous depression is associated with a major impairment of TSH secretion, which baseline TSH measurements in the morning and the evaluation of the TSH response to TRH may not reveal, and supports the case for some degree of central hypothyroidism in endogenous depression.
Endocrine study of anorexia nervosa.
The multiple endocrine abnormalities found are consistent with hypothalamic dysfunction and the etiology of this dysfunction remains for the endocrinologist highly controversial.
The nocturnal serum thyrotropin surge is abolished in patients with adrenocorticotropin (ACTH)-dependent or ACTH-independent Cushing's syndrome.
A substantial impairment of TSH secretion is shown, and in particular the loss of the nocturnal surge of the hormone, in patients with Cushing's syndrome.