BACKGROUND: Tirzepatide, a dual glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) receptor agonist, induces potent appetite suppression and substantial weight loss. Increasing access to incretin-based therapies through online services has raised concerns regarding metabolic and psychiatric complications, particularly in vulnerable individuals. We report a case of starvation ketosis associated with self-administered tirzepatide, followed by the clinical recognition of anorexia nervosa.
CASE PRESENTATION: A 21-year-old woman with no prior formal psychiatric or metabolic diagnoses had a 2-month history of dieting behaviors and intermittent binge-purge symptoms before tirzepatide initiation. Seeking further weight loss, she obtained tirzepatide through an online medical service and self-administered 2.5 mg weekly for approximately 4 weeks, followed by 5.0 mg weekly for another month, without direct medical supervision. She reportedly stated during the online consultation that she was overweight. Her body weight decreased from 47 kg to 41 kg (BMI 17.9 to 15.6 kg/m²). Approximately 2 months after initiation, she developed severe nausea, bilious vomiting, and presyncope, requiring emergency admission. Tirzepatide had been discontinued shortly before admission because of nausea. Laboratory evaluation revealed marked ketonemia (serum 3-hydroxybutyrate 2057 µmol/L), normoglycaemia (glucose 79 mg/dL), mildly elevated anion gap, normal HbA1c (5.1%), and no clinically significant acidaemia. She had no history of SGLT2 inhibitor use or habitual alcohol consumption. She was diagnosed with starvation ketosis and improved with intravenous glucose infusion and nutritional support. Shortly after discharge, psychiatric evaluation by a board-certified psychiatrist led to a diagnosis of anorexia nervosa, binge-eating/purging type. At early follow-up, body weight had increased to 42 kg, the Eating Attitudes Test-26 (EAT-26) score decreased to 14, but serum 3-hydroxybutyrate remained elevated at 166 µmol/L. At later outpatient reassessment several months later, body weight remained 42 kg, serum 3-hydroxybutyrate had normalized to 24 µmol/L, and the EAT-26 score was 16; however, her drive for thinness persisted.
CONCLUSIONS: This case highlights that unsupervised tirzepatide use may be associated with starvation ketosis and the clinical recognition or exacerbation of eating-disorder psychopathology. Metabolic recovery did not parallel full improvement in eating-disorder symptoms, underscoring the need for careful screening, longitudinal psychiatric follow-up, and interdisciplinary management when incretin-based therapies are used.
