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Background Although vaccination against coronavirus disease (COVID-19) has several side effects, hypopituitarism due to hypophysitis has rarely been reported. Case presentation An 83-year-old healthy woman, who had received her fourth COVID-19 vaccine dose 2 days before admission, presented to the emergency department with difficulty moving. On examination, impaired consciousness (Glasgow Coma Scale: 14) and fever were observed. Computed tomography and magnetic resonance imaging of the head revealed swelling from the sella turcica to the suprasellar region. Her morning serum cortisol level was low (4.4 μg/dL) and adrenocorticotropic hormone level was normal (21.6 pg/mL). Central hypothyroidism was also suspected (thyroid stimulating hormone, 0.46 μIU/mL; free triiodothyronine, 1.86 pg/mL; free thyroxine, 0.48 ng/dL). Secondary adrenocortical insufficiency, growth hormone deficiency, delayed gonadotropin response, and elevated prolactin levels were also observed. After administration of prednisolone and levothyroxine, her consciousness recovered. On the 7th day of admission, the patient developed polyuria, and arginine vasopressin deficiency was diagnosed using a hypertonic saline test. On the 15th day, the posterior pituitary gland showed a loss of high signal intensity and the polyuria resolved spontaneously. On the 134th day, the corticotropin-releasing hormone loading test showed a normal response; however, the thyrotropin-releasing hormone stimulation test showed a low response. The patient’s disease course was stable with continued thyroid and adrenal corticosteroid supplementation. Conclusions Herein, we report a rare case of anterior hypopituitarism and arginine vasopressin deficiency secondary to hypophysitis following COVID-19 vaccination.

Wilson’s disease (WD) is an autosomal recessive disorder caused by defective function of the copper-transporting ATP7B protein. Symptoms are typically related to the brain and liver, while endocrinologic abnormalities are rare. Here, we reported a 12-year-old female patient that was initially presented with unusual skin darkening and low serum level of adrenocorticotropic hormone and diagnosed as having adrenocortical insufficiency. We further screened the mutation in ATP7B by direct DNA sequencing and found compound heterozygous mutations: a known pathogenic mutation in exon8:c.2333G>T (Arg778Leu) inherited from her mother and a variant in intron4:c.1707 + 5G>A inherited from her father. To explore the pathogenicity of the intronic variant, a minigene splicing assay was used to determine the effects of the splicing variant by analyzing reverse transcription PCR of ATP7B minigene transcript production. The result indicated that the c.1707 + 5G>A variant resulted in exon 4 skipping. We herein identified that 1707 + 5G>A intron 4 variant is a pathogenic mutation. Molecular genetic analysis and laboratory examination definitely confirmed the patient’s condition as WD. Clinical status improved considerably after penicillamine treatment. Our results extended the mutation spectrum of ATP7B gene and highlighted the importance of molecular genetic analysis for the accurate diagnosis of atypical WD. WD may have diverse presentations and should be considered in children especially presenting with adrenocortical insufficiency as initial symptom, and this study highlights the importance of screening for hormone abnormal in WD.