Endocrine disorders are important complications of PID. Analysis of the endocrine manifestations in patients with PID in a large-scale study may provide further insights into the relationship between the immune and endocrine systems.

These results indicate that STAT5B may therefore play a role in regulating the cholesterol metabolism in children with GHD.

Hajdu-Cheney syndrome is an autosomal dominant disorder characterized by acroosteolysis of the distal phalanges associated with digit abnormalities, distinctive craniofacial changes, dental anomalies, and a proportionate short stature. The pubertal development of children with Hajdu-Cheney syndrome is usually normal in the literature, although we here first describe a girl who was found to have Hajdu-Cheney syndrome accompanied with premature ovarian failure. She showed a follicle-stimulating hormone-dominant response on luteinizing hormone-releasing hormone test and did not show any sex differentiation abnormality or adrenal steroid hormone deficiency. On the basis of the findings in our patient, premature ovarian failure may be a complication of Hajdu-Cheney syndrome and thus an early endocrinological evaluation of patients is important.

An 81‐year‐old woman with a history of hypertension and Alzheimer's disease presented to the emergency department because of impaired consciousness. Physical examination revealed acute progressive generalized flaccid paralysis, hypertension, respiratory failure, and pupillary dilation. Although the patient did not complain of headache, head magnetic resonance angiography and magnetic resonance imaging showed multifocal segmental cerebral vasospasm and cerebral infarction in the left occipital lobe. Her family reported that although she did not have a license to cook pufferfish, she was in the habit of eating pufferfish. We subsequently detected tetrodotoxin in the patient's urine, and she was diagnosed with tetrodotoxin poisoning. As the symptoms of tetrodotoxin intoxication improved, head magnetic resonance angiography showed the disappearance of the multifocal segmental cerebral vasospasm. The patient's clinical course and imaging findings were consistent with reversible cerebral vasoconstriction syndrome (RCVS). Sympathetic overactivity after tetrodotoxin intoxication possibly caused the development of RCVS, and RCVS could not be ruled out even in the absence of the typical thunderclap headache. Magnetic resonance angiography is a useful modality when performing repeated examinations.

Guillain–Barré syndrome (GBS) usually has a good prognosis; however, patients may develop sequelae without prompt treatment. We herein describe an 81-year-old woman who developed acute-onset excruciating thigh pain and weakness in her lower extremities after spinal surgery. We diagnosed acute inflammatory demyelinating polyradiculoneuropathy by a nerve conduction study, which showed findings of demyelination without cerebrospinal fluid analysis because of a spinal prosthesis. Although anti-GM1 and anti-GalNAc-GD1a antibodies were positive, the patient was clinically diagnosed with acute inflammatory demyelinating polyradiculoneuropathy (a subtype of GBS), not acute motor axonal neuropathy. She recovered well with immunoglobulin therapy. A literature review of 18 cases revealed that unexplained weakness, areflexia, and numbness of the extremities after spinal surgery, a shorter time from spinal surgery to symptom onset to general GBS, abnormal nerve conduction study results, normal spinal imaging findings, and the development of atypical symptoms such as cranial and autonomic nerve syndrome and respiratory failure are useful for diagnosing GBS when cerebrospinal fluid examination cannot be performed after spinal surgery.