Alpha1-acid glycoprotein (AGP), also known as oral mucus protein (ORM), is an acute phase positive protein. AGPs have various biological activities, such as drug transport, immune regulation, maintenance of capillary barrier, regulation of lipid metabolism, etc. AGP mainly exists in liver cells, but it is also expressed in other tissue cells, such as adipose tissue, brain tissue, endothelial cells and immune cells. This article mainly reviews the application of AGP in pulmonary diseases, and the role,significance and related new developments in different systemic diseases.

A 48-year-old female patient received chemotherapy with etoposide and carboplatin combined with whole brain radiotherapy for small cell lung cancer located in the right lung with brain metastasis. An IV infusion of toripalimab 240 mg once per 21 days in the 4th cycle of chemotherapy was combined due to tumor progression, and no radiotherapy was given again. After 7 courses of chemotherapy, the patient received monotherapy with toripalimab. On the 2nd day after the 5th administration of toripalimab, the patient developed obvious fatigue, nausea, vomiting, and repeated fever. Laboratory tests showed decreased corticotropin and cortisol (1.5 μg/L, 3.9 μg/L), increased prolactin (127.6 μg/L), and normal thyroid function. Excluding tumor occupation by pituitary magnetic resonance imaging, it was considered as hypophysitis caused by toripalimab. Symptoms disappeared after hydrocortisone replacement therapy was given. After the 9th administration of toripalimab, the patient developed polyuria, thirst, and nocturia. Laboratory tests showed decreased urine specific gravity and urine osmolality (1.010, 132 mmol/L). Diabetes insipidus as the manifestation of hypophysitis caused by toripalimab was considered. The above symptoms were improved after discontinuation of toripalimab and administration of desmopressin. After more than 3 months of the treatment, symptoms of diabetes insipidus disappeared. Then desmopressin was discontinued and diabetes insipidus did not recur.

A 48-year-old female patient received chemotherapy with etoposide and carboplatin combined with whole brain radiotherapy for small cell lung cancer located in the right lung with brain metastasis. An IV infusion of toripalimab 240 mg once per 21 days in the 4th cycle of chemotherapy was combined due to tumor progression, and no radiotherapy was given again. After 7 courses of chemotherapy, the patient received monotherapy with toripalimab. On the 2nd day after the 5th administration of toripalimab, the patient developed obvious fatigue, nausea, vomiting, and repeated fever. Laboratory tests showed decreased corticotropin and cortisol (1.5 μg/L, 3.9 μg/L), increased prolactin (127.6 μg/L), and normal thyroid function. Excluding tumor occupation by pituitary magnetic resonance imaging, it was considered as hypophysitis caused by toripalimab. Symptoms disappeared after hydrocortisone replacement therapy was given. After the 9th administration of toripalimab, the patient developed polyuria, thirst, and nocturia. Laboratory tests showed decreased urine specific gravity and urine osmolality (1.010, 132 mmol/L). Diabetes insipidus as the manifestation of hypophysitis caused by toripalimab was considered. The above symptoms were improved after discontinuation of toripalimab and administration of desmopressin. After more than 3 months of the treatment, symptoms of diabetes insipidus disappeared. Then desmopressin was discontinued and diabetes insipidus did not recur.