**5. Type 1 Diabetes Mellitus**

Type 1 diabetes induced by ICI treatment results from the destruction of β-cells by ICIs and is reportedly more frequent with the use of anti-PD1/anti-PD-L1 antibodies. However, the reported incidences are 2.0% and 0.4% with nivolumab and pembrolizumab; thus, it seems to be a less common irAE [12]. The incidence of type I diabetes after ipilimumab treatment is even lower [20,42]. However, fulminant type I diabetes mellitus can worsen rapidly and prove fatal, and it is necessary to consider the possibility of this complication when administering ICIs. The time from anti-PD-1 therapy initiation to the onset of type 1 diabetes has been reported to be 13–504 days [43]. Symptoms include dry mouth, polydipsia, and polyuria due to hyperglycemia in mild-to-moderate cases. Severe disease is associated with ketosis, ketoacidosis, general fatigue, and disturbed consciousness, with further progression resulting in coma.

Fulminant type I diabetes mellitus exhibits a hyperacute onset over several days, and endogenous insulin is depleted at the time of diagnosis [44]. On the other hand, type I diabetes mellitus develops relatively slowly over the course of several weeks.

Because β-cell dysfunction is generally irreversible, it is important to make a diagnosis and initiate treatment before the development of ketoacidosis. Diabetes mellitus should be suspected when symptoms of hyperglycemia appear and fasting blood sugar and random blood sugar levels exceed 126 and 200 mg/mL, respectively. In such cases, definite diagnosis and diagnosis of the disease type should be performed.

Blood glucose levels may be elevated to approximately 200–300 mg/dL, although elevation to approximately 1000 mg/dL is also possible. The HbA1c level is also elevated, notwithstanding it is lower relative to the blood glucose level. The C peptide level gradually decreases in serum and urine, and anti-glutamic acid decarboxylase antibodies are generally absent.

#### **6. Treatment**
