title: Diabetes mellitus with Laron syndrome: case report.
abstract: There are different opinions concerning changes in glucose metabolism in patients with Laron syndrome. In this paper we discuss the treatment results of our patient with Laron syndrome who developed diabetes during late adolescence. A 19-year-old boy with Laron syndrome was referred to our clinic for follow-up. He had been diagnosed with Laron syndrome (LS) at 4 years old and rIGF-1 therapy was initiated. After 4 months the treatment was discontinued. At the age of 17, rIGF-1 therapy was restarted. A height gain of 8.8 cm. was observed during the 2-year treatment period. He was admitted to our hospital at the age of 19 years following discontinuation of the therapy. At that time, his height was 142 cm, and weight for height was 136%. His blood glucose was 85 mg/dL (4.72 mmol/L), insulin was 26.39 pmol/L, and HbA1c was 5.4%. At the age of 20, when he has not been receiving IGF-1 therapy for 1 year, his weight for height was 143 cm. Laboratory evaluation revealed that fasting blood glucose was 176 mg/dL (9.77 mmol/L), fasting insulin was 29.86 pmol/L, and HbA1c was 7.5%. Primary insulin therapy was then initiated. His parents both had a diagnosis of type 2 diabetes. Insulin therapy was switched to oral antidiabetic (OAD) therapy at the end of the second year because of a normal C-peptide level of 0.8 nmol/L under insulin therapy. After 6 months of OAD, HbA1c was 5.7%. The treatment was then switched to IGF-1 therapy, but his blood glucose profile was impaired and OAD therapy was restarted. In conclusion, we observed that genetic susceptibility and abdominal obesity caused type 2 diabetes in this patient. We believe that oral antidiabetic agents and life-style changes may be the appropriate approach when diabetes is developed in LS patients.
authors.forename: Sebahat Yılmaz
authors.initials: SY
authors.lastname: Agladıoglu
authors.forename: Semra
authors.initials: S
authors.lastname: Cetınkaya
authors.forename: Senay
authors.initials: S
authors.lastname: Savas Erdeve
authors.forename: Asan
authors.initials: A
authors.lastname: Onder
authors.forename: Havva Nur Peltek
authors.initials: HN
authors.lastname: Kendırcı
authors.forename: Veysel Nijat
authors.initials: VN
authors.lastname: Bas
authors.forename: Zehra
authors.initials: Z
authors.lastname: Aycan
mesh_terms: D000328:Adult; D003924:Diabetes Mellitus, Type 2 / Q000188:drug therapy / Q000209:etiology*; D004198:Disease Susceptibility; D016903:Drug Monitoring; D006801:Humans; D007004:Hypoglycemic Agents / Q000627:therapeutic use; D007328:Insulin / Q000627:therapeutic use; D007334:Insulin-Like Growth Factor I / Q000235:genetics / Q000627:therapeutic use; D046150:Laron Syndrome / Q000150:complications / Q000188:drug therapy / Q000503:physiopathology*; D008297:Male; D008687:Metformin / Q000627:therapeutic use; D056128:Obesity, Abdominal / Q000150:complications / Q000503:physiopathology*; D011994:Recombinant Proteins / Q000627:therapeutic use; D016896:Treatment Outcome; D055815:Young Adult
chemical_list: D007004:Hypoglycemic Agents; C583557:IGF1 protein, human; D007328:Insulin; D011994:Recombinant Proteins; D007334:Insulin-Like Growth Factor I; D008687:Metformin