Werner syndrome, also called adult progeria, is a heritable autosomal recessive 
human disorder characterized by the premature onset of numerous age-related 
diseases including juvenile cataracts, dyslipidemia, diabetes mellitus (DM), 
osteoporosis, atherosclerosis, and cancer. Werner syndrome is a segmental 
progeroid syndrome whose presentation resembles accelerated aging. The most 
common causes of death for WS patients are atherosclerosis and cancer. A 
40-year-old female presented with short stature, bird-like facies, canities with 
alopecia, scleroderma-like skin changes, and non-healing foot ulcers. The 
patient reported a history of delayed puberty, abortion, hypertriglyceridemia, 
and juvenile cataracts. A clinical diagnosis of WS was made and subsequently 
confirmed. We discovered two WRN gene mutations in the patient, Variant 1 was 
the most common WRN mutation, nonsense mutation (c.1105C>T:p.R369Ter) in exon 9, 
which caused a premature termination codon (PTC) at position 369. Variant 2 was 
a frameshift mutation (c.1134delA:p.E379KfsTer5) in exon 9, which caused a PTC 
at position 383 and has no published reports describing. Patients with WS can 
show a wide variety of clinical and biological manifestations in 
endocrine-metabolic systems (DM, thyroid dysfunction, and hyperlipidemia). 
Doctors must be cognizant of early manifestations of WS and treatment options.