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Introduction Werner syndrome (WS), also known as adult progeria, is a rare autosomal recessive syndrome caused by pathogenic loss of function of the WRN gene on chromosome 8p12. WS is characterized by signs of premature aging in young adults, including short stature, graying of hair, bilateral cataracts, and scleroderma-like skin changes. A thin, high-pitched voice is characteristic of patients. In addition, diabetes mellitus, cardiovascular disease and osteoporosis can also be seen at an increased rate. Patients have an increased thyroid neoplasms, malignant melanoma and meningioma. There is no specific or effective treatment for this rare syndrome. In this case, we aimed to present our patient with this rare syndrome. Clinical case A 28-year-old male patient was admitted for diabetes regulation and foot ulcers. In the patient's history, it was learned that he did not gain weight and did not gain sufficient height since the age of 14. He had been receiving insulin therapy for uncontrolled diabetes for about 10 years. He had cataract surgery at the age of 18. In our evaluation, there were scleroderma-like skin changes on the distal parts of both lower extremities. The patient's hair turned gray. His voice was high-pitched. Two of his siblings looked like him. One sibling who looked like him died at the age of 34. In the laboratory tests; FPG:306 mg/dL and HbA1C:11. The patient had hypergonadotropic hypogonadism. Rheumatological disease examination was normal. No pathological features were observed in lower extremity doppler examinations. Werner syndrome was considered in the patient who did not have sufficient height growth during adolescence, graying of the hair, a history of cataracts, scleroderma-like skin changes, and an elderly appearance. Malignancy scans of the patient were found to be normal. Genetic counseling was given to the patient and his family. The patient was taken to outpatient follow-up. Conclusion Werner syndrome is a rare disease. It is important to recognize patients in the early period, to prevent disease-related complications, especially in terms of the risk of malignancy development.

Introduction Cushing's disease caused by pituitary corticotropin (ACTH)-secreting tumors. These tumors are almost always benign and are usually microadenomas. In 30 to 40 percent, the microadenoma is so small that it is not detectable by magnetic resonance imaging (MRI). Primary therapy consists of transsphenoidal surgery or pituitary irradiation. Patients who fail this first approach can be treated either by repeat transsphenoidal surgery, medical therapy, radiotherapy, or, as a final resort, surgical or medical adrenalectomy. Clinical Case A 38-year-old male patient presented with headache and fatigue. The laboratory examinations reviewed ACTH depending Cushing's syndrome. A suspicious lesion in the pituitary with no contrast enhancement was observed in Sella MRI. Cavernous sinus sampling consistent with central sources. He was operated in 2018 for pituitary Cushing's disease. Reticulin framework disrupted compatible with adenoma but, ACTH could not be stained in immunohistochemical staining for technical reasons. Due to the high cortisol levels of the patient in the postoperative follow-up, the patient underwent bilateral adrenalectomy in 2019. Because of active Cushing's disease, patient was re-evaluated in 2022. In laboratory examinations, HGB 16.6 g/dL, WBC 6400 /uL, NEU 3200 /uL, PLT 228000 uL, cre 0.76 mg/dL, TSH 1.5 mIU/L, FT4 1.2 ng/dl, FSH 4.6 U/L, LH 7.98 U/L, PTH 23.7 ng/L, PRL 17 µg/L, Total Testosterone 571 ng/dl, Progesterone 0.06 µg/L, GH 0.04 ug/L, IGF1 83 µg/L were detected. Basal cortisol was 35 ug/dl and ACTH 67 ng/L. Cortisol with 1 mg of DST resulted in 28 ug/dl. 2 mg DST resulted in cortisol 38 ng/L. Free cortisol in the urine was found to be 281 mg/day (n<130 mg/day). Empty sella was observed in sella MR. No prominent contoured lesion was observed in the pituitary gland. Adrenal gland was not observed in the Abdominal MRI. No tumor was detected in Thorax CT. The patient's pasireotide 0.3 mg 1×1 treatment was continued. Metyropane 250 mg 2×1 was added to the treatment. Conclusion In Cushing's disease, the ACTH-secreting adenoma may be too small to be detected.

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