선현우

187

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Systolic blood pressure predict new onset metabolic unhealthy : 4yr longitudinal retrospective study

1건양대병원 내분비내과, ²성균관대학교 강북삼성병원 내분비내과

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선현우

, 홍주영

, 김종대

, 임동미

, 박근용

, 박세은

, 박철영

, 이은정

, 오기원

, 이원영

Background/Aims: It is well known that hypertension and diabetes is closely associated. But, There is a only one report that hypertension raid risk of in- cident diabetes in non-diabetic subjects. It is not known whether hypertension cause metabolic derangement. So, we investigated whether hypertension cause new onset metabolic unhealthy in metabolic healthy subjects through a 4 year retrospective longitudinal study. Being metabolically healthy was de- fined by having two or more than metabolic abnormalities among four components of metabolic syndrome besides WC criteria plus insulin resistence status 1) sRystemic blood pressure ≥ 130 mmHg and/or diastolic blood pressure ≥ 85 mmHg or on antihypertensive treatment 2) Triglyceride ≥ 150 mg/dL 3) Fasting glucose ≥ 100 mg/dL 4) HDL-cholesterol ≤ 40 mg/dL in men, 50 mg/dL in women 5) HOMA-IR ≥ 90th percentile Methods: A total 10,901 Koreans who underwent consecutive comprehensive health check-ups at both 2005 and 2009 were assessed via longitudinal analysis. A 7124 Subjects that have new onset metabolic unhealthy were assessed at baseline. The odds ratio (OR) for new-onset metabolic unhealthy was analyzed according to systolic blood pressure quartile. Results: At baseline, there are 7124 Subjects that have new onset metabolic unhealthy. During a median follow-up of 48.7 months, 1008 subject (14.1%) have new-onset metabolic unhealthy. As a result, If systolic blood pressure is higher, the incidence of metabolic unhealthy subjects is increased. Systolic blood pressure predicted new onset metabolic unhealthy; the OR (95% CI) for incident metabolic unhealthy was 1.015 (1.008-1.021) per 1mmHg, after full adjustment (p<0.001) in a multivariate binary linear regression analysis. Systolic pressure is categorized into quartile. In multivariate analysis for incident metabolic unhealthy(table 2), the OR (95% CI) of the 4th quartile compared to the 1st quartile of systolic blood pressure for incident metabolic unhealthy was 1.979 (1.006-3.893) after full adjustment (p=0.048). P for trend of quartile group was <0.001. Conclusions: High systolic blood pressure predict new onset metabolic unhealthy in metabolic healthy subjects in 4year longitudinal retrospective study.

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Delayed diagnosis of pseudohypoparathyroidism misrecognized as primary hypothyroidism in adulthood

1경희대학교 의과대학 내과학교실, ²강동경희대병원 내분비대사내과

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박성준

, 한아림

, 황유철

, 정인경

, 안규정

, 정호연

, 전지은

hormone (PTH). The patients show the clinical features of hypoparathyroidism but have elevated serum PTH level and physical appearances of Albright's hereditary osteodystrophy (AHO). We report a case of 21-year-old man misrecognized as primary hypothyroidism in late childhood which was finally proven to be PHP. The patient was diagnosed with primary hypo- thyroidism(thyroid-stimulating hormone [TSH] 41 mIU/ℓ) and vitamine D deficiency at age 9.

He was treated with levothyroxine, but TSH level was never normalized despite good compliance. On examination, he was mildly obese (body mass index 25.3 kg/㎡) with a height of 154.7, at Tanner stage-5 of puberty, and had a round face with short neck [Figure 1]. He had con- tracted hands, and brachydactyly of 3rd and 4th metacarpal bones [Figure 2]. Laboratory findings showed low ionized calcium and elevated intact PTH levels, but normal phosphorus and 25-OH vitamine D levels (1.1 mmol/ℓ, 101.6 pg/㎖, 3.4 ㎎/㎗, and 25.5 ng/㎖, respectively). He had sub- clinical hypothyroidism with a serum TSH level of 8.8 mIU/ℓ and free T4 level of 1.36 ng/㎗, without autoimmune antibodies. Thyroid ultrasonography revealed atrophic thyroid with hetero- geneous parenchyma. Other pituitary hormones including growth hormone were within the nor- mal range. Bone mineral density by dual-energy X-ray was within the normal range. PTH re- sistance was suspected and Ellsworth-Howard test was performed. Urinary cyclic adenosine monophosphate and phosphate levels remain unchanged after exogenous PTH administration [Table 1]. GNAS gene sequencing identified a heterozygous missense mutation. As described above, he had features of AHO and PTH resistance with coexisting TSH resistance, which was consistent with PHP type 1a. He was given oral calcium supplement, calcitriol, and levothyroxine. He is currently on regular follow up with routine tests of calcium, phosphorus, PTH and TSH levels, 24-hour urinary calcium–creatinine ratio for titration of therapy.

Keywords: Albright hereditary osteodystrophy, hypoparathyroidism, hormone resistance, Ellsworth-Howard test, GNAS mutation test