- The Effects of Alendronate in Bone Metabolism of Primary Osteoporosis.
-
Hyo Jeong Kim, Jee Won Park, Soo Jin Kim, Kwan Woo Lee, Hyeon Man Kim, Yoon Sok Chung
-
J Korean Endocr Soc. 2003;18(1):56-62. Published online February 1, 2003
-
-
-
 Abstract
 PDF
- BACKGROUND
To evaluate the effects of alendronate in preventing bone loss at the spine and hip in Korean cases of primary osteoporosis, we treated 138 patients with 10 mg of alendronate daily. Of the 138 patients treated, 50 were treated for one complete year, and at their final visit, measurements were taken to assess the completed outcome of the reatment, and the results from this small group were compared with those of the rest. The way this has been written causes ambiguity concerning exactly who was being studied. Check that my rewrite of this section conveys correctly the group that was studied, and how. METHODS: The serum levels of calcium(Ca) and phosphorous(P), total alkaline phosphatase(ALP), the urine calcium creatinine ratio(Uca/cr) and urine deoxypyridinoline(DPD) were measured before, during, and after the 1 year treatment period. The bone mineral densities(BMDs) at the spine and hip were also measured before and after the treatment period. New clinical fractures and side effects, were evaluated during the treatment period. RESULTS: The total serum ALP and urine DPD were decreased significantly, after the treatment period, by 38.3 and 40.5% respectively. The bone mineral density at the spine and hip were significantly increased after 1 year, by 6.7 and 2.0%, respectively. Of the 50 subjects who had completed a full year of treatment, only 4(8%) had developed new clinical fractures. Of the 138 patients who had been treated, 8(5.8%) discontinued the medication due to side effects. Of these, 7 had gastrointestinal symptoms, and 1 had skin eruption. CONCLUSION: Alendronate significantly decreased the total serum ALP and urine DPD and significantly increased spine and hip bone mineral density. Alendronate 10mg was effective in preventing bone loss in Korean cases of primary osteoporosis.
- A Case of Type Ia Glycogen Storage Disease.
-
Young II Choi, Young In Choi, Jee Won Park, Yoon Sok Chung, Hyon Ju Kim
-
J Korean Endocr Soc. 1999;14(4):786-792. Published online January 1, 2001
-
-
-
Abstract
PDF
- Glycogen storage diseases are inherited disorders of carbohydrate metabolism caused by a deficiency of enzymes that are involved in degradation of glycogen in the liver. The accumulation of glycogen occurs in the liver and other organs. Type Ia is the most common form and clinically may manifest of glycogen storage disease itself rather than growth hormone deficiency. But in this case the patient showed exceptional extreme growth retardation. Growth hormone stimulation test with clonidine and L-dopa revealed that the patient had growth hormone deficiency. Therefore, we report of a case of glycogen storage disease type Ia with the presence of GH deficiency with review of literature. A 16-year-old male was admitted for the evaluation of hepatomegaly and extreme short stature. The height was 113.5cm, less than third percentile of same age group, and compatible with fiftieth percentile of height of 6 years of age. After laboratory work up including liver biopsy, he was diagnosed with type I glycogen storage disease. The patient was presented with metabolic acidosis, hyperuricemia, and hypoglycemia. Hypoglycemia was managed with frequent feeding with high starch diet and intravenous glucose infusion. Metabolic acidosis was treated with sodium bicarbonate. Secondary hyperuricemia was treated with allopurinol. The patient is being followed at out-patient clinic with clinical improvement after of GH administration.
|
KES
