| PrefaceBecause of active vitamin D also named 1. 25(OH)2D3 declining ,the most of chronic renal failure uremic patients have to endure hy-pocalcemia, hypophosphatemia, secondary hyperparathyroidism (SHPT) and immunity confusion. aD3 is nonactive vitamin D before C25 hydrooxyaction in liver cell, so it become 1.25(OH)2D3. The active vitamin D can improve Ca, P to be absorbed in intestine and renal tube and inhibit parathyroid cell proliferation to decrease the product of PTH. Some foreign latest research show the active vitamin D can inhibit the synthesis of IL -2 and Ig . As a result the SIL-2R increases compensatedly. The active vitamin D is like cortisone with immu-nosuppressive activity. The controversy has been existing in which is the best administration and the immunoregulationn to uremic patents since the vitamin D was adopted. Some scholars believe vitamin D routine therapy with few adverse reactions. But the other think the vitamin D pulse therapy is more reliable than routine therapy which only compensates physiological requirements . There are few reports on aD3 pulse therapy. This experiment will aim at discussing the curative affection on Ca, P, SHPT and immunity between the routine and pulse administration, while establishing secured rapid and beneficial treatment. Now I will show the result;Material1. Sample: 55 nondialysis urimic patients with hypocalcemia, hy-perphosphatemia and SHPT, age 44. 7±10. 1 years old. They have not adopted Ca, vitamin D, and cortisone. To divide the patients into two teams at random the pulse therapy team including 30 person; the routine therapy team including 25 person. The control team is composed of 10 health person who were in harmony with uremic patients in age and sex.2. Apparatus: DP IMMULTTE ANALYSOR. HITACH 7170 AUTOMATIC BIOCHEMISTRY ANALYSOR.3. Reagent. PTH reagent from DP COMPANY. IL-2, SIL-2R regent from BECKMAN COMPANY.MethodFirst, to take venous blood of all sample with empty stomach before experiment and to examine Ca, P, PTH, IL-2, SIL-2R and ALT. Second , the person in pulse team administer aD3 1ug and Ca-CO3 0. 5 Qd Po, as well as the person in routine team take aD30. 25ug and CaCO3 0. 5 Qd Po. The other treatments are same. I will test those indexes again after two weeks. Third, the data was statistically analyzed. To express all tested indexes in form of mean ± SD. Student s t test, P <0. 05 as significant limit.ResultCRF vs control: the Ca. concentration came down by 24. 8% (1. 91 ±0.28vs2.54±0.16mmol/l p <0.01) ;IL-2 dropped by 35.2% (5.31±2. 07vs8. 19±2. 17ug/L p<0.05) The P concentration increased by 65.2%(2.28±0.68vsl.38±0.11mmol/1) ;the SIL-2Rgrew by 3. 67 folds(1561±637. 06vs334 ± 181IU/mi) , as weU as PTH rising 10. 1folds(p <0. 01).The routine team self - contrast: PTH declined 32. 1% (573. 16 ±414. 39vs389. 17 ± 181. 86Pg/ml p <0. 05). But the variances of P, SIL - 2R, Ca, IL - 2 and ALT are not significant (P>0.05 ).The self - contrast in pulse team. PTH descended 59. 9% (562. 06 ±403. 22 vs225. 4±175. 45Pg/ml P <0.01). P concentration was fallen by 26.2% (2. 29 ±0. 69vsl. 69 ±0. 65mmol/l) ;IL-2 went down by 17. 6% ( 5. 28 ± 2. 03vs4. 32 ± 2. 17ug/L) ; Ca was raised by 22. 1% ( 1. 90 ± 0. 31vs2. 32 ± 0. 24mmol/L); SIL-2R went up 14. 1% (1770. 32±873. 79vs1551. 64 ± 857. 96IU/ml p < 0.05).The tested indexes of pulse therapy vs those of routine team: Ca 2. 32 ± 0. 24vs2. 01 ± 0. 18mmol/L; SIL - 2R 1770. 32 ± 873.79 vsl519.52±624.78IU/ml;P 1.69 ±0. 65vs2. 19 ±0. 49mmol/L;IL -24. 32 ±2. 17vs5.33 ± 1. 83ug/L;PTH 225. 24 ± 1775.43vs389. 17 ± 181. 86Pg/ml. P <0. 05. There were not hypercalcemia during experiment. I also did not find progressive nausea and vomiting. Each ALT is not beyond the normal limitation.DiscussThe shortage of active vitamin D is the primary cause of hypocal-cemia, hyperphosphatemia and SHPT. Kidney is an important organ where the active vitamin D is synthesized.Because of the impaired kidney falls the quantity and activity of... |
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