卡马西平、丙戊酸钠、托吡酯对3～12岁癫(癎)儿童骨代谢的影响

目的探讨抗癫痫（EP）药物（AEDs）卡马西平（CBZ）、丙戊酸钠（VPA）、托吡酯（TPM）对EP患儿骨代谢影响。方法实验组为90例3～12岁原发性EP患儿,根据治疗药物不同随机分为CBZ、VPA、TPM组各30例。除口服上述药物外未予其他任何药物治疗,疗程6～12个月。于治疗前和治疗后3、6个月分别测定骨密度（BMD）、骨碱性磷酸酶（BAP）、血钙、磷、碱性磷酸酶（ALP）。对照组为30例未治疗原发性EP患儿,同期检测上述指标。对上述骨代谢指标进行评价。结果实验组治疗前后BMD、BAP、钙、磷、ALP与对照组比较无显著性差异（Pa〉0.05）。实验组CBZ、VPA、TPM治疗前后5种骨代谢指标比较亦无显著性差异（Pa〉0.05）。结论短期服用CBZ、VPA、TPM对3～12岁EP患儿骨代谢无影响。     

卡马西平、丙戊酸钠、托吡酯对3～12岁癫癎儿童骨代谢的影响

目的探讨抗癫癎(EP)药物(AEDs)卡马西平(CBZ)、丙戊酸钠(VPA)、托吡酯(TPM)对EP患儿骨代谢影响。方法实验组为90例3～12岁原发性EP患儿,根据治疗药物不同随机分为CBZ、VPA、TPM组各30例。除口服上述药物外未予其他任何药物治疗,疗程6～12个月。于治疗前和治疗后3、6个月分别测定骨密度(BMD)、骨碱性磷酸酶(BAP)、血钙、磷、碱性磷酸酶(ALP)。对照组为30例未治疗原发性EP患儿,同期检测上述指标。对上述骨代谢指标进行评价。结果实验组治疗前后BMD、BAP、钙、磷、ALP与对照组比较无显著性差异(Pa>0.05)。实验组CBZ、VPA、TPM治疗前后5种骨代谢指标比较亦无显著性差异(Pa>0.05)。结论短期服用CBZ、VPA、TPM对3～12岁EP患儿骨代谢无影响。     

糖皮质激素对肾病综合征患儿骨代谢的影响

目的 探讨糖皮质激素（GC）治疗对肾病综合征（NS）患儿骨代谢的影响。方法选择初发特发性肾病综合征（INS）患儿48例，予以GC治疗，并辅以钙尔奇D片，分别在GC治疗前（活动期）、激素治疗尿蛋白转阴后（缓解期）及肾病持续缓解5个月时（恢复期）检测血清骨钙蛋白（BGP）、骨特异性碱性磷酸酶（BALP）、甲状旁腺素（PTH）和钙水平。以同期儿保科体检的30例健康儿童为对照。结果INS患儿活动期血清BGP、钙水平较对照组明显降低（P〈0．01），血清BALP、FPTH较对照组明显升高（P〈0．01）。缓解期血清BGP最著低于活动期（P〈0．01）；血清BALP较活动期明显下降（P〈0．01），但与对照组比较无显著性差异（P〉0．05）；血清VFH高于活动期（P〈0．05）；血清钙高于对照组（P〈0．01），与活动期无显著性差异（P〉0．05）。NS患儿恢复期血清BGP、BALP、PTH、钙与对照组比较均无显著性差异（P〉0．05）。结论NS本身和GC治疗均可引起患儿骨代谢异常，但只要合理应用激素并及时补充VitD和钙制剂，骨代谢异常可以逆转。     

拉莫三嗪、丙戊酸钠对癫(癎)儿童认知功能的影响

目的：探讨拉莫三嗪（LTG）和丙戊酸钠（VPA）对癫痫儿童认知功能的影响。方法：首次确诊的癫痫患儿76例中，36例用LTG单药治疗，40例用VAP单药治疗。用药6个月前后对二组进行智力（IQ）测定。同时选取20例健康儿童作为健康对照组。结果：1．癫痫患儿语言智商（VIQ）、操作智商（PIQ）和总智商（FIQ）明显低于健康对照组，各项分测验得分亦均降低（Pa〈0．05）。2．癫痫患儿用LTG治疗6个月后VIQ、PIQ、FIQ及各项分测验得分较用药前无明显变化（Pa〉0．05）；癫痫患儿用VPA治疗6个月后VIQ、PIQ、FIQ无明显变化（Pa〉0．05），而在分测验中知识项得分用药后比用药前显著提高（P〈0．05），编码、木块图项得分显著下降（Pa〈0．05）。结论：癫痫患儿易发生认知功能损害，且损害无选择性；癫痫患儿服用LTG 6个月后对认知功能无影响；服用VPA 6个月后FIQ未见明显变化，但在木块图和编码上有降低，而在知识项得分用药后比用药前提高，表明VPA主要影响右脑功能，而对左脑无影响。     

食物过敏患儿综合营养干预后生长发育与营养状况监测北大核心CSCD

目的对食物过敏患儿采用综合营养干预后,监测患儿生长发育与营养状况,探讨营养干预的重要性。方法对158例2岁以下食物过敏患儿,按照其有无接受营养干预分为干预组和对照组。干预组患儿定期由营养医师指导患儿饮食及必要时补充营养素（钙、铁、锌）、益生菌。对照组仅由儿科医师诊治时口头指导。2组患儿随诊6个月后测量身长、体质量等体格指标,评价其生长发育状况,检测其血清生化指标,评估患儿膳食营养摄入情况。结果营养干预后干预组营养不良发生率（17．6％）明显低于对照组（37．0％）,差异有统计学意义（Х^2=22．03,P〈0．05）。干预组血清锌、铁的水平明显高于对照组,差异均有统计学意义1（88．5±9．6）μmol／L比（68．2±8．5）μmol／L,t=12．264,P〈0．01;（18．6±3．4）mmoL／L比（12．8±2．7）mmol／L,t=10．762,P〈0．05]。干预组〉6～24月龄患儿钙、锌日摄入量,〉12～24月龄患儿蛋白质日摄入量均明显高于对照组,差异均有统计学意义[（596．1±110．3）mg比（412．8±89．3）mg,t=4．011,P〈0．05;（10．7±3．7）mg比（7．3±2．1）mg,t：5．367,P〈0．05;（42．8±9．4）g比（33．2±8．2）g,t=3．245,P〈0．05）。结论食物过敏患儿存在营养不良风险,营养干预可明显降低食物过敏患儿营养不良及铁、锌、钙缺乏的发生率,应规范指导过敏患儿的科学喂养。     

丙戊酸钠对癫痫患儿血小板水平的影响

目的探讨丙戊酸钠对癫痫患儿血小板数目的影响。方法对48例确诊的癫痫患儿行丙戊酸钠单药治疗，在服用前、服用6个月、1年时分别采其中指外周血，对其血小板数目进行测定，并与33例健康儿童对照。结果治疗组服用丙戊酸钠6个月、1年时的血小板值明显低于治疗前（P 〈 0．01）；且明显低于对照组同期水平（P 〈 0．05，P 〈 0．01），用药时间越长，降低越明显。结论丙戊酸钠可降低血小板数目，提示丙戊酸钠治疗期间血象检测的必要。     

托吡酯治疗后癫(癎)患儿体重和血浆甘丙肽的变化

目的探讨癫痫患儿托吡酯治疗后体重变化与血浆甘丙肽的关系。方法对服用托吡酯的61例癫痫患儿用放射免疫法测定治疗前后血浆甘丙肽浓度和观察身高、体重变化,并以16例健康儿童作为对照。结果①服托吡酯后22例（36．1％）体重下降,该组甘丙肽浓度降低有统计学意义（t=2．91,P〈0．01）。体重增加组甘丙肽变化没有统计学意义（t=1．67,P〉0．05）。对照组甘丙肽变化无统计学意义（t=1．72,P〉0．05）。②体重下降组中18例（81．8％）患儿食欲变差,与体重增加组相比,差异有统计学意义（X^2=28．50,P〈0．001）。③食欲差组甘丙肽浓度降低有统计学意义（t=4．84,P〈0．001）,而食欲好组下降无统计学意义（t=1．04,P〉0．05）。④癫痫患儿治疗后体重指数的下降[（17．48±2．22）kg／m^2比（15．24±2．38）kg／m^2]有统计学意义（t=8．628,P〈0．01）。对照组是增加的。结论服用托吡酯后部分癫痫患儿体重会有显著下降和食欲减退,同时伴有血浆中甘丙肽水平显著的下降。提示托吡酯治疗引起的体重降低和食欲减退可能与甘丙肽浓度降低有关。     

癫痫患儿血清S-100β、胶质纤维酸性蛋白变化的意义

目的 探讨癫痫发作患儿及治疗后血清S-100β、胶质纤维酸性蛋白（GFAP）的变化。方法 采用双抗体夹心酶联免疫吸附法对41例癫痫患儿在癫痫发作24h内、用药4、12周分别进行定量测定其血清S-100β、GFAP蛋白水平，并与30例健康儿童进行比较。采用SPSS11．0软件进行分析。结果 发作后24h：癫痫组患儿血清S-100β、GFAP蛋白水平均显著高于对照组（Pa〈0．01）；婴儿痉挛症组血清S-100β、GFAP蛋白水平明显高于其他各组（Pa〈0．01）；局限性发作与全面性发作组比较，2组S-100β、GFAP蛋白水平无显著性差异（P〉0．05）。用药后4周：癫痫组血清S-100β、GFAP水平较前明显下降，但仍高于健康对照组（P〈0．01）。用药后12周：根据癫痫控制标准，控制23例，显效12例，有效4例，无效2例；各组S-100β、GFAP蛋白水平明显下降，无效组与其他各组比较，S-100β、GFAP蛋白水平仍高（P〈0．05）；其余各组比较无显著差异。癫痫患儿血清S-100β、GFAP蛋白水平经直线相关分析呈高度正相关（r=0．54P〈0．01）。结论 血清S-100β、GFAP水平在发作后癫痫患儿明显升高，临床控制效果与S-100β、GFAP蛋白水平高低、下降速度有关，二者可作为早期预测脑损伤、损伤程度并判断预后的指标之一。     

托吡酯对癫(癎)患儿骨代谢的影响

目的探讨抗癫癇药托吡酯(topiramate,TPM)对癫癇患儿骨代谢的影响。方法对单独服用托吡酯组32例、丙戊酸钠组45例和卡马西平组31例的癫癇患儿及36例未用药物治疗的癫癇患儿进行血钙、磷、碱性磷酸酶和骨密度的测定。结果血钙浓度TPM组和VPA组均较对照组高,CBZ组则较对照组低(P均<0.05);血磷浓度TPM组与CBZ组均较正常对照组低(P<0.05),VPA组与对照组相比差异无统计学意义(P>0.05);血碱性磷酸酶各组间差异无统计学意义(P>0.05)。骨密度测定,发现3个治疗组患儿均有不同程度的骨密度降低(P<0.05),并且和服药时间呈显著负相关。结论新型抗癫癇药如托吡酯亦可导致癫癇患儿骨代谢异常,且骨密度与服药时间呈负相关。     

常用抗癫癎药物对小儿机体诱变作用

目的　通过检测外周血淋巴细胞姊妹染色体交换 (SCE)频率及血清叶酸 (FA)水平 ,研究抗癫药物 (AEDs)对机体的诱变作用及其对FA代谢的影响 ,寻求抗诱变作用的途径。方法　选择癫患儿 90例 ,依据应用AEDs不同分组 ,检测各组用药前后SCE频率及FA水平 ,以及补充FA后两指标变化。结果　服用卡马西平 (CBZ)和丙戊酸钠 (VPA)的癫患儿 ,服药后较服药前血清FA明显降低 ,SCE频率显著升高 ,而补充服用FA后两指标有明显改善。结论　CBZ、VPA对小儿机体具有诱变作用 ,但硝基安定无明显诱变作用。FA能够减轻AEDs对机体的诱变作用。     

The effects of antiepileptic drugs on the relationships between leptin levels and bone turnover in prepubertal children with epilepsy

Antiepileptic drugs (AED) had an effect on bone metabolism in children. This study was conducted in order to determine the relationships between serum leptin levels, bone mineral density (BMD) and bone turnover markers in epileptic children. Fifty-three patients were treated with valproic acid (VPA) and 23 with carbamazepine (CBZ) monotherapy; 50 healthy children were included in the study as controls. Serum alkaline phosphatase (ALP) and cross-linked C-telopeptide (CTx) levels were statistically significantly higher in the CBZ group than in the VPA group and the control group (p < 0.0001, p < 0.010, respectively). Serum osteocalcin and ALP levels were significantly lower in the VPA group than in the control group (P < 0.012, P < 0.030, respectively). Although we found slightly higher serum leptin levels in both the CBZ and VPA groups, they were not significantly different from the control group (P > 0.05). We demonstrated that the markers of bone formation and resorption increased with CBZ and decreased with VPA treatment without affecting BMD and vitamin D levels in prepubertal epileptic children.     

托吡酯和卡马西平对癫癎患儿骨代谢的影响

目的：探讨抗癫癎药托吡酯(topiramate,TPM)和卡马西平(carbamazepine,CBZ)对癫癎患儿骨代谢的影响。方法：对63例单独服用TPM和CBZ的癫癎患儿及36例未用药物治疗的癫癎患儿（对照组）进行血钙、磷、碱性磷酸酶和骨密度的测定。结果：TPM组血钙浓度2.41±0.17 mmol/L,较对照组的2.26±0.11 mmol/L高,CBZ组2.15±0.26 mmol/L,较对照组低（均P0.05）。与对照组比较,TPM和CBZ组患儿均有不同程度的骨密度降低(P<0.05)。结论：托吡酯和卡马西平均可引起血钙、磷的异常变化和骨密度的降低。［中国当代儿科杂志,2010,12（2）：96-98］     

Thyroid function and volume in epileptic children using carbamazepine, oxcarbazepine and valproate

BACKGROUND: The aim of the present study was to investigate the effects of carbamazepine (CBZ), oxcarbazepine (OXC), and valproic acid (VPA) on thyroid function and volume in epileptic children. METHODS: Fifty-three epileptic children (age, 3-17 years) treated with OXC (n = 10), CBZ (n = 12), or VPA (n = 31) at least for 1 year were evaluated in terms of thyroid hormones, thyroid-stimulating hormone (TSH) levels, response to thyrotropin-releasing hormone (TRH) stimulation test, and thyroid volumes. RESULTS: The patients in the OXC and CBZ groups had similar total thyroxin (TT4) and free T4 (fT4) median levels that were significantly lower than those of the VPA group (P < 0.016). Total tri-iodothyrosin median levels were lower in the CBZ group compared to the VPA group (P < 0.016). Basal TSH levels and thyroid volumes were similar in all groups (P > 0.016). One child from the OXC group (10%), one from the CBZ group (%8.3), and six from the VPA group (19.3%) had hypothyroidic status according to the TRH stimulation test. No statistically significant correlations were found between thyroid gland volume and thyroid function variables and between anti-epileptic drug receiving time and thyroid function or thyroid volume, respectively, in any of the groups (P > 0.05). CONCLUSIONS: Thyroid function should be evaluated periodically in children using CBZ, OXC or VPA. The children taking VPA seems to be at greater risk compared to children onr CBZ or OXC therapy. Except for the basal TSH values in the VPA group, the parameters predictive for the subclinical hypothyroid status remain to be evaluated in further studies.     

Bone mineral metabolism changes in epileptic children receiving valproic acid

OBJECTIVE: The aim of this study was to evaluate bone mineral density (BMD) in epileptic children receiving valproic acid (VPA) and to determine differences between osteopenic and non-osteopenic children. METHODS: Thirty-three epileptic children, receiving VPA for at least 6 months, were compared with 33 healthy children for BMD. BMD was measured by dual-energy X-ray absorptiometry at lumbar vertebrae, femoral neck and greater trochanter. Serum calcium, phosphorus, alkaline phosphates, osteocalcin and VPA levels were also determined. RESULTS: Patient's osteocalcin levels were significantly higher (P = 0.02) and femur and trochanter BMD values were significantly lower (P = 0.04 and P = 0.03, respectively). Duration of VPA therapy was significantly longer and doses of VPA were significantly higher in seven osteopenic patients compared with 26 non-osteopenic patients. Osteopenic patients (4.6 +/- 2.4 years) were younger than non-osteopenic patients (7.8 +/- 3.2 years) (P = 0.01). CONCLUSION: Long-term and high dose VPA therapy may cause osteopenia, primarily in younger epileptic children. These patients should be followed closely by BMD measurements.     

Bone mineral density and metabolism in children with congenital hypothyroidism after prolonged l-thyroxine therapy

Abstract The effect of long-term l -thyroxine (LT4) replacement therapy on bone mineral density and on biochemical markers of bone turnover were studied in children with congenital hypothyroidism (CH). Forty-four children and adolescents (mean age 8.5 ± 3.5 years) with primary CH who began LT4 replacement therapy within the first month of life were studied. Bone mineral density (BMD) of the lumbar vertebrae and the upper femoral bone was measured by dual energy X-ray absorptiometry. Serum osteocalcin (OC) and bone alkaline phosphatase were measured as markers of bone formation and urinary deoxypyridinoline was taken as a marker of bone resorption. Bone mineral densities of CH children were not different from those in age-matched controls. The biochemical markers of bone turnover were normal except for the serum OC levels which were found to be higher than in controls and positively correlated with the free thyroid hormone levels (for FT4 r = 0.42, p = 0.02). Eight CH children demonstrated low BMD values (below -1 SDS) at - 2 ± 0.7 SDS for the lumbar spine and - 1.6 ± 0.5 SDS for the femoral site. These eight children showed lower mean weight ( p < 0.05) and their dietary calcium intake tended to be less ( p < 0.06) than that seen in the normal BMD group. In conclusion, our results show that LT4 replacement therapy for 8 years is not detrimental to the skeletal mineralization of CH children. As in a healthy population, weight and current intake of calcium seem to be major determinants of bone density. Dietary recommendations, especially when calcium intake is below the recommended dietary allowance, may have to be reconsidered.     

Serum lipid profile in children receiving anti-epileptic drug monotherapy: is it atherogenic?

The effect of anti-epileptic drugs (AEDs) on serum lipid profile is controversial in children as well as in adults. We longitudinally studied serum lipid profile in 34 newly diagnosed epileptic children receiving AED monotherapy with valproic acid (VPA), carbamazepine (CBZ) or phenobarbital (PB). Serum levels of total cholesterol (TC), high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), triglycerides (TGs), apolipoprotein Al (Apo A1) and apolipoprotein B (Apo B) were measured at baseline and after 2 years of AED monotherapy. Atherosclerotic indices of TC/ HDL-C and Apo A1/Apo B ratios were calculated. Although there were some alterations in serum lipid profile with AED without statistical significance, the atherosclerotic indices of TC/HDL-C and Apo A1/Apo B ratios did not change significantly after 2 years of monotherapy. Only serum TGs levels significantly decreased with VPA monotherapy. These data suggest that 2 years AED monotherapy with VPA, CBZ or PB did not cause a significant level of concern for an atherogenic effect in children with epilepsy.     

Bone mineral status in ambulatory pediatric patients on long-term anti-epileptic drug therapy

BACKGROUND: For ambulatory pediatric outpatients,reports of abnormalities of bone metabolism associated with anti-epileptic drugs are inconsistent and may be difficult to interpret. METHODS: The effects of long-term anti-epileptic therapy (mainly valproic acid and/or carbamazepine) on bone mineral status were evaluated in ambulatory epileptic patients(seven males and 11 females) aged 5.5-15.9 years.Bone mineral density (BMD) at the lumbar spine was measured by dual-energy X-ray absorptiometry and markers of bone and mineral metabolism were determined. RESULTS: The mean BMD was decreased by 9% in our patients relative to the control, and five patients (all males)showed osteopenia, defined as BMD SD scores less than - 1.5.Serum levels of minerals, intact parathyroid hormone and 1alpha,25(OH)2 vitamin D were within the normal ranges. In most patients, serum levels of intact osteocalcin, carboxyterminal propeptide of type I procollagen and pyridinoline cross-linked telopeptide of type I collagen were reduced relative to the corresponding mean control values. The BB genotype by BsmI restriction fragment length polymorphism, associated with low BMD, was not found in our patients. The dietary calcium intake in the osteopenic patients was significantly lower than that of the non-osteopenic patients. CONCLUSIONS: Our results indicate that long-term anti-epileptic treatment induces a state of decreased bone turnover in children, resulting in osteopenia preferentially in males. The alterations may be due, at least in part, to direct effects of the drugs on bone cells; and that low calcium intake could be an aggravating factor for anti-epileptic-associated osteopenia.