老年男性骨质疏松与相关影响因素的关系

目的 测定老年男性不同年龄组骨密度及有关的影响因素,以探讨老年男性骨质疏松的发生与有关影响因素的关系,为防治老年男性骨质疏松症提供依据。方法 双能量X线骨密度测定仪测定前臂骨密度;全自动生化分析法测定血清钙（Ca)、磷（P）;放免法测定甲状旁腺素（PTH）、降钙素（CT）、1,25（OH）2D3、25（OH）D3、白介素－6（IL－6）。97例老年男性分为骨质疏松组与非骨质疏松组,并与60岁以下男性 进行比较。结果 老年男性骨密度、CT,1,25（OH2）D3、25（OH）D3随年龄增长而降低,PTH、IL－6随着年龄增长而升高（P＜0．05）。骨质疏松组与非骨质疏松组比较,PTH、IL－6二明显升高,CT、25（OH）D3、1,25（OH）2D33明显下降（P＜0．05－0．001）。结论 骨质疏松有关影响因素的改变使骨吸收增加,骨形成降低,导致骨丢失,引发骨质疏松症。     

老年男性2型糖尿病患者骨密度及骨代谢生化指标的研究

目的：探讨老年男性2型糖尿病患骨密度改变及其机制，以了解2型糖尿病是否易合并骨质疏松及其特点。方法：测定70例老年男性2型糖尿病患及60例年龄、体重指数相匹配的健康对照的骨密度，血清骨钙素（BGP）、抗酒石酸酸性磷酸酶（TRAP）、碱性磷酸酶（ALP）、尿钙（Ca）、尿羟脯氨酸（HOP）、空腹及餐后血糖、糖化血红蛋白（HbA1c）等，两组进行比较。结果：老年男性2型糖尿病患较健康对照组骨密度显降低。BGP浓度显低于对照组（P＜0．001）；TRAP、甲状旁腺素（PTH）、尿钙、HOP显高于对照组（P＜0．05）、糖尿病患BMD与病程、年龄、HbA1C、FBG、PBG呈显负相关，与平均体重指数（BMI)呈正相关。结论：老年男性2型糖尿病患较易患骨质疏松，其骨改变特点是：骨吸收增加，骨形成下降；发病机理主要是血糖升高，钙的排出增多和继发性甲状旁腺功能亢进以及胰岛功能减退。     

慢性肝病患者血清VitD3水平与骨代谢的关系

检测了部分慢性乙型肝炎(下简称慢乙肝)及肝硬化患者的血清1,25(OH)2D3、骨钙素(BGP)、甲状旁腺素(PTH)、钙、磷及尺桡平均密度(BMD),并与对照组比较.结果两组患者血清1,25(OH)2D3、BGP及BMD值均明显下降,肝硬化组下降尤为显著.肝硬化组血清PTH显著升高.两组患者血钙明显降低,而血磷三组间无差异.1,25(OH)2D3水平与BGP、BMD呈显著正相关;PTH与血钙、BMD无相关性.提示慢性肝病患者存在以骨形成减少为主的骨代谢紊乱,其中血清1,25(OH)2D3减少为关键因素,PTH虽升高,但与肝病患者骨密度变化无相关.     

健骨颗粒对去卵巢骨质疏松模型鼠钙调节激素的影响

目的:探讨健骨颗粒对骨质疏松模型鼠三种主要钙调节激素水平的影响.方法:切除雌性大鼠卵巢建立绝经后骨质疏松症病理模型,分别喂服健骨颗粒、骨松宝和生理盐水,用放射免疫测定法检测血清甲状旁腺激素(PTH)、1,25-二羟维生素D3[1,25-(OH)2D3]、降钙素(CT)和雌二醇(E2)水平.结果:卵巢切除后随着血清E2水平的下降,1,25-(OH)2D3、CT含量明显下降(P＜0.01或P＜0.05),而PTH却显著上升(P＜0.01).用药后健骨颗粒组血清1,25-(OH)2D3、CT水平显著回升(P＜0.01或P＜0.05),而PTH浓度出现下降(P＜0.01).E2与CT、1,25-(OH)2D3呈正相关,而与PTH呈负相关;PTH与1,25-(OH)2D3、CT呈负相关,1,25-(OH)2D3与CT呈正相关.结论:健骨颗粒能通过协调骨质疏松模型鼠血清PTH、1,25-(OH)2D3、CT三种钙调节激素浓度,改善因E2下降对骨代谢产生的副作用,这可能是健骨颗粒有效防治骨质疏松症的主要作用机制之一.     

老年男性抑郁情绪对原发性骨质疏松症骨代谢影响

目的研究老年男性抑郁情绪对原发性骨质疏松症骨代谢的影响。方法选取于我院老年科住院的老年男性原发性骨质疏松患者68例,老年抑郁量表(GDS)评估抑郁值,根据抑郁评分分为抑郁组和正常组。化学发光免疫分析法测定血清甲状旁腺激素(PTH)、25-羟基-维生素D(25-OH-Vit D)、骨钙素(BGP)、Ⅰ型胶原交联氨基末端肽(INTP)、Ⅰ型胶原交联羧基末端肽(ICTP)水平,比较两组PTH、25-OH-Vit D、BGP、INTP、ICTP水平,分析抑郁评分与PTH、25-OH-Vit D、BGP、INTP、ICTP相关性,探讨抑郁情绪对骨质疏松骨代谢影响的途径。结果 (1)抑郁组骨密度明显低于正常组(P=0.01),而年龄、体重指数均无差别。(2)两组间PTH、25-OH-Vit D水平无差别,抑郁组血清BGP水平低于正常组,而血清INTP、ICTP水平高于正常组。(3)抑郁评分与PTH、25-OH-Vit D无相关性,与BGP呈正相关(r=0.172,P=0.04),与INTP、ICTP呈负相关(r=-0.265,P=0.00;r=-0.198,P=0.02)。结论老年男性抑郁情绪增加骨破坏而加重骨质疏松。     

补肾壮骨颗粒剂对老年男性骨转换指标的影响

目的 观察补肾健脾活血中药对老年男性骨密度(BMD)、骨特异性碱性磷酸酶(BAP)、抗洒石酸酸性磷酸酶5b(TRAP5b)、氨基端和中段骨钙素(BGP)的影响.方法 采用自身前后对照的方法,临床选取符合骨量减少及骨质疏松患者的老年男性病例35例,平均年龄(75.56±5.8)岁,给予口服补肾壮骨颗粒剂,钙尔奇D片和法能胶丸做为基础用药.分别测定服药前及服药半年后患者BMD、BAP、TRAP5b、BGP4项骨转换指标,并将服药前后测定值做比较.结果 服药半年后患者的BMD及BAP较服药前升高明显(P＜0.05),有统计学意义;TRAP5b较服药前降低(P＜0.05),有统计学意义;而BGP服药前后改善不明显,(P＞0.05),无统计学意义.结论 补肾健脾活血中药与钙剂、维生素D联合应用,能抑制骨吸收,降低血清TRAP5b;促进骨形成,提高血清BAP及BGP含量,减缓骨量丢失,提高骨密度,有效防治老年男性骨质疏松症.     

1084例女性TRACP、CTX-1、BALP、BGP、钙磷代谢指标 与BMD相关性

目的研究女性抗酒石酸酸性磷酸酶（TRACP)、I型胶原交联C-末端肽（CTX4)、骨碱性磷酸酶（BALP)、骨钙素 (BGP)、25著维生素D3(25( OH) D3)、甲状旁腺素（PTH)、降钙素（CT)与股骨颈BMD的相关性。方法采用Discovery WA型 骨密度仪检测股骨颈BMD,采用酶标免疫分析仪检测TRACP、CTX4、BALP、BGP、25 ( OH) D3、PTH、CT。将1084例受试者检 测结果按5岁为年龄段分组,应用SPSS 13. 0分析软件进行统计分析。结果25 (OH) D3、PTH、CT在35 ~ 50岁年龄段各组间 不存在差异;50岁以后25 (OH) D3开始下降,与丽D呈正相关;CT降低出现在65 ~ 79岁年龄段,与丽D显著正相关。35 ~ 45岁年龄段TRACP、CTX4与BMD呈负相关,而BALP、BGP与BMD呈正相关;50 -60岁年龄段BALP、BGP明显升高, TRACP、CTX4、BALP、BGP均与BMD呈负相关;65岁以后BALP、BGP开始下降,BALP、BGP与骨密度呈正相关,TRACP、CTX- 1与骨密度呈负相关。结论TRACP、CTX4、BALP、BGP、25 ( OH) D3、PTH、CT监测骨代谢水平为骨质疏松诊断、鉴别诊断提 供了分子生物学依据。     

绝经后妇女血清调钙激素水平与骨代谢关系探讨

目的 探讨绝经后妇女血清调钙激素水平对骨形成、骨吸收及骨密度的影响。方法 142名健康绝经后妇女测定血雌二醇（E2）、睾酮（T）、总三碘甲状腺原氨酸（TT3）、总甲状腺素（TT4)、甲状旁腺激素全段（PTH－SP）、降钙素（CT）、骨钙素（BGP）、尿脱氧吡啶啉（DPD）、尿肌酐（Cr）。双能X线骨密度仪测定腰椎、髋部、前臂骨密度（BMD）,对检测结果进行分析。结果 本组骨质疏松患病率为60．48％,低骨量32．39％,正常骨量7．13％。血清6种调钙激素中T、E2、TT3、TT4、CT与BMD、BGP呈正相关,与年龄负相关;PTH－SP与BMD呈负相关,与年龄、DPD／Cr呈正相关。结论 绝经后妇女血调钙激素水平影响骨形成、骨吸收和骨密度,使骨代谢趋向于负平衡,是绝经后妇女易发生骨质疏松症的重要原因。     

慢性乙肝性肝硬化症男性患者血清性激素、钙调节激素和骨转换指标的变化

目的　慢性严重肝脏损害常合并肝性骨病。为了探讨终末期肝病患者的钙调节激素变化和骨转换率状态 ,我们回顾性分析了 17例乙肝后肝硬化失代偿的男性患者 ,并和年龄、身高、体重相匹配的健康男性进行对照研究。方法　肝硬化组和对照组均检测其血清性激素 [雄激素 (T)、雌激素 (E2 ) ],钙调节激素 [甲状旁腺素 (PTH)、降钙素 (CT)和 2 5羟维生素D3(2 5 -OHVD3) ]和骨转换指标 [血清骨钙素 (BGP)和尿脱氧吡啶啉 肌酐比值 (Dpd Cr) ]以及钙 (Ca2 + )、磷 (PO3- )和碱性磷酸酶 (ALP)。结果　显示与对照组相比 ,肝硬化组血清T明显降低、E2 水平和E2 T比值显著升高 ;血清PTH显著升高、2 5 -OHVD3明显降低 ,而CT差异不大。其中E2 升高和 2 5 -OHVD3降低有极显著意义。肝硬化组血清BGP和Ca2 + 水平明显降低、尿Dpd Cr比值和尿Ca2 + Cr比值明显升高。而血清CT和PO3- 差异不大。结论　我们认为慢性严重肝硬化患者骨量减低 ,呈现出骨形成降低、骨吸收增强之特征 ,与维生素D和性激素代谢异常有关 ,而PTH升高乃继发性改变     

666例维汉老年男性骨代谢水平、骨密度测定分析

目的 探讨汉族和维吾尔族老年男性骨代谢水平的特点,了解一定年龄范围内男性骨质疏松的特点.方法 选择符合研究对象的666名老年汉族和维吾尔族男性,测量骨密度(BMD)、骨碱性磷酸酶(BAP)、骨钙素(BGP)、抗酒石酸酸性磷酸酶(TRACP-5b)、25羟基维生素D3(25-( OH) VD3),按BMD值分为正常组、骨量减少组和骨质疏松组并进行比较.结果 OP患病率随年龄增加而增加,与年龄呈正相关.单因素方差分析,维吾尔族、汉族老年男性在年龄、BGP、TRACP-5b中差异有统计学意义(P＜0.05).统计学两两比较:汉族老年男性骨质疏松组TRACP-5b高于正常组及骨量减少组,骨质疏松组BGP骨量明显高于正常组(P＜0.05);维吾尔族骨量减少组的25-( OH) VD2、25-(OH)VD3与正常组存在差异,维吾尔族老年男性骨质疏松组年龄明显高于正常组.同组比较中:正常组、骨质疏松组中,维吾尔族25-(OH)VD2、25-(OH)VD3水平明显低于汉族(P＜0.05),正常组中维吾尔族老年男性BAP、BGP水平高于汉族老年男性(P＜0.05);同组中,维吾尔族年龄均低于汉族年龄(P＜0.05).结论 BGP、TRACP-5b在汉族老年男性中可以较早的反应骨代谢水平的差异性,可以作为骨质疏松症的早期检测指标;维吾尔族老年男性和汉族老年男性在维生素D代谢上可能存在着差异并影响到骨代谢.     

90例2型糖尿病合并慢性并发症的骨代谢的变化

目的 探讨2型糖尿病合并慢性并发症骨代谢的改变和机制。方法 测定90例2型糖尿病合并慢性并发症及70例2型糖尿病无并发症患与年龄，体重指数相匹配100例健康对照组的骨密度，血清骨钙素（BGP），钙（Ga)，尿羟脯氨酸（HOP），空腹及餐后2h的血糖，糖化血红蛋白（HbAlc)等进行比较。结果 2型糖尿病合并慢性并发症组BMD明显下降，FBG，PBG，尿HOP均高于2型糖尿病无慢性并发症组，BMD与糖尿病的病程，FBG，PBG，尿HOP呈显的负相关。结论 2型糖尿病合并慢性并发症组，糖尿病病程长，血糖高，BMD下降，比2型糖尿病无慢性并发症患更易患骨质疏松，骨吸收大于骨形成，骨矿含量明显下降。     

中老年2型糖尿病患者骨代谢特点及骨量丢失危险因素分析

目的 探讨中老年2型糖尿病(type 2 diabetes mellitus,T2DM)患者骨代谢特点及骨量丢失危险因素.方法 选择中老年T2DM患者612例(男296例,女316例),根据骨密度(bone mineral density,BMD)水平分为骨量正常组(108例)、骨量减少组(281例)、骨质疏松组(22...     

The relationship of vitamin D status to bone mineral density in an Italian population of postmenopausal women

Several authors have found a relationship between vitamin D status and bone mineral density (BMD). To our knowledge, no previous studies on this topic have been carried out on the Italian postmenopausal population. We studied this relationship retrospectively in 156 Italian postmenopausal women. We also investigated the relationship between parathyroid hormone (PTH) and BMD. Measurements of BMD were taken at the lumbar spine and upper femur by dual X-ray absorptiometry. Serum 25(OH)D (calcidiol), 1,25(OH)2D (calcitriol), PTH, calcium, phosphorus, creatinine, osteocalcin and urinary calcium and phosphorus were measured according to the current laboratory methods of analysis. We found a positive statistically significant correlation between BMD, both at the spine and hip, and 25(OH)D, and a negative statistically significant correlation between BMD and PTH. No statistically significant correlation was found between BMD and 1,25(OH)2D. Crude logistic regression showed age, 25(OH)D and PTH were significant predictors of low BMD, while 1,25(OH)2D was not. Backward logistic regression showed 25(OH)D was the best predictive model for spine osteoporosis together with age, and on its own it was the best predictive model for femoral neck osteoporosis.No funding sources supported this publication.     

鲑鱼降钙素结合脉冲电磁场治疗脊髓损伤致骨质疏松症的临床效果

目的观察鲑鱼降钙素联合低频脉冲电磁场治疗脊髓损伤所致骨质疏松症的临床效果。方法 2012年9月至2015年9月本科收治的脊髓损伤致骨质疏松症患者90例,按随机数字表法将其分为降钙素组(n=30)、电磁场组(n=30)及联合治疗组(n=30)。降钙素组给予鲑鱼降钙素治疗,电磁场组给予低频脉冲电磁场进行治疗,联合治疗组给予低频脉冲电磁场联合鲑鱼降钙素治疗,共3个月。测定治疗不同时间段患者疼痛视觉模拟评分(VAS),腰椎及股骨颈骨密度(BMD)及甲状旁腺素(PTH)、骨钙素(BGP)、1,25-双羟维生素D3[1,25-(OH)2D3]等生化指标的变化情况。结果治疗1、2、3个月及6个月后联合治疗组患者VAS评分显著低于降钙素组及电磁场组。治疗后,联合治疗组腰椎及股骨颈骨密度均显著高于降钙素组及电磁场组(P0.05);联合治疗组PTH、BGP均显著低于降钙素组及电磁场组(P0.05),1,25-(OH)2D3显著高于降钙素组及电磁场组(P0.05)。结论低频脉冲电磁场联合鲑鱼降钙素可有效减轻脊髓损伤所致骨质疏松症患者的骨性疼痛程度,提升患者骨密度。     

Biochemical parameters associated with low bone density in healthy men and women.

A causal role in age-related bone loss has been attributed to alterations in vitamin D status, the bone mineral regulating hormones, and/or renal function. We assessed biochemical parameters of bone metabolism and renal function in healthy subsets of young and old men (n = 191) and women (n = 120) and evaluated the relationships between these parameters and bone mineral density (BMD) in the radius, spine, and femur. There were no significant associations between BMD at any site and serum 25-OHD, 1,25-(OH)2D, PTH, or creatinine clearance in either young men or in young or old women, after controlling for age. In old men, however, lower radius BMD was significantly related to higher PTH and higher 1,25-(OH)2D and marginally related to lower 25-OHD values. In young men, there were unexpected but significant associations between lower femoral neck BMD and higher serum osteocalcin and urinary calcium/creatinine excretion after age adjustment. In old women, lower spine and radius BMD was also significantly correlated with higher serum osteocalcin. In this healthy, vitamin D-replete population, there were significant cross-sectional declines in BMD in the femur in young and old men and at all sites in old women. Elevated remodeling may be an important feature that contributes to reduced femoral BMD in young men and reduced spine and radius BMD in old women. However, compromised renal function or levels of 1,25-(OH)2D or elevated PTH appear to be neither necessary nor relevant as determinants of osteopenia in the spine or femur in these normal, healthy men and women.     

Remarkable increase in lumbar spine bone mineral density and amelioration in biochemical markers of bone turnover after parathyroidectomy in elderly patients with primary hyperparathyroidism: a 5-year follow-up study

We evaluated the efficacy of parathyroidectomy (PTX) on bone mineral density (BMD) and hormonal and biochemical markers of bone metabolism in elderly primary hyperparathyroidism (PHPT) patients, and followed these patients for 5 years after PTX. Eleven PHPT patients were enrolled and were followed for 5 years by measuring lumbar spine BMD (LSBMD), femoral BMD (FBMD), radial BMD (RBMD), parathyroid hormone (PTH), 1,25-dihydroxyvitamin D [1,25(OH)₂D], serum calcium (SCa), inorganic phosphate (iP), bone-specific alkaline phosphatase (BAP), intact osteocalcin (IOC), urinary excretion of type I collagen cross-linked N-telopeptide (NTx), and urinary deoxypyridinoline (DPD). PTX produced significant increases in LSBMD of 12%, 19%, and 29% as compared with pretreatment levels after 1, 3, and 5 years, respectively (P < 0.01, compared to baseline), whereas there was no significant increase in FBMD and a slight decrease in RBMD. SCa and iP levels remained normal over the five years. PTX also resulted in significant decreases in PTH, 1,25(OH)₂D, BAP, IOC, NTx, and DPD that continued for at least 3 years after PTX. In conclusion, PTX seemed effective to normalize various markers of bone metabolism in elderly PHPT patients and is recommended to patients with low LSBMD to prevent future fractures. On the other hand, the use of PTX for low FBMD or RBMD patients requires further discussion.     

老年2型糖尿病双能X线及定量CT测量骨密度的临床分析

目的 探讨老年2型糖尿病临床与不同骨密度(BMD)测定方法之间的关系和特点。方法 测定45例老年2型糖尿病患者的空腹(FBG)及餐后血糖(PBG)、糖化血红蛋白(HbAlc)、胆固醇(TC)、甘油三脂(TG)、骨钙素(BGP)、血清Ⅰ型胶原C端肽(CICP)、血清骨特异性碱性磷酸酶(B-ALP)、尿吡啶啉(Pyd)、脱氧吡啶啉(D-Pyd)、尿羟脯胺酸(Hyp),对同一病人同时行双能X线测定(DEXA)及定量CT测定(QCT),并进行分组比较。结果 本组45例病人中同时用DEXA及QCT测定骨密度均有骨质疏松者18例,占45％(18/40),其中男性4例,女性14例,女性占骨质疏松组的77.78％(14/18)。单用DEXA测量出骨质疏松者23例,单用QCT测量出骨质疏松者21例,其中5例有2例示QCT正常,而用DEXA测定有骨质疏松;3例用QCT测定已有腰椎骨质疏松,而DEXA示腰椎正常,但股骨颈部有骨质疏松。结论 老年2型糖尿病的骨质疏松与糖尿病病程、餐后血糖、胆固醇密切相关。骨形成指标(BGP、CICP)在骨质疏松组中非但不降,反比非骨质疏松组有明显升高。本研究显示老年2型糖尿病同时用DEXA及QCT测定骨密度有很好的相关性,r=0.770,P<0.01,故仅做腰椎QCT也可作为老年2型糖尿病骨质疏松的诊断依据。     

Vitamin D depletion following burn injury in children: a possible factor in post-burn osteopenia

BACKGROUND: Children burned > 40% total body surface area (TBSA) have chronically low bone mineral density (BMD) and increased risk for fractures and adult-onset osteoporosis. Because they are advised to avoid sunlight to prevent burn scar hyperpigmentation, we hypothesized that they develop vitamin D depletion, which could contribute to post-burn osteopenia. METHODS: We studied 24 children, ages 5-20 years, burned > or = 40% TBSA 7.1 +/- 3.8 (SD) years, range 1.9-13.3 years, previously (n = 12) and 2.0 +/- 0.2, range 1.4-2.1 years, previously (n = 12), of which half received recombinant human growth hormone during the first post-burn year. We measured lumbar spine BMD, serum 25-hydroxyvitamin D (25(OH)D), 1,25-dihydroxyvitamin D (1,25(OH)2D), intact PTH (iPTH), and osteocalcin. RESULTS: Serum 25(OH)D was low in 10/11 patients and 1,25(OH)2D was low in 5/11 at 7 years post-burn. Serum 25(OH)D was low in 10/12, while 1,25(OH)2D was low in 0/12 at 2 years; osteocalcin was low in 9/12 in the 7-year group; iPTH levels were in the lowest quartile in 5/12 patients at 7 years and 10/12 patients at 2 years. Serum 25(OH)D levels correlated with BMD z-scores, r = 0.53, p < 0.05, and inversely with iPTH levels, r = -0.66, p < 0.05, in the 7-year group. CONCLUSION: Burned children have low circulating levels of 25(OH)D which correlated with BMD z-scores, suggesting that post-burn vitamin D depletion may play a role in the chronically low bone density observed in these children.     

Exogenous PTH and Endogenous 1,25‐Dihydroxyvitamin D Are Complementary in Inducing an Anabolic Effect on Bone

PTH and 1,25(OH)₂D each exert dual anabolic and catabolic skeletal effects. We assessed the potential interaction of PTH and 1,25(OH)₂D in promoting skeletal anabolism by comparing the capacity of exogenous, intermittently injected PTH(1‐34) to produce bone accrual in mice homozygous for the 1α(OH)ase‐null allele [1α(OH)ase^?/? mice] and in wildtype mice. In initial studies, 3‐mo‐old wildtype mice were either injected once daily (40 μg/kg) or infused continuously (120 μg/kg/d) with PTH(1–34) for up to 1 mo. Infused PTH reduced BMD, increased the bone resorption marker TRACP‐5b, and raised serum calcium but did not increase serum 1,25(OH)₂D. Injected PTH increased serum 1,25(OH)₂D and BMD, raised the bone formation marker osteocalcin more than did infused PTH, and did not produce sustained hypercalcemia as did PTH infusion. In subsequent studies, 3‐mo‐old 1α(OH)ase^?/? mice, raised on a rescue diet, and wildtype littermates were injected with PTH(1–34) (40 μg/kg) either once daily or three times daily for 1 mo. In 1α(OH)ase^?/? mice, baseline bone volume (BV/TV) and bone formation (BFR/BS) were lower than in wildtype mice. PTH administered intermittently increased BV/TV and BFR/BS in a dose‐dependent manner, but the increases were always less than in wildtype mice. These studies show that exogenous PTH administered continuously resorbs bone without raising endogenous 1,25(OH)₂D. Intermittently administered PTH can increase bone accrual in the absence of 1,25(OH)₂D, but 1,25(OH)₂D complements this PTH action. An increase in endogenous 1,25(OH)₂D may therefore facilitate an optimal skeletal anabolic response to PTH and may be relevant to the development of improved therapeutics for enhancing skeletal anabolism.