[原创] 请版主辟专栏讨论铜结合剂治疗癌症

heping

QUOTE:

以下是引用球在2008-8-30 9:07:06的发言：

有基础理论和临床数据没有？

拿出来给大家学习一下了！

The Cp response to TM-induced copper deficiency is monotonic and exhibits little intersubject variability; therefore, there is essentially no risk of sudden changes or unpredictable fluctuations that might make dose management difficult. Following Cp levels once every 1–2 weeks is adequate to monitor copper status early in therapy. As a corollary, overtreatment is easily detectable and correctable. Using the six times/day dose regimen borrowed from our Wilson’s disease work and initial TM doses ranging from 90–120 mg/day, the serum Cp was reliably lowered to 50% of baseline in 17 of 18 patients and to 20% of baseline in 14 of 18 patients. Reduction to 50% of baseline was achieved, on average, in 30 days, with further reduction to Cp levels of 5–10 mg/dl taking 20–30 days. Although this rate of decrease in Cp is reasonable for the initial treatment of early malignant lesions or in the adjuvant setting, in widely metastatic advanced cancer, this rate of decrease will not be sufficiently rapid to prevent some disease progression during induction of copper deficiency in a significant number of patients. Because loading dose variations of 90–120 mg/day do not appear to affect the rate of Cp reduction, and given the typical daily intake of copper with food, we conclude that higher doses in-between meals will likely be required to accelerate the rate of induction of copper deficiency. A follow-up trial is under way to test this hypothesis.

As a result of this study, it is apparent that with our present TM dose regimens, there is considerable lag between the initiation of TM therapy and the reduction of copper levels in tumors to a likely antiangiogenic level. Further retarding the ability to reach antiangiogenic levels of copper deficiency is the likelihood that most tumors sequester copper (42, 43, 44, 45) . Thus, it is reasonable to hypothesize that additional time may be required to deplete the tumor microenvironment to an effectively low level of copper, which is defined as a level low enough to inhibit angiogenesis. It is difficult to estimate this time accurately from our study. Thus, patients with very rapidly progressive large tumors may be relatively poor candidates for this approach to antiangiogenesis therapy as a single modality.

Another level of complexity is added by the fact that in bulky disease, initially effective antiangiogenesis may cause brisk tumor necrosis, as was documented in the mass shown in Fig. 3 . Tumor lysis may result in the release of additional copper from the dying cells. In the case of the patient whose mass is shown in Fig. 3 , a transient rise in Cp was observed at approximately the same time as the ultrasound suggested that the large tumor mass might be undergoing central necrosis due to a significant decrease in blood flow. For these reasons, we conclude that a period of 60–90 days of Cp at the target level of 20% of baseline is a reasonable starting point for evaluation of response to anticopper therapy in future trials in patients with measurable disease. In the two patients who exhibited partial regression of lung lesions, tumor control may have begun earlier. It is also interesting to note that in both of these patients, the lung parenchymal metastases were the sites of tumor regression. It is possible that mild clinical copper deficiency impairs superoxide dismutase function (46) so that under conditions of high oxidant stress, such as those present in the lung, the metastatic foci are more susceptible to oxidative damage.

Despite individual differences, the use of three-dimensional ultrasound to determine the total blood flow to a given mass demonstrates that maintenance of mild copper reduction to 20% of baseline induced for at least 8 weeks appears sufficient to alter tumor blood flow. Due to the relative insensitivity of CAT to the blood flow or metabolic status of the lesions, parallel imaging modalities, as demonstrated here for three-dimensional ultrasound, will be required to assess functional response in addition to tumor size.

In light of the data presented above, we advance the preliminary conclusion that the size of solid tumors of a variety of types may be stabilized or decreased by TM, given sufficient time in a state of mild clinical copper deficiency represented by a decrease in Cp to or below 20% of baseline, as defined by this study. Among the patients maintained at the target Cp level for more than 90 days, a significant proportion of cases (five of six) were stabilized, with no detriment to their quality of life. However, in this population of patients with advanced disease, only 39% of those treated were able to be maintained at the target Cp for this duration.

The pattern and speed of progression observed in these patients have also provided useful preliminary information. One patient achieved stable disease at all sites but one and has chosen to remain on TM therapy due to disease stabilization at the more life-threatening sites of disease (bowel and paratracheal lymph nodes; the site of progression in this patient with melanoma is a large adrenal metastasis. This and other observations in this trial suggest that whereas copper deficiency may be generally inhibitory of angiogenesis, heterogeneity of tumor type and the specific location of metastases may modulate the response to this therapeutic modality. The small number of patients in this study and the design of this study preclude more detailed conclusions regarding efficacy at specific metastatic sites. Because it appears that lesions progress at a much faster rate on copper repletion than while on TM therapy, future trials may formally incorporate the use of adjunct modalities, either systemically or loco-regionally, to address the specific sites of progression while allowing the patients to remain in a copper-deficient state.

We report preliminary observations of combination therapies of TM with radiotherapy, trastuzumab, and IFN- without apparent exacerbation of toxicity of the added modality. Taken as a whole, the safety and preliminary efficacy data derived from this trial support the conduct of additional studies designed to test the specific efficacy of TM alone or in combination for the treatment of early metastatic disease, minimal disease, and in adjuvant high-risk clinical settings, including chemoprevention.

heping

QUOTE:

以下是引用球在2008-8-30 9:07:06的发言：

有基础理论和临床数据没有？

拿出来给大家学习一下了！

REFERENCES

 

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heping

QUOTE:

以下是引用球在2008-8-30 9:07:06的发言：

有基础理论和临床数据没有？

拿出来给大家学习一下了！

25. Engleka K. A., Maciag T. Inactivation of human fibroblast growth factor-1 (FGF-1) activity by interaction with copper ions involves FGF-1 dimer formation induced by copper-catalyzed oxidation. J. Biol. Chem., 267: 11307-11315, 1994.[Abstract/Free Full Text]
26. Shing Y. Heparin-copper biaffinity chromatography of fibroblast growth factors. J. Biol. Chem., 263: 9059-9062, 1988.[Abstract/Free Full Text]
27. Patstone G., Maher P. Copper and calcium binding motifs in the extracellular domains of fibroblast growth factor receptors. J. Biol. Chem., 271: 3343-3346, 1996.[Abstract/Free Full Text]
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29. Parke A., Bhattacherjee P., Palmer R. M., Lazarus N. R. Characterization and quantification of copper sulfate-induced vascularization of the rabbit cornea. Am. J. Clin. Pathol., 137: 1121-1142, 1988.
30. Raju K. S., Alesandrii G., Zinche M., Gullino P. M. Ceruloplasmin, copper ions, and angiogenesis. J. Natl. Cancer Inst., 69: 1183-1188, 1982.
31. Ziche M., Jones J., Gullino P. M. Role of prostaglandin E and copper in angiogenesis. J. Natl. Cancer Inst., 69: 475-482, 1982.
32. Brem S. S., Zagzag D., Tsanaclis A. M. C., Gatley S., Elkouby M. P., Brien S. E. Inhibition of angiogenesis and tumor growth in the brain. Suppression of endothelial cell turnover by penicillamine and the depletion of copper, an angiogenic cofactor. Am. J. Pathol., 137: 1121-1142, 1990.[Abstract]
33. Brem S., Tsanaclis A. M., Zagzag D. Anticopper treatment inhibits pseudopodial protrusion and invasive spread of 9L gliosarcoma cells in the rat brain. Neurosurgery, 26: 391-396, 1990.[CrossRef][Medline]
34. Brewer G. J., Dick R. D., Yuzbasiyan-Gurkin V., Tankanow R., Young A. B., Kluin K. J. Initial therapy of patients with Wilson’s disease with tetrathiomolybdate. Arch. Neurol., 48: 42-47, 1991.[Abstract]
35. Brewer G. J., Dick R. D., Johnson V., Wang Y., Yuzbasiyan-Gurkan V., Kluin K., Fink J. K., Aisen A. Treatment of Wilson’s disease with ammonium tetrathiomolybdate. I. Initial therapy in 17 neurologically affected patients. Arch. Neurol., 51: 545-554, 1994.[Abstract]
36. Brewer G. J., Johnson V., Dick R. D., Kluin K. J., Fink J. K., Brunberg J. A. Treatment of Wilson’s disease with ammonium tetrathiomolybdate. II. Initial therapy in 33 neurologically affected patients and follow-up with zinc therapy. Arch. Neurol., 53: 1017-1025, 1996.[Abstract]
37. Brewer G., Merajver S. Treatment of metastatic cancer with the anticopper, antiangiogenic drug, tetrathiomolybdate. J. Investig. Med., 47: 223A 1999.
38. Linder M. C., Houle P. A., Isaacs E., Moor J. R., Scott L. E. Copper regulation of ceruloplasmin in copper-deficient rats. Enzyme (Basel), 24: 23-35, 1979.[Medline]
39. Carson P. L., Fowlkes J. B., Roubidoux M. A., Moskalik A. P., Govil A., Normolle D., LeCarpentier G., Nattakom S., Helvie M. R. J. M. 3-D color Doppler image quantification of breast masses. Ultrasound Med. Biol., 24: 945-952, 1998.[CrossRef][Medline]
40. LeCarpentier, G. L., Tridandapani, P. B., Fowlkes, J. B., Roubidoux, M. A., Moskalik, A. P., and Carson, P. L. Utility of 3D ultrasound in the discrimination and detection of breast cancer. RSNA EJ, in press, 1999.
41. Takahashi K., Mulliken J. B., Kozakewich H. P., Rogers R. A., Folkman J., Ezekowitz R. A. Cellular markers that distinguish the phases of hemangioma during infancy and childhood. J. Clin. Investig., 93: 2357-2364, 1994.
42. Arnold M., Sasse D. Quantitative and histochemical analysis of Cu, Zn, and Fe in spontaneous and induced primary tumors in rats. Cancer Res., 21: 761-766, 1961.
43. Apelgot S., Copey J., Fromentin A., Guille E., Poupon M. F., Rousel A. Altered distribution of copper (⁶⁴Cu) in tumor-bearing mice and rats. Anticancer Res., 6: 159-164, 1986.[Medline]
44. Gullino P. M., Ziche M., Alessandri G. Gangliosides, copper ions and angiogenic capacity of adult tissues. Cancer Metastasis Rev., 9: 239-251, 1990.[CrossRef][Medline]
45. Fuchs M. G., Sacerdote de Lustig E. Localization of tissue copper in mouse mammary tumors. Oncology (Basel), 46: 183-187, 1989.[Medline]
46. Culotta V. C., Klomp L. W. J., Strain J., Casareno R. L. B., Krems B., Gitlin J. D. The copper chaperone for superoxide dismutase. J. Biol. Chem., 272: 23469-23472, 1997.[Abstract/Free Full Text]

heping

 

刚刚在网上找了一篇青霉胺片的介绍, 供各位参考.

 

http://www.newdruginfo.cn/Html/rheum/rheum/3827344383.html

青霉胺片

青霉胺用于类风湿性关节炎、慢性活动性肝炎、硬皮病、口眼干燥、关节炎综合征等自身免疫性疾病，可见有明显的疗效；对类风湿性关节炎，可减轻关节疼痛、肿胀及渗液情况，晨起关节僵硬、血沈率等临床症状明显改善；可使慢性活动性肝炎病人转氨酶下降或转为正常。用于治疗硬皮病，可使皮肤胶原交叉联结减少，张力增加。治疗重金属中毒、风湿关节炎。

	药名	青霉胺片	通用名	青霉胺片
	药品剂型	片剂	药品规格	0.125g*100片
	生产厂家	上海医药（集团）有限公司信谊制药总厂	批准文号	国药准字H31022286
	药品单位	瓶	价格	￥90元 [购药指南]

青霉胺片说明书：

药品名：青霉胺片

性状：本品为包衣片，除去包衣后显白色

药理毒理：
1．络合作用。 ①重金属中毒，本品能络合铜、铁、汞、铅、砷等重金属，形成稳定和可溶性复合物由尿排出。其驱铅作用不及依地酸钙钠，驱汞作用不及二巯丙醇；但本品可口服，不良反应稍小，可供轻度重金属中毒或其他络合剂有禁忌时选用。 ②Wilson病，是一种常见染色体隐性遗传疾病，主要有大量铜沉积于肝和脑组织，引起豆状核变性和肝硬化，本品能与沉积在组织的铜结合形成可溶性复合物由尿排出。 ③胱氨酸尿及其结石，本品能与胱氨酸反应形成半胱氨酸－青霉胺二硫化物的混合物，从而降低尿中胱氨酸浓度；该混合物的溶解度要比胱氨酸大50倍，因此能预防胱氨酸结石的形成；长期服用6～12个月，可能使已形成的胱氨酸结石逐渐溶解。
2．抗类风湿关节炎：治疗类风湿关节炎的作用机制尚未明了。用药后发现有改善淋巴细胞功能，明显降低血清和关节囊液中的IgM类风湿因子和免疫复合物的水平，但对血清免疫球蛋白绝对值无明显降低。体外有抑制T细胞的活力，而对B细胞无影响。本品还能抑制新合成原胶原交叉连接，故也用于治疗皮肤和软组织胶原病。

药代动力学：
在胃肠道吸收约57%。血药浓度1小时达高峰。主要贮存于皮肤和血浆。t1/2为90小时。同于与蛋白质结合，即使停药3个月，体内仍有痕迹存在。本品在肝脏代谢，氧化为二硫化物，迅速由尿排出，24小时排出80%。

适应症：
适用于重金属中毒、肝豆状核变性（wilson病）、胱氨酸尿及其结石，亦治疗其他药物无效的严重活动性类风湿关节炎。

用法用量：
1.成人常用量：每日1g（8片），分4次口服。Wilson病和类风湿性关节炎患者初用时，每日口服125-250mg（1-2片），以后每1-2月增加125-250mg（1-2片），常用维持量为250mg（2片），每日4次，最大量一般每日不超过1.5g（12片）。胱氨酸尿患者的本品用量可参考尿中胱氨酸排出量而定，最大量每日为2g（16片）。有结石的患者，每日要求尿中排出胱氨酸100mg以下，无结石患者每日尿中排出胱氨酸100-200mg。重金属中毒用量每日为0.5-1.5g（4-12片）。
2.小儿常用量：按体重每日30mg/KG，分2-3次口服。

结药说明：
本品应每日连续服用。即使暂时停药数日，再次用药时亦会可能发生过敏反应，因此又要从小剂量开始。长期服用本品应加用维生素B6 每日25mg，以补偿所需要的增加量。手术患者在创口未愈时，每日剂量限制在250mg。出现不良反应要减少剂量或停药。有造血系统和肾功能损害应视为严重不良反应，必须停药。Wilson病服用本品1-3个月才见效。类风湿关节炎服本品2-3个月奏效，若治疗3-4个月无效时，则应停用本品，改用其他药物治疗。

不良反应：
1、常见的有厌食、恶心、呕吐、溃疡病活动、口腔炎和溃疡。 20%服药者有味觉异常。 2、过敏反应有皮肤瘙痒、荨麻疹、发热、关节疼痛和淋巴结肿大。其他皮肤反应包括狼疮样红斑和天疱样皮损。 3、本品抑制原胶原交叉连接，使皮肤变脆和出血，并影响创口愈合。 4、少数服药者发生白细胞减少，其他造血系统损害有粒细胞缺乏症、再生障碍性贫血、嗜酸粒细胞增多、溶血性贫血和血小板减少性紫癜。 5、6%-20%服药者出现蛋白尿、有时有血尿和免疫复合物膜型肾水球肾炎所致的肾病综合症。 6、个别出现秃发、胆汁潴留、Goodpasture综合症、重症肌无力和耳鸣，实验室检查有lgA降低。药物不良反应大多在停药后自动缓解和消失。过敏反应用肾上腺皮质激素和抗组胺药物治疗有效。味觉异常，除Wilson病患者外，可用4%硫酸铜溶液 5～10滴，加入果汁中口服，每日2次，有助于味觉恢复。

禁忌：1．肾功能不全、孕妇及对青霉素类药过敏的患者禁用。 2．粒细胞缺乏症，再生障碍性贫血患者禁用。

注意事项：1、青霉素过敏患者，对本品可能有过敏反应。 2、白细胞计数和分类、血红蛋白、血小板和尿常规等检查应在服药初6个月内每2周检查1次，以后每月1次。 3、肝功能检查应每6个月1次，以便早期发现中毒性肝病和胆汗潴留。 4、Wilson病患者初次应用本品时应在服药当天留24小时尿测尿酮，以后每3个月如法测定1次。 5、本品应每日连续服用，即使暂时停药数日，再次用药时亦可能发生过敏反应，因此又要从小剂量开始。长期服用本品应加用维生素B6每日25mg,以补偿所需要的增加量。 6、手术患者在创口未愈合时，每日剂量限制在250mg。 7、出现不良反应要减少剂量或停药。 8、有造血系统和肾功能损害应视为严重不良反应，必须停药。 9、Wilson病服本品1~3个月才见效。类风湿关节炎服本品2~3个月奏效，若治疗3~4个月无效时，则应停服本品，改用其他药物治疗

孕妇及哺乳期妇女用药：本品可影响胚胎发育。动物实验发现有骨骼畸形和腭裂等。患有类风湿关节炎和胱氨酸尿的孕妇，在妊娠期服用本品曾报道其出生婴儿有发育缺陷，因此，孕妇应忌服。若必须服用，则每日剂量不超过1g。预计孕妇需作剖腹产者，应在妊娠末6周起，到产后伤口愈口前剂量每日限在250mg。

老年患者用药：65岁以上老人服用容易有造血系统毒性反应

药物相互作用：本品可加重抗疟药、金制剂、免疫抑制剂、保泰松对造血系统和肾脏的不良反应。口服铁剂患者，本品宜在服铁剂前2小时口服，以免减弱本品疗效

规格：0.125*100片

有效期：２年

批准文号：国药准字Ｈ３１０２２２８6

生产企业：上海医药（集团）有限公司信谊制药总厂

heping

QUOTE:

以下是引用球在2008-8-30 9:07:06的发言：

有基础理论和临床数据没有？

拿出来给大家学习一下了！

QUOTE:

球，　你好．

QUOTE:

我自己顶自己一下．　希望听到你和大家的见解．

QUOTE:

 

heping

QUOTE:

以下是引用球在2008-8-30 9:07:06的发言：

有基础理论和临床数据没有？

拿出来给大家学习一下了！

矿物锌

锌是人体300多酶所需的一种微量金属。它不是铜的螯合剂. 它只是阻止肠道对膳食所含的铜的吸收。它诱导细胞的肠道产生金属硫蛋白（ MT ），其对铜有非常高的亲和力, 使铜从粪便中排出。这意味着，任何新进入人体铜没有达到血液循环系统。锌的应用较早，威尔森氏症患者经常使用它控制病情.

人体正常锌水平范围为60至150MCG/ dl . 缺锌或低于锌水平以下是癌症患者常见的.  缺锌是导致免疫受到抑制的原因，因为锌是多种酶的T细胞发挥其功能和调节作用的所必需的。

即使每日按150毫克服用锌, 使血清锌的范围保持在140至160MCG/ dl ，锌降铜的效果仍是极其缓慢的。目前的估计需要70-90天可降低铜大约25MCG/ dl,  CP约5-7毫克/ dl。尽管高量的锌减少体内铜的速度很慢, 但它仍是用以增强机体免疫功能的健康补充. 特别是它能阻止血管的生成从而有效延缓癌增长的长期效用不可低估.

[此贴子已经被作者于2008-9-9 6:41:26编辑过]