我父亲肺鳞癌的治疗贴(2014年3月1日驾鹤西去）

老马，我想问一下，我爸爸吃了40天的特罗凯，是从化疗完毕就立即开始吃的，这一点我当初也不同意，因为觉得化疗完了立即上特根本无法判断特是否有效，毕竟化疗可以坚持一段时间，结果吃了半个月去医院复查，大夫说效果非常好，其实我当时就很怀疑了，因为我跟爸爸通电话觉得爸爸状态不是很好，可能是CT的反应比身体的反应要慢些，大夫坚持说效果很好，直到一个月去复查，胸水就抽了就来，住了十几天还是让吃特，最终医院大夫终于根据CT宣布特无效，进展，进行了爸爸今年的第六次化疗，用的恩度，效果还可以，昨天医生跟妈妈说，要给爸爸放疗，说是放疗可以让爸爸的胸膜固定，可以控制胸水，爸爸这次抽的已经是血性的胸水了，我看了治疗胸水的方法，并没有放疗可以控制胸水这一说啊，化疗完了接着放疗，有没有治疗过度的嫌疑呢？？？？？？   我怀疑特就从来没有生效过，可怜我妈妈还给我爸爸买的正版特，心疼，我想这次出院后，在下一个化疗周期开始时不化疗了，骗爸爸吃2992，您觉得可以么？？？？爸爸再也不吃靶向了，说我们全家都骗他。不知道如果特无效，联用184会怎么样？？？？爸爸说我们拿他试药，可是他不明白，药不试试怎么知道有没有效果呢？？？？？？

有胸水不适合放疗。
骗吃2992，难度比较大，因为2992很容易腹泻。
" E# p; L, ~* S  V6 Q3 H- e特无效，联184也难的。
你老爸可能还是只有放疗和化疗可用。

今天体重56kg，辛伐他汀改成10mg每天。
老爸开始练习祝总骧教授“312”经络锻炼法。

Purpose: To assess the efficacy and toxicity of relatively low-dose docetaxel (60 mg/m2) for previously treated advanced non-small-cell lung cancer (NSCLC). Patients and methods: Patients with advanced (clinical stage IIIA–IV) NSCLC who had previously undergone at least one series of chemotherapy were enrolled. Previous paclitaxel use was allowed, but docetaxel was not. Docetaxel was administered at an initial dose of 60 mg/m2 intravenously on day 1 over 90 min every 3 weeks. Results: From June 1997 to November 1999, 22 patients were entered into this study. The total number of cycles delivered to 22 patients was 53, with a median per patient of 2. Four patients achieved a partial response (PR), and the overall response rate was 18.2% (95% confidence interval 5.1–40.3%). The median time to progression was 13.7 weeks. The median survival time was 7.8 months, and the 1-year survival rate was 25%. About 73% of patients experienced grade 3 or 4 neutropenia. Neutropenic fever was observed in four patients (18%). Non-hematologic toxicities were generally mild. No treatment-related deaths occurred. Conclusions: Although the validity of the results of this study is limited due to the small and monoracial study population examined, low-dose (60 mg/m2) docetaxel for previously treated advanced NSCLC appears to yield antitumor activity and survival benefit comparable to those obtained with the conventional dose (100 mg/m2).

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低剂量化疗主要是抗血管生成了。如果联合口服CTX 50mg 每天，效果会更好。

用CTX不合算。
) y9 W- @6 g) C8 L* ~CTX的毒副作用
   (1)恶性肿瘤
. j2 R! {3 \' z9 t  （2）出血性膀胱炎  据报道，口服CTX治疗病人约5%~17%可发生出血性膀胱炎。因此，CTX治疗病人应勤饮水、多排尿，对神经性膀胱病人可能需要导尿或膀胱冲冼。
   ( 3)对血液系的影响  CTX主要损伤骨髓干细胞。CTX冲击治疗后7~10天淋巴细胞计数出现减少，10至14天中性粒细胞开始减少，但21~28天后中性粒细胞计数开始恢复。除非长疗程治疗（≥2年），一般血小板减少较少发生。
   (4)对性腺的损害  CTX对卵泡内的粒膜细胞有毒性作用，使血清雌二醇和黄体酮水平减低，抑制卵泡细胞的成熟，减少卵泡的排出数量，最终彻底导致卵巢功能衰竭。研究表明，随年龄的增大，卵巢对CTX毒性的耐受性越低。此外，CTX亦能损害男性睾丸生精能力，这与CTX的疗程长短有关。CTX累积总剂量应<150mg/kg。

Could Less be More? Low-Dose Chemotherapy Goes on Trial
: F, d5 S! o/ b% a! G/ K" FKen Garber
4 j- i; O7 D1 T! L- h2 ?) R0 iJudah Folkman, M.D., is accustomed to skeptics. When he first proposed, 30 years ago, the existence of a protein in the blood that blocked tumor blood vessel growth, the idea was almost universally ridiculed. Antiangiogenesis, of course, is now mainstream.
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5 o0 @2 a+ C. M+ ^3 K" RIn April 2000, Folkman offered a new heresy: continuous, low-dose chemotherapy that, by targeting the endothelial cells that form the tumor’s blood supply, might work against drug-resistant tumors.

% m4 ~& P2 r' T, w. W/ U“We said that, in some patients, you may be able to rescue them by changing the schedule and doing antiangiogenic chemotherapy,” said Folkman. The idea, also dubbed “low-dose” or “metronomic” chemotherapy, challenged the long-entrenched “more is better” orthodoxy, and many oncologists openly scoffed.

Now Folkman’s idea is being put to the test. Three North American clinical trials of metronomic chemotherapy are under way. Each uses low-dose, continuous chemotherapy in combination with commercially available antiangiogenesis drugs.
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3 p- V; n/ u4 ?+ X) q“The animal experiments are promising, the concept is plausible, and well designed clinical trials should be used to evaluate it,” said Ian Tannock, M.D., Ph.D., professor of medical oncology at the University of Toronto. Tannock leads one of the trials, using low-dose cyclophosphamide and Celebrex (celecoxib) to treat metastatic renal cancer. But, Tannock cautioned, “There’s certainly no basis for using it outside the setting of a clinical trial.”

In this trial, patients receive a daily 50mg/m2 oral dose of cyclophosphamide indefinitely until the cancer progresses or toxicities emerge. By comparison, Tannock noted that a typical standard regimen would include cyclophosphamide doses of 500 to 1000 mg/m2 intravenously every 3 weeks.
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Low-dose/antiangiogenic/metronomic chemotherapy has precedents. “Using low-dose chemotherapy is not a new idea,” said Robert Kerbel, Ph.D., of the University of Toronto. “In fact, there are oncologists who will say to you, ‘Hell, we’ve been using low-dose chemotherapy, or some kind of continuous regimen . . . for years.’ ” Anecdotal reports of responses to low-dose palliative chemotherapy are common. In childhood leukemia, continuous “consolidation therapy” lasting 3 years is now standard.

“Eighty-two percent of the last 400 kids I’ve taken care of with leukemia are alive and well, and 89% are alive at 11 years, and it’s all metronomic,” said pediatric oncologist Barton Kamen, M.D., Ph.D., of the Cancer Institute of New Jersey, Princeton. “Did I win because I was killing the vasculature in the bone marrow? I can’t tell you that. But I can tell you that the use of chronic, repetitive low-dose medicine, regardless of the target, works—absolutely works.”

Others are skeptical. “Gee, it sounds wonderful, but there [are a lot] of good theories out there,” said Roy Baynes, M.D., Ph.D., director of the bone marrow transplant program at Wayne State University in Detroit. “I would just make a plea, before everyone jumps overboard—let’s get the data.”
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The antiangiogenic chemotherapy theory originated in the early 1990s with Tim Browder, M.D., an oncology fellow in Folkman’s laboratory. Browder and Folkman were puzzled that chemotherapy, which was known to have antiangiogenic effects, always led to resistance. Tumor endothelial cells, in theory, should not become resistant to chemotherapy because they lacked the tumor’s genetic instability. Why, then, didn’t chemotherapy work better?

- B: P/ c! l2 X/ Q“I had this discussion many times with Browder,” Folkman recalled. “Browder came back and said, ‘I think the reason that chemotherapy doesn’t act all the time on endothelial cells is they keep stopping [treatment]—taking vacations, treatment vacations.’” Browder reasoned that giving chemotherapy continuously would prevent endothelial cell recovery and effectively starve tumors of their blood supply.
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Proving the theory took years of exhaustive laboratory work, culminating in Browder and Folkman’s April 2000 paper in Cancer Research. Working in mice, Browder showed that continuous low-dose cyclophosphamide could cure otherwise invariably fatal tumors. After creating a super-resistant tumor line, Browder then showed that low-dose cyclophosphamide could greatly slow tumor growth and improve survival.
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# e' L2 V* d" c, O: oThe drug’s antiangiogenic effects, a variety of careful assays demonstrated, were responsible. “The tumor would be drug resistant ... but the endothelial cell would not,” said Folkman. “And you could get [disease] control.”
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Kerbel, at the same time, published results showing that a combination of low-dose vinblastine and an anti-VEGF (vascular endothelial growth factor) receptor antibody could completely eradicate tumors in mice. “The tumors completely regressed,” Kerbel recalled. “They never came back during 7 months of continuous therapy.” This and Browder and Folkman’s work together laid the theoretical groundwork for today’s clinical trials.

Besides Tannock’s renal cancer trial, two other human trials are under way. Rena Buckstein, M.D., of the Toronto Sunnybrook Regional Cancer Center, is leading a multicenter trial also using low-dose cyclophosphamide with celecoxib to treat non-Hodgkin’s lymphoma.
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Meanwhile, oncologists at the Dana Farber Cancer Institute, Boston, are undertaking separate pediatric and adult trials using a combination of two chemotherapy agents—low-dose cyclophosphamide and etoposide—and two antiangiogenic drugs, celecoxib and thalidomide.

“I think this has immense promise, and it deserves to be tested,” said principal investigator Mark Kieran, M.D., Ph.D. “If the philosophy is right, we will at least see a little bit of activity.”
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1 T5 y/ F: h: p9 t) j. H* jKerbel said he is worried that, because celecoxib and thalidomide are not the optimal antiangiogenic agents, these trials will not demonstrate metronomic therapy’s true potential. Experimental drugs targeting VEGF or the VEGF receptor would theoretically be more potent, but drug companies will only test such drugs against standard-dose chemotherapy, to advance their chances of Food and Drug Administration approval. “It’s a bit frustrating,” said Kerbel, who added that he hopes that the early trials will show enough effect to convince drug companies to test their new agents with low-dose chemotherapy.

Although results in mice and anecdotal reports in humans seem to favor the metronomic idea, there is at least one big worry: resistance. While antiangiogenesis, in theory, bypasses the genetic instability that leads to tumor resistance, in some of Browder and Folkman’s experiments the tumors eventually returned.
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* W, s- F5 E& h: u“Even if you target the vasculature, there may be ways that you still nevertheless get resistance,” said Kerbel. For example, tumors may evolve to survive in relatively hypoxic conditions. Or, in response to stress, they may secrete cytokines or growth factors that promote angiogenesis.

“A tumor could escape an angiogenesis inhibitor,” admitted Folkman, who, nevertheless, is not worried. “We’ve actually seen that, but it turns out that now you just give more angiogenesis inhibitor, and you override it.”
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Some think that metronomic chemotherapy not only blocks angiogenesis but also directly targets tumors. “I believe that metronomics is working whether the vasculature really turns out to be the target or not,” said Kamen. The anti-inflammatory effects of low-dose chemotherapy may, Kamen speculated, allow natural killer cells better access to tumors. And since many chemotherapy drugs only work against dividing cells in the process of synthesizing new DNA—the so-called “S phase”—continuous chemotherapy is necessary to kill all tumor cells present, in Kamen’s view. Higher doses, if given intermittently, will not help. “You can’t kill a cell twice,” said Kamen. “That’s what it comes down to.”
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Skeptics counter that high doses are absolutely necessary to eradicate tumors. “Systematic undertreatment compromises outcome,” Wayne State’s Baynes said.

So the fate of metronomic chemotherapy rests on the clinical trials. Even if they succeed, it will not be easy to convince oncologists to abandon the “maximum tolerated dose” philosophy.
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“There’s this view: If you’re not vomiting and you’re not having your hair fall out, then there’s probably nothing happening to your tumor,” said Kerbel. “That’s a very entrenched view among oncologists. Since that’s been a prevailing way of doing things for decades, it’s not easy, based on a couple of early clinical trials, to turn that around.”
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. B0 t5 ^. R3 AFolkman is more optimistic, since many doctors have already used low-dose chemotherapy successfully without knowing why it works. “Clinicians come up all the time and say, ‘I want to tell you a secret. I never stop chemotherapy,’” Folkman said. “‘I keep giving it, but I was afraid to mention it, because everyone thought I was giving homeopathic doses.’” Now, Folkman said, “They have an explanation.” All that’s missing is the proof.

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低剂量CTX还是很安全的，我看过病例，最长连续使用65个月。每天50mg口服，工作生活如常。
实际上我们不需要连续使用这么长时间，1、2个月就行了。

英雄武松 发表于 2012-12-1 20:07

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- w$ s  O  U, C. j+ k) Q0 j2 E我妈每天上午一盒舒化奶。舒化奶不坏肚子，其他的奶制品吃了坏肚子。
从明天起，就买乳铁蛋白舒化奶了。

哪里有卖乳铁蛋白舒化奶

, q% i, N2 S" Z& w, a# e' z3 I2012-12-11，去省人民医院检查胸腹部B超，还有血常规，T淋巴亚组细胞、肝、肾功能、肿瘤指标，以及抽血做生物治疗。
5 o5 w9 q, i* p, H- S- x& P胸腹部B超结果：无胸水、肝，肾、肾上腺、胃、前列腺无异常。
9 ?' N" @; S+ [/ R血常规：白细胞6200，血小板28万，血红蛋白10.5克。
肿瘤指标：cea 5.4，ca125 64.6 cy211 7，C反应蛋白18（应该是炎症的原因）
肝功能正常，肾功能中尿素8.40，略超（正常上限是7.14)。
T淋巴亚组细胞数据比上次有改善。