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David Hanson
03.10.95

1935 / Class of '94 / Type: IgA / Stem Cell Transplant, Aggressive MM / Died 3-10-95

Here's the basic gist of Dave's story: I am afraid it may unduly scare people. His case was unusually aggressive.

He was diagnosed in April of 1994, at the age of 59, when a routine blood test showed anemia. After a retest, which also showed not only low red cell count, but also a low white cell count, the doctor did a sed rate test. When his sed rate came out 120 his doctor immediately sent him to an oncologist who did a serum electrophoresis and a bone marrow aspiration and made the diagnosis. His IgA was 3900 and his bone marrow showed 60-70 percent plasma cells but all the rest of the tests that were done at that time looked good. His x-rays showed no lesions, he had no protein in his urine and his calcium and creatinine were normal. Except for the anemia he was asymptomatic, with no bone pain at all.

The doctor sent us for a consultation to see whether perhaps a bone marrow transplant would be a possible option for him. At that time we were told that he was too old for an allogeneic transplant (he was soon to turn 60), though an autologous one could be considered. We were quoted statistics, however, which didn't seem to show any greater results from an autologous transplant than from Melphalan - Prednisone treatment and he felt that the odds as then described to him didn't justify disrupting his life and work schedule.

Dave started with MP in June of 1994. After two rounds he didn't seem to be responding. His IgA after the first round had gone up to 4600 and after the second it was 4200, still above that at diagnosis. (In retrospect I think he was responding to a degree, but that his fast moving cancer was growing back just about as fast as it was being killed by the Melphalan.) Since his white cells (which had been low before treatment even) weren't tolerating the MP we tried switching to high dose Dexamethasone (which is the drug that gives most of the effect of VAD for those who respond).

Unfortunately, he didn't respond at all to it and after two 3-week rounds his myeloma had run away, leading quickly (by early October) to compression fractures and hypercalcemia and he was in miserable shape. (This after being basically asymptomatic until September.) We went back to the MP supporting it with GCSF (Neupogen) so that his white cell count could recover between treatments. He also started on monthly Aredia treatments. This fairly quickly (maybe three or four rounds) brought his IgA back down to about where it had been at diagnosis, but the MP and the myeloma cells seemed to fight to about a draw at that point and we kept trying it too long. Compression fractures (in almost every vertebra of his spine, leading to a loss of four inches in his height) and fractured ribs had left him unable to even turn over and it was a long, slow road to regaining some mobility. We continued the Melphalan treatments, as the IgA continued to go down ever so slowly. But after about eight months the myeloma seemed to have built up resistance to the Melphalan, his IgA suddenly started soaring, his calcium got out of control and his platelets started drastically falling.

When the cancer broke loose from the Melphalan (climbing in a few weeks from about 3,000 to 7,000) we immediately went to Arkansas where he was given CDEP, a high dose treatment with four drugs: Cytoxan, Dexamethasone, etoposide (sometimes called VP-16) and cisplatin. He had a miraculous, though brief, response. By four weeks his IgA was down to about 1800 and he was feeling much better than he had for months. However, by the time they collected his stem cells three weeks later, the IgA had already jumped up and when he had his transplant the next week it was already up to 2800.

The previous treatment with Melphalan (11 rounds) led to difficulty collecting stem cells. He didn't succeed in collecting right after the CDEP but a couple of weeks later, after some rest and stimulation with high doses of GCSF, he did produce enough for two transplants. They were considered "poor quality", though, which meant they engrafted slowly and he was transfusion dependent (for both red cells and platelets) longer than most people after transplant.

He had his first (and what turned out to be his only) transplant in September, as soon as the stem cells were collected. He had it out-patient. The induction treatment with the stem-cell transplant (high dose Melphalan) brought his IgA down to almost normal readings (a low of 627 about 7 weeks after transplant), though cancer cells were still present. We went home expecting to have the second transplant in a 3 or 4 months and hoping that the second PSCT, with total body radiation added to the treatment, would put him into complete remission.

Unfortunately, the aggressiveness of his myeloma wasn't to allow that. We stepped up the schedule for the transplant when we saw that the IgA was going up fast (doubling in about three weeks), but it was high enough and his marrow was enough compromised by the time we were ready for the transplant that a last minute decision was made to try to "cool down" the myeloma before doing the transplant. He was given an attenuated CDEP treatment instead, to which he again responded well initially (going from 4850 to 2140 in 2 weeks), but this time it started soaring again within three weeks and the decision was to try a different approach, an intensive VAD (which Dave had never had) treatment with double the adriamycin. By the time his counts had recovered to the point he could have this treatment the IgA was already up to 5900. When his myeloma failed to respond to the VAD treatment his marrow completely failed and we had to head home for what we knew would be a very rapid end. Luckily, things moved so rapidly that he wasn't in pain. He passed away two weeks after we got home, on March 10.

We will never know what might have happened if Dave had started aggressive treatment earlier. Looking back at his test results, though, it seems pretty clear to me that there was a definite change in his myeloma's response to Melphalan after the successive small doses. The fact that he still had a good, though temporary, response to it in large doses with the transplant makes me wonder whether if that treatment had been given early (before the small doses built up the myeloma's resistance), it might not have knocked the myeloma back significantly enough to have given him a long remission.

Certainly the improvement we saw with the intensive therapy (both the CDEP and the transplant) was spectacular, though unfortunately brief. It did, however, give Dave the immense pleasure of being able to help out in another family medical crisis that happened to occur during the two month partial remission that he did achieve. We would not have been able to be of any help had he not had the transplant, and that meant an awful lot to him. Our nine month stay (broken only by that two month period) was a very intense experience. Dave kept up his good spirits (with some inevitable low spots) through all the side effects of the chemo treatments. We were lucky to be matched to a wonderful Patient-Partner in Little Rock who made us feel completely at home there. Dave also found great support in both the BMT-talk and later the hem-onc online email support groups and we made very meaningful connections with several myeloma patients through the groups. He became known as quite a vocal advocate of the internet at the Little Rock clinic.


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