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Old 09-24-2007, 10:03 AM   #1
Lani
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Exclamation bones of breast cancer patients aged prematurely by treatment

Bones of Breast Cancer Patients Aged Prematurely by Treatment: Presented at ASBMR [Doctor's Guide]
HONOLULU, HAWAII — September 20, 2007 — Women who are under treatment for early-stage breast cancer are likely to have a low bone mineral density (BMD) and are at increased risk of osteopaenia and osteoporosis, researchers noted here at the 29th Annual Meeting of the American Society for Bone and Mineral Research.
Chemotherapy, radiation therapy, aromatase inhibitors and other treatments for breast cancer all put this population at increased risk for osteoporotic fractures, stated Pauline M. Camacho, MD, Associate Professor of Medicine, Division of Endocrinology and Metabolism, and Director, Osteoporosis and Metabolic Bone Disease Center, Loyola University Health System, Maywood, Illinois, United States.
Dr. Camacho and colleagues conducted a retrospective chart review of 238 postmenopausal women referred to their centre for the management of osteoporosis or osteopaenia.
Patients were divided into those without a history of breast cancer (174 patients), and those with early-stage breast cancer (64 patients) who were receiving or being considered for adjuvant hormonal therapy with aromatase inhibitors.
The mean age of those with breast cancer was 59.5 years compared with 64.2 years for those without. Serum 25-hydroxy-vitamin D levels were 28.7 ng/mL in those without breast cancer and 34.03 ng/mL in those with the disease. Spine T scores were lower, and femoral-neck bone mineral density (BMD) were significantly lower in controls than in those with early-stage cancer, perhaps because the cancer patients were receiving closely monitored health care, Dr. Camacho said.
More than three-quarters of both groups had at least one secondary cause of osteoporosis. The most common secondary cause was vitamin-D deficiency in both groups, which was seen in 37.5% of the breast-cancer group and 51.1% of the group without breast cancer.
A new diagnosis of a secondary cause, however, was seen more often in those with breast cancer, which Dr. Camacho said was a significant finding.
"There is a growing trend toward switching adjuvant treatment from tamoxifen to aromatase inhibitors as adjuvant treatment for breast cancer," Dr. Camacho noted. "Since there is such a high prevalence of secondary causes of osteoporosis, physicians should be cautious about prescribing or continuing these patients on adjuvant therapy with aromatase inhibitors.Tamoxifen should be considered, since it is bone-sparing," she advised.

ABSTRACT: Prevalence of Secondary Causes of Osteoporosis Among Breast Cancer Patients with Osteoporosis and Osteopenia [American Society for Bone and Mineral Research]
Purpose: The main objective of this study was to determine the prevalence of secondary causes of osteoporosis among breast cancer patients being evaluated for osteopenia (low bone mass) and osteoporosis.
Methods: We conducted a retrospective chart review of 238 postmenopausal women consecutively referred to Loyola University Medical Center Endocrinology clinics from 2000-2005, for the management of osteoporosis or osteopenia. Patients were divided into two groups: those without a history of breast cancer or NBC group (N=174), and those with breast cancer or BC group (N=64). The BC group was comprised of patients with early stage breast cancer in the midst of or considering adjuvant hormonal therapy with aromatase inhibitors. Histories and biochemical data from their initial consultation were analyzed. Statistical analysis of each patient population was performed to elucidate the prevalence of secondary causes of osteoporosis in patients with breast cancer relative to the group of patients without breast cancer.
Results: The demographics of the two groups differed in age (64.2 ± 14.2 in NBC versus 59.5 ± 10.6 in BC group, p=0.015), mean weight (63.5 ± 13.7 in NBC versus 73.62 ± 20.95 kg in BC, p <0.001), 25 OH Vitamin D levels (28.7 ± 13.1 in NBC versus 34.03 ± 15.1 ng/ml in BC, p = 0.019) and degree of bone loss (spine T score of -1.966± 1.34 in NBC versus-0.918± 1.41 in BC, p < 0.001). The presence of at least one secondary cause of osteoporosis was seen in 78.1% of the breast cancer patient group (excluding cancer-related therapies), and in 77 % of the non-breast cancer group. Newly diagnosed metabolic bone disorders were seen in 57.8% of the breast cancer population. The most common secondary cause in both groups was vitamin D deficiency, which was seen in 37.5% of the breast cancer group and 51% of the non-breast cancer group. In the BC group, this was followed by idiopathic hypercalciuria (15.6% versus 8% in NBC, trend towards higher prevalence in BC than the NBC group p=0.085), normocalcemic hyperparathyroidism (3.1%) and primary hyperparathyroidism (1.6%).
Conclusion: We found a high prevalence of secondary causes of osteoporosis among breast cancer patients undergoing or considering adjuvant hormonal therapy with aromatase inhibitors. Previously published reports of bone loss and fractures seen in patients on such agents may have been partly due to the presence of these disorders. It is prudent to obtain a baseline DXA and to screen patients with breast cancer for secondary causes of bone loss.
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Old 09-24-2007, 10:20 AM   #2
Lani
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now that I have (I hope not) alarmed you--bisphosphonate more than counteracts AIbone

effect--hot off the press:

American Society for Bone and Mineral Research 29th Annual Meeting
Risedronate More Than Counteracts Bone-Depleting Effects of Aromatase Inhibitors


September 24, 2007 (Honolulu) — Not only is aromatase inhibitor–induced damage to bone corrected, but bone mineral density (BMD) is improved to above-baseline levels when postmenopausal women with hormone receptor–positive breast cancer on aromatase inhibitors have the bisphosphonate risedronate (Actonel, Procter and Gamble Pharmaceuticals, Inc) added to their treatment regimen.

The 12-month results of the Study of Anastrozole with the Bisphosphonate Risedronate (SABRE) were presented here during the American Society for Bone and Mineral Research 29th Annual Meeting by lead investigator Richard Eastell, MD, professor of medicine and the Academic Unit of Bone Metabolism at the University of Sheffield, United Kingdom.

SABRE was a multicenter study consisting of 234 postmenopausal women with hormone receptor–positive early-stage breast cancer. Mean age was 64 years (range, 45 – 91 years).

Subjects were categorized into 3 groups according to fracture risk. Those in the high-risk group (38 women) had a lumbar spine or hip BMD T-score below ?2.0 and a history of "fragility fracture" or were at high risk of fracture. Those with a moderate fracture risk (154 women) had T-scores below ?1.0 but at least ?2.0 or above and a history of fragility in a first-degree relative, early menopause or advanced age, low body weight (less than 127 lbs), or a current smoker. Those with the lowest fracture risk (42 women) had T-scores of ?1.0 and above and no history of fractures or fragility.

All subjects had received the aromatase inhibitor anastrazole 1 mg/day for 2 years. They were given calcium 500 mg daily or vitamin D 200 IU daily.

Women in the high fracture risk group were prescribed risedronate 35 mg a week. Moderate-risk patients were randomly assigned to receive risedronate 35 mg/week or placebo, whereas women in the lowest-risk group did not receive bisphosphonate therapy.

At 12 months, BMD in the high-risk group had increased significantly at the lumbar spine (approximately 3.0%; P < .0001) and hip (>1.0%; P = .012). BMD in the low-risk group had decreased numerically at the lumbar spine (P = .3511) and hip (P = .4918), but the change was not statistically significant.

In moderate fracture risk patients, the increase in BMD was significantly greater at the lumbar spine in those on risedronate compared with those on placebo (>1.0%; P < .0001), as well as at the hip (approximately 1.0%; P = .002).

There was also a significant decrease in bone turnover markers between all risedronate-treated women and placebo-treated women. Low-risk women had an increase in serum C-terminal cross-linking telopeptide of type 1 collagen and bone alkaline phosphatase, indicating that bone degradation was taking place.

Ten women withdrew from the study, all because of adverse effects related to the aromatase inhibitor. There was 1 nontreatment related death during the year of follow-up.

"In postmenopausal women with breast cancer who are already at moderate to high risk of fragility fracture and are scheduled for treatment with anastrazole, bone health can be managed according to established guidelines," Dr. Eastell told meeting attendees. "For patients who are already at risk, risedronate at the licensed dose was sufficient to prevent a decrease in BMD and an increase in bone turnover."

In an interview with Medscape, Pauline Camacho, MD, professor of medicine at Loyola University in Chicago, Illinois, commented, "There is a trend toward switching women over to aromatase inhibitors from tamoxifen.... Physicians need to carefully calculate if this switch is necessary.

"Tamoxifen is bone-sparing. If women could be maintained on it rather than switching to an aromatase inhibitor, that would be helpful [to bone health]," Dr. Camacho added.

"Women on aromatase inhibit should be evaluated as if they were much older than their chronological age[, and] serum vitamin D levels should also be evaluated," she said. "Vitamin D deficiency is very common. In 37.5% of women, levels are not where they should be."

In addition, Dr. Camacho recommended routine monitoring of parathyroid hormone levels, serum calcium, 24-hour urinary calcium excretion, and calcium/creatinine clearance.

Dr. Eastell received funding from AstraZeneca. Dr. Camacho reports no relevant financial relationships.

American Society for Bone and Mineral Research 29th Annual Meeting: Abstract M300. Presented September 17, 2007.
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Old 09-24-2007, 10:31 AM   #3
chrisy
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Lani, thanks for the roller coaster ride! LOL
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Chris in Scotts Valley
June 2002 extensive hi grade DCIS (pre-cancer-stage 0, clean sentinal node) Mastectomy/implant - no chemo, rads. "cured?"
9/2004 Diag: Stage IV extensive liver mets (!) ER/PR- Her2+++
10/04-3/05 Weekly Taxol/Carboplatin/Herceptin , complete response!
04/05 - 4/07 Herception every 3 wks, Continue NED
04/07 - recurrence to liver - 2 spots, starting tykerb/avastin trial
06/07 8/07 10/07 Scans show stable, continue on Tykerb/Avastin
01/08 Progression in liver
02/08 Begin (TDM1) trial
08/08 NED! It's Working! Continue on TDM1
02/09 Continue NED
02/10 Continue NED. 5/10 9/10 Scans NED 10/10 Scans NED
12/10 Scans not clear....4/11 Scans suggest progression 6/11 progression confirmed in liver
07/11 - 11/11 Herceptin/Xeloda -not working:(
12/11 Begin MM302 Phase I trial - bust:(
03/12 3rd times the charm? AKT trial

5/12 Scan shows reduction! 7/12 More reduction!!!!
8/12 Whoops...progression...trying for Perjeta/Herceptin (plus some more nasty chemo!)
9/12 Start Perjeta/Herceptin, chemo on hold due to infection/wound in leg, added on cycle 2 &3
11/12 Poops! progression in liver, Stop Perjeta/Taxo/Herc
11/12 Navelbine/Herce[ptin - try for a 3 cycles, no go.
2/13 Gemzar/Carbo/Herceptin - no go.
3/13 TACE procedure
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Old 11-26-2007, 12:46 PM   #4
Christine MH-UK
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Some recent research suggests benefit of exercise

I found this on Medline:</PRE>
1: Oncol Nurs Forum. 2007 May;34(3):627-33.Exercise effects on bone mineral density in women with breast cancer receivingadjuvant chemotherapy.Schwartz AL, Winters-Stone K, Gallucci B.The Scottsdale Healthcare Cancer Research Endowed Chair, Arizona StateUniversity, Phoenix, AZ, USA. annaschwartz@peoplepc.comPURPOSE/OBJECTIVES: To test the effects of aerobic and resistance exercise onchanges in bone mineral density (BMD) in women newly diagnosed with stage I-IIIbreast cancer receiving chemotherapy. DESIGN: Randomized clinical trial. SETTING:Two National Cancer Institute-designated cancer centers in metropolitan areas.SAMPLE: 66 women with stage I-III breast cancer beginning adjuvant chemotherapy. METHODS: Participants were randomized to aerobic or resistance exercise and usualcare. At the beginning of chemotherapy and at six months, patients completedexercise testing and BMD assessment of the lumbar spine by dual energy x-rayabsorptionetry. MAIN RESEARCH VARIABLES: BMD, aerobic capacity, and musclestrength. FINDINGS: The average decline in BMD was -6.23% for usual care, -4.92% for resistance exercise, and -0.76% for aerobic exercise. Aerobic exercisepreserved BMD significantly better compared to usual care. Premenopausal womendemonstrated significantly greater declines in BMD than postmenopausal women.Aerobic capacity increased by almost 25% for women in the aerobic exercise group and 4% for resistance exercise. Participants in the usual care group showed a 10%decline in aerobic capacity. CONCLUSIONS: The data suggest that weight-bearingaerobic exercise attenuates declines in BMD and that aerobic and resistanceexercise improve aerobic capacity and muscle strength at a time when womengenerally show marked declines in functional ability. IMPLICATIONS FOR NURSING:Exercise may prevent or at least minimize bone loss observed during chemotherapy and may prevent or delay the long-term effects of osteoporosis.Publication Types: Comparative Study Randomized Controlled TrialPMID: 17573321 [PubMed - indexed for MEDLINE]</PRE>
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Old 11-26-2007, 12:59 PM   #5
hutchibk
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"Furthermore, supplementation of systemic anticancer therapy with bisphosphonates or other therapeutic approaches is suggested for prevention of SREs (skeletal related events)."

(and Zolondronic Acid is something to keep an eye on too...)

http://www.springerlink.com/content/m174r20h8u0837p1/
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Brenda

NOV 2012 - 9 yr anniversary
JULY 2012 - 7 yr anniversary stage IV (of 50...)

Nov'03~ dX stage 2B
Dec'03~
Rt side mastectomy, Her2+, ER/PR+, 10 nodes out, one node positive
Jan'04~
Taxotere/Adria/Cytoxan x 6, NED, no Rads, Tamox. 1 year, Arimadex 3 mo., NED 14 mo.
Sept'05~
micro mets lungs/chest nodes/underarm node, Switched to Aromasin, T/C/H x 7, NED 6 months - Herceptin only
Aug'06~
micro mets chest nodes, & bone spot @ C3 neck, Added Taxol to Herceptin
Feb'07~ Genetic testing, BRCA 1&2 neg

Apr'07~
MRI - two 9mm brain mets & 5 punctates, new left chest met, & small increase of bone spot C3 neck, Stopped Aromasin
May'07~
Started Tykerb/Xeloda, no WBR for now
June'07~
MRI - stable brain mets, no new mets, 9mm spots less enhanced, CA15.3 down 45.5 to 9.3 in 10 wks, Ty/Xel working magic!
Aug'07~
MRI - brain mets shrunk half, NO NEW BRAIN METS!!, TMs stable @ 9.2
Oct'07~
PET/CT & MRI show NED
Apr'08~
scans still show NED in the head, small bone spot on right iliac crest (rear pelvic bone)
Sept'08~
MRI shows activity in brain mets, completed 5 fractions/5 consecutive days of IMRT to zap the pesky buggers
Oct'08~
dropped Xeloda, switched to tri-weekly Herceptin in combo with Tykerb, extend to tri-monthly Zometa infusion
Dec'08~
Brain MRI- 4 spots reduced to punctate size, large spot shrunk by 3mm, CT of torso clear/pelvis spot stable
June'09~
new 3-4mm left cerrebellar spot zapped with IMRT targeted rads
Sept'09~
new 6mm & 1 cm spots in pituitary/optic chiasm area. Rx= 25 days of 3D conformal fractionated targeted IMRT to the tumors.
Oct'09~
25 days of low dose 3D conformal fractionated targeted IMRT to the bone mets spot on rt. iliac crest that have been watching for 2 years. Added daily Aromasin back into treatment regimen.
Apr'10~ Brain MRI clear! But, see new small spot on adrenal gland. Change from Aromasin back to Tamoxifen.
June'10~ Tumor markers (CA15.3) dropped from 37 to 23 after one month on Tamoxifen. Continue to monitor adrenal gland spot. Remain on Tykerb/Herceptin/Tamoxifen.
Nov'10~ Radiate positive mediastinal node that was pressing on recurrent laryngeal nerve, causing paralyzed larynx and a funny voice.
Jan'11~ MRI shows possible activity or perhaps just scar tissue/necrotic increase on 3 previously treated brain spots and a pituitary spot. 5 days of IMRT on 4 spots.
Feb'11~ Enrolled in T-DM1 EAP in Denver, first treatment March 25, 2011.
Mar'11~ Finally started T-DM1 EAP in Denver at Rocky Mountain Cancer Center/Rose on Mar. 25... hallelujah.

"I would rather be anecdotally alive than statistically dead."
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Old 11-26-2007, 03:36 PM   #6
suzan w
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Great info...as I had severe osteoporosis before my diagnosis...now, after A/C, herceptin and Arimidex....phew...I have been taking Actonel and Fosomax for almost 7 years now and wonder about the long term effects of that??!! And...what is the opinion...is Actonel better than Fosomax??
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Suzan W.
age 54 at diagnosis
5/05 suspicious mammogram-left breast
5/05 biopsy-invasive lobular carcinoma with LCIS,8mm tumor,stage 1 grade 2, ER+ PR+ Her2+++
6/14/05 bilateral mastectomy, node neg. all scans neg.
Oncotype DX-high risk
8/05-10/05 4 rounds A/C
10/05 -10/06 1 yr. herceptin
arimidex-5 years
2/14/08 started daily self administered injections..FORTEO for severe osteoporosis
7/28/09 BRCA 1 negative BRCA2 POSITIVE
8/17/09 prophylactic salpingo-oophorectomy
10/15/10 last FORTEOinjection
RECLAST infusion(ostoeporosis)
6/14/10 5 year cancerversary!
8/2010-18%increase in bone density!
no further treatments
Oncologist says, "Go do the Happy Dance"
I say,"What a long strange trip its been"
'One day at a time'
6-14-2015. 10 YEAR CANCERVERSARY!
7-16 to 9-16. Extensive (and expensive) dental work done to save teeth. Damage from osteoporosis and chemo and long term bisphosphonate use
6-14-16. 11 YEAR CANCERVERSARY!!
7-20-16 Prolia injection for severe osteoporosis
2 days later, massive hive outbreak. This led to an eventual dx of Chronic Ideopathic Urticaria, an auto-immune disease from HELL.
6-14-17 12 YEAR CANCERVERSARY!!
still suffering from CIU. 4 hospitilizations in the past year

as of today, 10-31-17 in remission from CIU and still, CANCER FREE!!!
6-14-18 13 YEAR CANCERVERSARY!! NED!!
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Old 11-26-2007, 06:44 PM   #7
hutchibk
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I have learned that the predominant thinking is after 2-3 years on bisphosphenate, they are leaning towards switching us to Zometa on an every 3 month infusion. That's what Dr. Ueno at MD Anderson who is working on a current study suggested last weekend at the conference I went to and that is also what my onc told me a couple of months ago he was leaning towards... we just scheduled my bone density last week so he can make his determination.
__________________
Brenda

NOV 2012 - 9 yr anniversary
JULY 2012 - 7 yr anniversary stage IV (of 50...)

Nov'03~ dX stage 2B
Dec'03~
Rt side mastectomy, Her2+, ER/PR+, 10 nodes out, one node positive
Jan'04~
Taxotere/Adria/Cytoxan x 6, NED, no Rads, Tamox. 1 year, Arimadex 3 mo., NED 14 mo.
Sept'05~
micro mets lungs/chest nodes/underarm node, Switched to Aromasin, T/C/H x 7, NED 6 months - Herceptin only
Aug'06~
micro mets chest nodes, & bone spot @ C3 neck, Added Taxol to Herceptin
Feb'07~ Genetic testing, BRCA 1&2 neg

Apr'07~
MRI - two 9mm brain mets & 5 punctates, new left chest met, & small increase of bone spot C3 neck, Stopped Aromasin
May'07~
Started Tykerb/Xeloda, no WBR for now
June'07~
MRI - stable brain mets, no new mets, 9mm spots less enhanced, CA15.3 down 45.5 to 9.3 in 10 wks, Ty/Xel working magic!
Aug'07~
MRI - brain mets shrunk half, NO NEW BRAIN METS!!, TMs stable @ 9.2
Oct'07~
PET/CT & MRI show NED
Apr'08~
scans still show NED in the head, small bone spot on right iliac crest (rear pelvic bone)
Sept'08~
MRI shows activity in brain mets, completed 5 fractions/5 consecutive days of IMRT to zap the pesky buggers
Oct'08~
dropped Xeloda, switched to tri-weekly Herceptin in combo with Tykerb, extend to tri-monthly Zometa infusion
Dec'08~
Brain MRI- 4 spots reduced to punctate size, large spot shrunk by 3mm, CT of torso clear/pelvis spot stable
June'09~
new 3-4mm left cerrebellar spot zapped with IMRT targeted rads
Sept'09~
new 6mm & 1 cm spots in pituitary/optic chiasm area. Rx= 25 days of 3D conformal fractionated targeted IMRT to the tumors.
Oct'09~
25 days of low dose 3D conformal fractionated targeted IMRT to the bone mets spot on rt. iliac crest that have been watching for 2 years. Added daily Aromasin back into treatment regimen.
Apr'10~ Brain MRI clear! But, see new small spot on adrenal gland. Change from Aromasin back to Tamoxifen.
June'10~ Tumor markers (CA15.3) dropped from 37 to 23 after one month on Tamoxifen. Continue to monitor adrenal gland spot. Remain on Tykerb/Herceptin/Tamoxifen.
Nov'10~ Radiate positive mediastinal node that was pressing on recurrent laryngeal nerve, causing paralyzed larynx and a funny voice.
Jan'11~ MRI shows possible activity or perhaps just scar tissue/necrotic increase on 3 previously treated brain spots and a pituitary spot. 5 days of IMRT on 4 spots.
Feb'11~ Enrolled in T-DM1 EAP in Denver, first treatment March 25, 2011.
Mar'11~ Finally started T-DM1 EAP in Denver at Rocky Mountain Cancer Center/Rose on Mar. 25... hallelujah.

"I would rather be anecdotally alive than statistically dead."
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