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Achievement of recommended treatment targets for bone and mineral metabolism in haemodialysis patients using paricalcitol: an observational study.

https://arctichealth.org/en/permalink/ahliterature136584
Source
Scand J Urol Nephrol. 2011 Apr;45(3):196-205
Publication Type
Article
Date
Apr-2011
Author
Anders Fernström
Jan Giæver
Barbara Granroth
Britta Hylander
Gert Jensen
Anders Christensson
Björn Wikström
Lars Weiss
Ulf Wrege
Stefan H Jacobson
Author Affiliation
Department of Nephrology, Linköping University/Linköping University Hospital, Linköping, Sweden. anders.fernstrom@lio.se
Source
Scand J Urol Nephrol. 2011 Apr;45(3):196-205
Date
Apr-2011
Language
English
Publication Type
Article
Keywords
Aged
Biomarkers, Pharmacological - blood - metabolism
Bone Density - drug effects
Bone Density Conservation Agents - administration & dosage - pharmacology - therapeutic use
Bone Diseases, Metabolic - drug therapy - etiology - metabolism
Bone and Bones - metabolism
Calcium - blood
Chronic Disease
Ergocalciferols - administration & dosage - pharmacology - therapeutic use
Female
Humans
Hyperparathyroidism, Secondary - complications - drug therapy - metabolism
Injections, Intravenous
Kidney Diseases - complications - metabolism - therapy
Male
Middle Aged
Observation
Parathyroid Hormone - metabolism
Phosphorus - blood
Prospective Studies
Renal Dialysis
Sweden
Abstract
Secondary hyperparathyroidism (SHPT) is a common problem among patients with chronic kidney disease (CKD) on haemodialysis. This study was conducted to assess the use, effectiveness and safety of intravenous paricalcitol in haemodialysis patients with various degrees of SHPT.
This observational, multicentre, prospective study was conducted in 14 Swedish dialysis centres from May 2007 to June 2008 and included 92 haemodialysis patients with a diagnosis of SHPT associated with CKD. The decision to initiate treatment with intravenous paricalcitol was made by the treating physician. No treatment algorithms were provided.
Mean patient age was 64 years. Of the 92 patients included, 74 had an intact parathyroid hormone (iPTH) level of >300 pg/ml at baseline. Median iPTH was 584 pg/ml in patients with a baseline PTH of >300 pg/ml. During follow-up there was a decrease in iPTH to 323 pg/ml at 6 months (-45%, p
PubMed ID
21366390 View in PubMed
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Adherence, preference, and satisfaction of postmenopausal women taking denosumab or alendronate.

https://arctichealth.org/en/permalink/ahliterature140933
Source
Osteoporos Int. 2011 Jun;22(6):1725-35
Publication Type
Article
Date
Jun-2011
Author
D L Kendler
M R McClung
N. Freemantle
M. Lillestol
A H Moffett
J. Borenstein
S. Satram-Hoang
Y-C Yang
P. Kaur
D. Macarios
S. Siddhanti
Author Affiliation
University of British Columbia, 600-1285 West Broadway, V6H 3X8 Vancouver, BC, Canada. kendler@ca.inter.net
Source
Osteoporos Int. 2011 Jun;22(6):1725-35
Date
Jun-2011
Language
English
Publication Type
Article
Keywords
Administration, Oral
Aged
Alendronate - administration & dosage - adverse effects - therapeutic use
Antibodies, Monoclonal - administration & dosage - adverse effects - therapeutic use
Antibodies, Monoclonal, Humanized
Bone Density - drug effects
Bone Density Conservation Agents - administration & dosage - adverse effects - therapeutic use
British Columbia
Epidemiologic Methods
Female
Humans
Injections, Subcutaneous
Medication Adherence - statistics & numerical data
Middle Aged
Osteoporosis, Postmenopausal - drug therapy - physiopathology - psychology
Patient Preference - statistics & numerical data
Patient Satisfaction - statistics & numerical data
Treatment Outcome
Abstract
In this study, 250 women with osteoporosis were randomized to 12 months with subcutaneous denosumab 60 mg every 6 months or oral alendronate 70 mg once weekly, then crossed over to the other treatment. The primary endpoint, treatment adherence at 12 months, was 76.6% for alendronate and 87.3% for denosumab.
The purpose of this study is to evaluate treatment adherence with subcutaneous denosumab 60 mg every 6 months or oral alendronate 70 mg once weekly.
In this multicenter, randomized, open-label, 2-year, crossover study, 250 postmenopausal women with low bone mineral density received denosumab or alendronate for 12 months, then the other treatment for 12 months. The alendronate bottle had a medication event monitoring system cap to monitor administration dates. Definitions were as follows: compliance, receiving both denosumab doses 6 (± 1) months apart or 80-100% of alendronate doses; persistence, receiving both denosumab doses and completing the month 12 visit within the visit window or = 2 alendronate doses in the final month; adherence, achieving both compliance and persistence. This report includes data from the first 12 months.
The primary study endpoint, adherence in the first 12 months, was 76.6% (95/124) for alendronate and 87.3% (110/126) for denosumab. Risk ratios for denosumab compared with alendronate at 12 months were 0.58 (p = 0.043) for non-adherence, 0.48 (p = 0.014) for non-compliance, and 0.54 (p = 0.049) for non-persistence. Subject ratings for treatment necessity, preference, and satisfaction were significantly greater for denosumab and ratings for treatment bother were significantly greater for alendronate. Adverse events were reported by 64.1% of alendronate-treated subjects and 72.0% of denosumab-treated subjects (p = 0.403). The most common adverse events were arthralgia, back pain, pain in extremity, cough, and headache (each in
PubMed ID
20827547 View in PubMed
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Advanced vertebral fracture among newly diagnosed children with acute lymphoblastic leukemia: results of the Canadian Steroid-Associated Osteoporosis in the Pediatric Population (STOPP) research program.

https://arctichealth.org/en/permalink/ahliterature152682
Source
J Bone Miner Res. 2009 Jul;24(7):1326-34
Publication Type
Article
Date
Jul-2009
Author
Jacqueline Halton
Isabelle Gaboury
Ronald Grant
Nathalie Alos
Elizabeth A Cummings
Maryann Matzinger
Nazih Shenouda
Brian Lentle
Sharon Abish
Stephanie Atkinson
Elizabeth Cairney
David Dix
Sara Israels
David Stephure
Beverly Wilson
John Hay
David Moher
Frank Rauch
Kerry Siminoski
Leanne M Ward
Author Affiliation
University of Ottawa, Ontario, Canada.
Source
J Bone Miner Res. 2009 Jul;24(7):1326-34
Date
Jul-2009
Language
English
Publication Type
Article
Keywords
Adolescent
Bone Density - drug effects
Canada - epidemiology
Child
Child, Preschool
Female
Glucocorticoids - administration & dosage - adverse effects
Humans
Infant
Infant, Newborn
Lumbar Vertebrae - injuries
Male
Osteoporosis - chemically induced - epidemiology
Precursor Cell Lymphoblastic Leukemia-Lymphoma - diagnosis - drug therapy - epidemiology
Prevalence
Spinal Fractures - chemically induced - epidemiology
Thoracic Vertebrae - injuries
Abstract
Vertebral compression is a serious complication of childhood acute lymphoblastic leukemia (ALL). The prevalence and pattern of vertebral fractures, as well as their relationship to BMD and other clinical indices, have not been systematically studied. We evaluated spine health in 186 newly diagnosed children (median age, 5.3 yr; 108 boys) with ALL (precursor B cell: N = 167; T cell: N = 19) who were enrolled in a national bone health research program. Patients were assessed within 30 days of diagnosis by lateral thoraco-lumbar spine radiograph, bone age (also used for metacarpal morphometry), and BMD. Vertebral morphometry was carried out by the Genant semiquantitative method. Twenty-nine patients (16%) had a total of 75 grade 1 or higher prevalent vertebral compression fractures (53 thoracic, 71%; 22 lumbar). Grade 1 fractures as the worst grade were present in 14 children (48%), 9 patients (31%) had grade 2 fractures, and 6 children (21%) had grade 3 fractures. The distribution of spine fracture was bimodal, with most occurring in the midthoracic and thoraco-lumbar regions. Children with grade 1 or higher vertebral compression had reduced lumbar spine (LS) areal BMD Z-scores compared with those without (mean +/- SD, -2.1 +/- 1.5 versus -1.1 +/- 1.2; p
Notes
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PubMed ID
19210218 View in PubMed
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Alendronate has a residual effect on bone mass in postmenopausal Danish women up to 7 years after treatment withdrawal.

https://arctichealth.org/en/permalink/ahliterature183631
Source
Bone. 2003 Sep;33(3):301-7
Publication Type
Article
Date
Sep-2003
Author
Yu Z Bagger
László B Tankó
Peter Alexandersen
Pernille Ravn
Claus Christiansen
Author Affiliation
Center for Clinical and Basic Research A/S, Ballerup Byvej 222, Ballerup, Denmark. yb@ccbr.dk
Source
Bone. 2003 Sep;33(3):301-7
Date
Sep-2003
Language
English
Publication Type
Article
Keywords
Adult
Alendronate - administration & dosage
Biological Markers
Bone Density - drug effects
Bone Remodeling - drug effects
Denmark
Female
Follow-Up Studies
Humans
Middle Aged
Osteoporosis, Postmenopausal - prevention & control
Postmenopause
Prospective Studies
Abstract
Alendronate has been shown to reduce bone turnover and increase bone mass. However, little is known about the duration of the effect on bone after treatment withdrawal. The aim of this study was to investigate the long-term effects on bone mineral density (BMD) and bone turnover of various alendronate regimens after treatment withdrawal. In this study, we followed 203 postmenopausal women who previously participated in two alendronate randomized placebo-controlled trials. Daily oral treatment with various doses of alendronate (2.5-20 mg) were given for 2, 4, or 6 yr followed by no treatment for 7, 5, or 3 yr, respectively. Bone mineral density of the lumbar spine, hip, and forearm was measured by dual-energy x-ray absorptiometry. Biochemical markers of bone turnover were induced serum C-terminal telopeptides of type I collagen (CTX) and osteocalcin. Women who received alendronate (2.5-10 mg per day) for 2 yr had a 3.8% higher BMD compared to those receiving placebo when assessed 7 yr after withdrawal. The residual effect was proportionally larger in women who had received treatment for 4 (5.9%, P=0.02) or 6 yr (8.6%, P=0.002), respectively. However, the largest residual effect was found in women treated with alendronate 20 mg per day for 2 yr (9.7%, P=0.01 vs. placebo). The rate of bone loss after alendronate withdrawal was comparable to the bone loss observed in the placebo group. Bone markers tended to reverse back to normal levels, but were still affected even several years after withdrawal of treatment. This study has demonstrated that the efficacy of alendronate in preventing bone loss was proportional to the duration of treatment. The rate of bone loss after withdrawal of alendronate corresponded to the normal postmenopausal rate of bone loss. A residual effect on BMD was found up to 7 yr after treatment withdrawal.
PubMed ID
13678770 View in PubMed
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ALX 111: ALX1-11, parathyroid hormone (1-84) - NPS Allelix, PREOS, PTH, recombinant human parathyroid hormone, rhPTH (1-84).

https://arctichealth.org/en/permalink/ahliterature71301
Source
Drugs R D. 2003;4(4):231-5
Publication Type
Article
Date
2003
Author Affiliation
Adis International Ltd.
Source
Drugs R D. 2003;4(4):231-5
Date
2003
Language
English
Publication Type
Article
Keywords
Bone Density - drug effects
Clinical Trials, Phase II
Drug Industry
Female
Humans
Injections, Subcutaneous
Middle Aged
Multicenter Studies
Osteoporosis, Postmenopausal - drug therapy - prevention & control
Parathyroid Hormone - administration & dosage - adverse effects - therapeutic use
Randomized Controlled Trials
Recombinant Proteins - administration & dosage - adverse effects - therapeutic use
Treatment Outcome
Abstract
ALX 111 [parathyroid hormone (1-84) - NPS Allelix, recombinant human parathyroid hormone, rhPTH (1-84), PREOS] is a full-length, recombinant human parathyroid hormone. It has potential as an anti-osteoporotic agent, due to its properties as a bone formation stimulant.This profile has been selected from R&D Insight, a pharmaceutical intelligence database produced by Adis International Ltd. It has been recommended that ALX 111 should be given for 1 to 2 years and may be given in combination with an antiresorptive agent, such as estrogen or a bisphosphonate. In December 1999, Allelix Biopharmaceuticals merged with NPS Pharmaceuticals. This combined company is operating as NPS Pharmaceuticals in the US and as NPS Allelix in Canada. The merger has enabled a phase III study of ALX 111 to begin in the US, Europe and South America. NPS harmaceuticals has signed an agreement with Bio-Imaging Technologies, which will provide all image handling and analysis for this trial. Until 1994, Allelix Biopharmaceuticals and Glaxo in Canada were involved in a joint venture to investigate the efficacy of ALX 111 in osteoporosis. Allelix was subsequently, until September 1998, collaborating with Astra of Sweden in developing ALX 111. Astra had acquired exclusive worldwide rights to ALX 111 and was responsible for development of the agent. However, Astra returned all rights to ALX 111 to Allelix as a result of its merger with Zeneca to form AstraZeneca. In December 1999, Allelix Biopharmaceuticals merged with NPS Pharmaceuticals. This combined company is operating as NPS Pharmaceuticals in the US and as NPS Allelix in Canada. The merger has enabled a phase III study of ALX 111 to begin in the US, Europe and South America. The phase III trial of ALX 111 for the treatment of osteoporosis has completed patient enrolment, and phase II trials have been completed in Canada and the Netherlands. The 18-month, phase III, multicentre, placebo-controlled trial (Treatment of Osteoporosis with Parathyroid Hormone; TOP) has been designed to assess the bone-building and fracture-reducing potential of the drug, and over 2600 postmenopausal women with osteoporosis who have not received previous drug therapy for osteoporosis have been enrolled. Treatment will be completed in September 2003, but more than 75% of patients enrolled in the TOP study have chosen to enrol in an Open Label Extension Study (OLES), which allows for a total treatment period of up to 24 months. NPS Pharmaceuticals has signed an agreement with Bio-Imaging Technologies, which will provide all image handling and analysis for this trial. In September 2002, NPS Pharmaceuticals announced that it has met its patient enrolment target (n > 150) for its POWER (PTH for Osteoporotic Women on Estrogen Replacement) study; a 24-month phase III trial initiated in Europe in November 2001. In this trial, women with osteoporosis receive SC injections of ALX 111 or placebo, in combination with their existing hormone replacement therapies, to test the bone building potential of the drug. In addition to the POWER study, a clinical trial sponsored by the National Institutes of Health (NIH) is being conducted to evaluate the potential of ALX 111 to build bone in combination with another osteoporosis medication. The 'PaTH' study (PTH/alendronate) is designed to assess the effect of various combinations and sequential uses of ALX 111 and Merck's Fosamax, a drug for slowing the loss of bone due to osteoporosis. The PaTH study, initiated in May 2000 and scheduled to conclude in September 2003, involved 238 patients with postmenopausal osteoporosis. It is thought that alendronic acid and ALX 111, when administered in combination, may act in an additive manner to treat osteoporosis because they act in different ways; alendronic acid acts to inhibit resorption and ALX 111 speeds up bone formation and resorption, with a net increase in formation. Results of this study are still being analysed but preliminary results appear to be positive. The effect of ALX 111 on bone cell cultures underare still being analysed but preliminary results appear to be positive. The effect of ALX 111 on bone cell cultures under conditions of microgravity was tested in orbit on the Space Shuttle Columbia, which was launched on 16 January 2003 but did not survive re-entry. This study was one in a series of studies known as 'OSTEO' and had been prepared by researchers from NPS Pharmaceuticals using Millenium Biologix' OSTEO Mini-Lab System. Under space flight conditions, astronauts experience a loss in bone density at a rate up to ten times faster than that of earth-bound patients with osteoporosis, and it was hoped that this study would indicate the mechanism of action of ALX 111 at cellular and genetic levels. The results of these studies were represented by the samples of human bone cells, which were lost during the re-entry tragedy.
PubMed ID
12848587 View in PubMed
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Associated response in bone and lipids during hormone replacement therapy.

https://arctichealth.org/en/permalink/ahliterature182171
Source
Maturitas. 2004 Jan 20;47(1):39-45
Publication Type
Article
Date
Jan-20-2004
Author
Anne Bloch Thomsen
Sandra Silvestri
Jens Haarbo
Claus Christiansen
Nina H Bjarnason
Author Affiliation
Center of Clinical Basic Research, Ballerup Byvej 222, 2750 Ballerup, Denmark. abt@ccbr.dk
Source
Maturitas. 2004 Jan 20;47(1):39-45
Date
Jan-20-2004
Language
English
Publication Type
Article
Keywords
Biological Markers - blood - urine
Bone Density - drug effects
Cholesterol, LDL - drug effects
Denmark
Double-Blind Method
Estradiol - pharmacokinetics - therapeutic use
Estrogen Replacement Therapy - methods
Female
Follow-Up Studies
Humans
Middle Aged
Norpregnenes - pharmacokinetics - therapeutic use
Osteoporosis, Postmenopausal - drug therapy - prevention & control
Progestins - pharmacokinetics - therapeutic use
Prospective Studies
Regression Analysis
Treatment Outcome
Abstract
In postmenopausal women, we investigated if the response in bone mineral density (BMD) was associated with the response in the atherogenic lipid profile during hormone replacement therapy.
We performed an exploratory, post-hoc analysis of data from a prospective double-blind placebo-controlled trial. Healthy postmenopausal women were randomised into five groups, each receiving different combinations of 17 beta-estradiol and gestodene or placebo. A total of 133 women completed the study. The study period was 3 years. The response in bone mass was expressed as the percentage change in BMD from baseline calculated by linear regression from semi-annual measurements. The change in lipid profile was evaluated as the average of three mid-cycle and end-cycle values in percentage from baseline in order to account for cyclic changes during sequential hormone therapy.
A significant correlation between the increase in BMD of the spine and hip and forearm with the decrease in serum low density lipoprotein (LDL) and cholesterol was found. Additionally, the decrease in atherogenic lipids correlated significantly with the response in biochemical bone markers for resorption and formation.
In conclusion, our study shows that it is the same women who have a favourable response in BMD as in the lipid-profile during hormone replacement therapy (HRT). The association is most likely driven by a common response in FSH to exogenous estradiol therapy. This indicates that common denominators for the response to HRT exist. Further studies are needed to explore and identify such predictors.
PubMed ID
14706764 View in PubMed
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Associations between dietary cadmium exposure and bone mineral density and risk of osteoporosis and fractures among women.

https://arctichealth.org/en/permalink/ahliterature125636
Source
Bone. 2012 Jun;50(6):1372-8
Publication Type
Article
Date
Jun-2012
Author
Annette Engström
Karl Michaëlsson
Marie Vahter
Bettina Julin
Alicja Wolk
Agneta Åkesson
Author Affiliation
Institute of Environmental Medicine, Karolinska Institutet, Box 210, S-171 77 Stockholm, Sweden.
Source
Bone. 2012 Jun;50(6):1372-8
Date
Jun-2012
Language
English
Publication Type
Article
Keywords
Aged
Bone Density - drug effects
Cadmium - administration & dosage - adverse effects - urine
Cohort Studies
Female
Food contamination - analysis
Fractures, Bone - epidemiology - etiology
Humans
Middle Aged
Multivariate Analysis
Osteoporosis - epidemiology - etiology
Prospective Studies
Risk factors
Sweden - epidemiology
Abstract
Osteoporosis and its main health outcome, fragility fractures, are large and escalating public health problems. Cadmium, a widespread food contaminant, is a proposed risk factor; still the association between estimated dietary cadmium exposure and bone mineral density (BMD) has never been assessed. Within a sub-cohort of the Swedish Mammography Cohort, we assessed dietary cadmium exposure based on a food frequency questionnaire (1997) and urinary cadmium (2004-2008) in relation to total-body BMD and risk of osteoporosis and fractures (1997-2009) among 2676 women (aged 56-69 years). In multivariable-adjusted linear regression, dietary cadmium was inversely associated with BMD at the total body and lumbar spine. After further adjustment for dietary factors important for bone health and cadmium bioavailability--calcium, magnesium, iron and fiber, the associations became more pronounced. A 32% increased risk of osteoporosis (95% CI: 2-71%) and 31% increased risk for any first incident fracture (95% CI: 2-69%) were observed comparing high dietary cadmium exposure (=13 µg/day, median) with lower exposures (
PubMed ID
22465267 View in PubMed
Less detail

Benchmark dose for cadmium-induced osteoporosis in women.

https://arctichealth.org/en/permalink/ahliterature143373
Source
Toxicol Lett. 2010 Aug 16;197(2):123-7
Publication Type
Article
Date
Aug-16-2010
Author
Yasushi Suwazono
Salomon Sand
Marie Vahter
Staffan Skerfving
Jonas Lidfeldt
Agneta Akesson
Author Affiliation
Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden.
Source
Toxicol Lett. 2010 Aug 16;197(2):123-7
Date
Aug-16-2010
Language
English
Publication Type
Article
Keywords
Bone Density - drug effects
Cadmium - toxicity - urine
Dose-Response Relationship, Drug
Environmental Pollutants - toxicity - urine
Female
Humans
Linear Models
Middle Aged
Osteoporosis, Postmenopausal - chemically induced
Sweden
Abstract
We applied a hybrid approach to estimate the benchmark dose (BMD) and the lower 95% confidence limit (BMDL) for cadmium-induced bone effects in a population with low environmental exposure. Morning urine samples were collected by 794 Swedish women, aged 53-64 years, participating in a population-based study. We measured urinary cadmium (U-Cd), a marker of long-term exposure, and bone mineral density, expressed as its T-score (reference: 20-year old women) of the non-dominant wrist. BMD and BMDL, adjusted for relevant covariates, corresponding to an additional risk (BMR) of 5% or 10% were calculated, with the background risk at zero exposure set at 1% or 5%. With a BMR of 5% and a background risk of having low bone mineral density (at U-Cd = 0) of 1% or 5% (corresponding to T-score cut-offs -2.75 and -2.09, respectively), the BMD of U-Cd ranged 1.8-3.7 microg/g creatinine, and the BMDL ranged 1.0-2.1 microg/g creatinine. For a 5% BMR of osteoporosis (T-score
PubMed ID
20493933 View in PubMed
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[Biological effects of vitamin K and concentration of vitamin K in Norwegian food]

https://arctichealth.org/en/permalink/ahliterature30249
Source
Tidsskr Nor Laegeforen. 2004 Jun 17;124(12):1650-4
Publication Type
Article
Date
Jun-17-2004
Author
Christian A Drevon
Hege Berg Henriksen
Marianne Sanderud
Thomas E Gundersen
Rune Blomhoff
Author Affiliation
Avdeling for ernaeringsvitenskap, Institutt for medisinske basalfag, Universitetet i Oslo, Postboks 1046 Blindern, 0316 Oslo. c.a.drevon@basalmed.uio.no
Source
Tidsskr Nor Laegeforen. 2004 Jun 17;124(12):1650-4
Date
Jun-17-2004
Language
Norwegian
Publication Type
Article
Keywords
Adult
Blood Coagulation - drug effects - physiology
Bone Density - drug effects - physiology
Calcinosis - prevention & control
Child
English Abstract
Female
Food analysis
Humans
Male
Nerve Degeneration
Norway
Nutritional Requirements
Osteoporosis - etiology - prevention & control
Vitamin K - administration & dosage - analysis - metabolism - physiology
Abstract
BACKGROUND: Vitamin K has several biological effects and dietary intake seems to be more important than previously believed because of low bioavailability of the vitamins from the colon. MATERIALS AND METHODS: Data from the literature were identified on PubMed, and data from NORKOST II (a dietary study from 1997 based on a nation-wide sample of respondents) were used to calculate dietary intake of vitamin K. RESULTS: The dietary intake of vitamin K in Norway seems to be
Notes
Comment In: Tidsskr Nor Laegeforen. 2004 Dec 16;124(24):3261; author reply 3261-215608790
PubMed ID
15229714 View in PubMed
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119 records – page 1 of 12.