title: Hypovitaminosis D, impaired bone turnover and low bone mass are common in patients with peripheral arterial disease.
abstract: Hypovitaminosis D is common in patients with peripheral arterial disease (PAD). Subsequent secondary hyperparathyroidism and osteomalacia contribute to bone pain and myalgias, and so aggravate clinical symptoms of claudication. We evaluated 95 out of 297 patients with angiographically confirmed PAD stages II (pain in the calves and/or thighs only during exercise) or IV (history of, or presence of local ulcers) and compared them with 44 matched healthy controls regarding their medical history, bone density measurements of the femoral neck and calcaneal bone ultrasound. Bone pain, myalgias and mobility restriction as well as routine laboratory parameters, serum vitamin D [25(OH)D], crosslaps (CTX), parathyroid hormone (PTH), osteocalcin (OC) and alkaline phosphatase (AP) were recorded and analysed. 25(OH)D was significantly lower in PAD IV patients (9.6+/-4.6 ng/ml, P<0.0001) as compared to PAD II stages and controls (19.0+/-7.6 and 19.1+/-9.1 ng/ml), paralleled by lower serum calcium [2.24+/-0.02 mmol/l, P=0.0002 versus PAD II (2.36+/-0.02) and P<0.0001 versus controls (2.39+/-0.02)] and higher iPTH serum levels (66.3+/-3.6 pg/ml, P<0.0001) as compared to PAD II patients (45.3+/-3.5) and healthy controls (38.5+/-2.4). Alkaline phosphatase and serum crosslaps values were significantly higher and age-adjusted bone density and bone ultrasound measurements significantly lower in PAD IV patients, who were also twice as likely to have bone pain and myalgias as PAD II patients. Bone ultrasound measurements correlated significantly with both clinical severity and pain as well as serological parameters of bone metabolism. Underlying PAD has a significant impact on bone density and metabolism as well as on bone and muscular pain. Patients with PAD are at high risk for osteoporosis and osteomalacia and should be regularly monitored and treated for their vitamin D deficiencies.
authors.affiliation: Department of Internal Medicine, Division of Endocrinology, University Medical Center, Graz, Austria.
authors.forename: Astrid
authors.initials: A
authors.lastname: Fahrleitner-Pammer
authors.forename: Andrea
authors.initials: A
authors.lastname: Obernosterer
authors.forename: Ernst
authors.initials: E
authors.lastname: Pilger
authors.forename: Harald
authors.initials: H
authors.lastname: Dobnig
authors.forename: Hans Peter
authors.initials: HP
authors.lastname: Dimai
authors.forename: Georg
authors.initials: G
authors.lastname: Leb
authors.forename: Stefan
authors.initials: S
authors.lastname: Kudlacek
authors.forename: Barbara M
authors.initials: BM
authors.lastname: Obermayer-Pietsch
mesh_terms: D015502:Absorptiometry, Photon; D000368:Aged; D000704:Analysis of Variance; D016723:Bone Remodeling; D016022:Case-Control Studies; D005260:Female; D006801:Humans; D008297:Male; D010018:Osteomalacia / Q000209:etiology / Q000378:metabolism / Q000503:physiopathology; D015663:Osteoporosis, Postmenopausal / Q000209:etiology* / Q000378:metabolism / Q000503:physiopathology; D016491:Peripheral Vascular Diseases / Q000150:complications* / Q000378:metabolism / Q000503:physiopathology; D012307:Risk Factors; D014808:Vitamin D Deficiency / Q000150:complications* / Q000378:metabolism / Q000503:physiopathology
references.citation: Eur J Clin Invest. 2000 Oct;30(10 ):895-9
references.pmid: 11029604
references.citation: J Gen Intern Med. 2002 Sep;17(9):663-9
references.pmid: 12220361
references.citation: Endocr Rev. 2001 Aug;22(4):477-501
references.pmid: 11493580
references.citation: Calcif Tissue Int. 1999 Jun;64(6):485-9
references.pmid: 10341020
references.citation: Calcif Tissue Int. 2003 Jul;73(1):15-20
references.pmid: 14506949
references.citation: Osteoporos Int. 1994;4 Suppl 1:71-6
references.pmid: 8081065
references.citation: Maturitas. 2003 Apr 25;44(4):259-65
references.pmid: 12697366
references.citation: J Gen Intern Med. 2001 Jun;16(6):384-90
references.pmid: 11422635
references.citation: Calcif Tissue Int. 2002 Jun;70(6):443-9
references.pmid: 11976772
references.citation: Lancet. 2002 May 18;359(9319):1761-7
references.pmid: 12049882
references.citation: Osteoporos Int. 2003 Jul;14(7):577-82
references.pmid: 12856111
references.citation: J Bone Miner Res. 2000 Jun;15(6):1113-8
references.pmid: 10841179
references.citation: Osteoporos Int. 1998;8(6):563-9
references.pmid: 10326062
references.citation: Calcif Tissue Int. 2000 Jun;66(6):419-24
references.pmid: 10821877
references.citation: Osteoporos Int. 2002 Jul;13(7):523-6
references.pmid: 12111011
references.citation: Clin Exp Rheumatol. 2003 Jan-Feb;21(1):103-6
references.pmid: 12673899
references.citation: N Engl J Med. 1998 Mar 19;338(12):777-83
references.pmid: 9504937
references.citation: N Engl J Med. 1992 Dec 3;327(23 ):1637-42
references.pmid: 1331788
references.citation: Eur J Clin Invest. 2003 Apr;33(4):323-31
references.pmid: 12662163
references.citation: J Gen Intern Med. 2002 Sep;17(9):733-5
references.pmid: 12220371
references.citation: J Bone Miner Res. 2003 Jul;18(7):1261-6
references.pmid: 12854836
references.citation: N Engl J Med. 1997 Sep 4;337(10):670-6
references.pmid: 9278463
references.citation: J Clin Endocrinol Metab. 2000 Nov;85(11):4125-30
references.pmid: 11095443
references.citation: J Clin Endocrinol Metab. 1996 Mar;81(3):1129-33
references.pmid: 8772587