Hypovitaminosis D, impaired bone turnover and low bone mass are common in patients with peripheral arterial disease.
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.
Fahrleitner-Pammer
Astrid
A
Department of Internal Medicine, Division of Endocrinology, University Medical Center, Graz, Austria.
Obernosterer
Andrea
A
Pilger
Ernst
E
Dobnig
Harald
H
Dimai
Hans Peter
HP
Leb
Georg
G
Kudlacek
Stefan
S
Obermayer-Pietsch
Barbara M
BM
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
Eur J Clin Invest. 2000 Oct;30(10 ):895-9
11029604
J Gen Intern Med. 2002 Sep;17(9):663-9
12220361
Endocr Rev. 2001 Aug;22(4):477-501
11493580
Calcif Tissue Int. 1999 Jun;64(6):485-9
10341020
Calcif Tissue Int. 2003 Jul;73(1):15-20
14506949
Osteoporos Int. 1994;4 Suppl 1:71-6
8081065
Maturitas. 2003 Apr 25;44(4):259-65
12697366
J Gen Intern Med. 2001 Jun;16(6):384-90
11422635
Calcif Tissue Int. 2002 Jun;70(6):443-9
11976772
Lancet. 2002 May 18;359(9319):1761-7
12049882
Osteoporos Int. 2003 Jul;14(7):577-82
12856111
J Bone Miner Res. 2000 Jun;15(6):1113-8
10841179
Osteoporos Int. 1998;8(6):563-9
10326062
Calcif Tissue Int. 2000 Jun;66(6):419-24
10821877
Osteoporos Int. 2002 Jul;13(7):523-6
12111011
Clin Exp Rheumatol. 2003 Jan-Feb;21(1):103-6
12673899
N Engl J Med. 1998 Mar 19;338(12):777-83
9504937
N Engl J Med. 1992 Dec 3;327(23 ):1637-42
1331788
Eur J Clin Invest. 2003 Apr;33(4):323-31
12662163
J Gen Intern Med. 2002 Sep;17(9):733-5
12220371
J Bone Miner Res. 2003 Jul;18(7):1261-6
12854836
N Engl J Med. 1997 Sep 4;337(10):670-6
9278463
J Clin Endocrinol Metab. 2000 Nov;85(11):4125-30
11095443
J Clin Endocrinol Metab. 1996 Mar;81(3):1129-33
8772587