Abstract
Patients with spinal cord injury (SCI) have an increased susceptibility to ulcers of the skin due to pressure. Immediately after the injury, SCI patients have a greatly increased degradation of collagen from both bone and skin. Loss of collagen from the skin could account for a reduction of the skin's ability to resist mechanical insults. This paper describes the results of an investigation into the role of collagen metabolism in the etiology of pressure ulcers. Skin biopsies have been obtained from healthy non-paralysed volunteers, and from insensitive and sensitive skin in SCI patients. The amino acid content of the insensitive skin was considerably lower than in sensitive skin. The activity of the enzyme lysyl hydroxylase was also lower in the insensitive skin. Lysyl hydroxylase activity in the sensitive skin was similar to enzyme activity in control skin biopsies of the same body area.
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Anderson P, Ardley M 1979 Psychosocial factors associated with pressure sores. Archives of Physical and Medical Rehabilitation 60: 341–346.
Bradford M M 1976 A rapid and sensitive method for the quantitation of microgram quantities of protein utilising the principle of protein-dye binding. Analytical Biochemstry 72: 248–254.
Cardus D, McTaggart W G 1984 Total body water and its distribution in men with spinal cord injury. Archives of Physical and Medical Rehabilitation 65: 509–512.
Chantraine A, Delnaide P A 1976 Hydroelectrolytic determination in paraplegics (Total body water; exchangeable sodium and total body potassium). Paraplegia 14: 138–145.
Chantraine A 1978 Actual concept of osteoporosis in paraplegia. Paraplegia 16: 51–58.
Claus-Walker J et al 1977 The urinary excretion of collagen degradation products by quadriplegic patients and during weightlessness. Journal of Bone and Joint Surgery 59(A): 209–212.
Claus-Walker J 1980 Clinical implications of the disturbance in calcium and collagen metabolism in quadriplegia. International Journal of Rehabilitation Research 3: (4)540-541.
Claus-Walker J, Halstead L S 1981 Metabolic and endocrine changes in spinal cord injury. Part I. The nervous system before and after transection of the spinal cord. Archives of Physical and Medical Rehabilitation 62: 595–601.
Claus-Walker J, Halstead L S 1982 Metabolic and endocrine changes in spinal cord injury. Part II. Section 1. Consequences of partial decentralisation of the automatic nervous system. Archives of Physical and Medical Rehabilitation 63(11): 569–575.
Claus-Walker J, Halstead L S 1982 Metabolic and endocrine changes in spinal cord injury. Part II, Section 2. Partial decentralisation of the autonomic nervous system, continued. Archives of Physical Medical Rehabilitation 63(11): 576–580.
Claus-Walker J, Halstead L S 1982 Metabolic and endocrine changes in spinal cord injury. Part III. Less quanta of sensory input plus bedrest and illness. Archives of Physical and Medical Rehabilitation 63(12): 628–631.
Claus-Walker J, Halstead L S 1982 Metabolic and endocrine changes in spinal cord injury. Part IV. Compounded neurologic dysfunctions. Archives of Physical and Medical Rehabilitation 63(12): 632–638.
Greenway R M et al 1970 Long-term changes in gross body composition of paraplegic and quadriplegic patients. Paraplegia 7: 301–318.
Hunt R K et al 1978 Anaerobic metabolism and wound healing: An hypothesis for the initiation and cessation of collagen synthesis in wounds. American Journal of Surgery 135: 328.
Hunter T, Rajan K T 1971 The role of ascorbic acid in the pathogenesis and treatment of pressure sores. Paraplegia 8: 211.
Lindan R et al 1980 Incidence and clinical features of autonomic dysreflexia in patients with spinal cord injury. Paraplegia 18: 285–292.
Mathias C J et al 1975 Plasma catecholamines, plasma renin activity and plasma aldosterone in tetraplegic man, horizontal and tilted. Clinical Science of Molecular Medicine 49: 291–299.
Miller R L 1972 Rapid assay for lysyl-protocollagen hydroxylase activity. Analytical Biochemistry 45: 202–210.
Nemethy G, Scheraga H A 1986 Stabilization of collagen fibrils by hydroxyproline. Biochemistry 25: 3184–3188.
Peterkofsky B, DiBlasio R 1975 Modification of the tritium release assays for prolyl and lysyl hydroxylases using Dowex-50 columns. Analytical Biochemistry 66: 279–286.
Pilonchery G et al 1983 Urinary elimination of glycosaminoglycans during the immobilization osteoporosis of spinal cord injury patients. Clinical Orthopoedics 174: 230–235.
Prockop D J et al 1979 The biosynthesis of collagen and its disorders. New EnglandJournal of Medicine 301: 13–23.
Rodriguez G P, Claus-Walker J 1984 Measurement of hydroxylysine glycosides in urine and its application to spinal cord injury. Journal of Chromatography 308: 65–73.
Rodriguez G P et al 1986 Adrenergic receptors in insensitive skin of spinal cord injury patients. Archives of Physical and Medical Rehabilitation 67: 177–180.
Singh J et al 1977 Urinary excretion of glycosaminoglycans in quadriplegia. Proceedings of the Society of Experimental Biological Medicine 156: 488–490.
Stover S L, Fine P R (eds) 1986 Spinal Cord Injury: The facts and figures. The University of Alabama at Birmingham, Alabama.
Traub W 1974 Some stereochemical implications of the molecular conformation of collagen. Israel Journal of Chemistry 12: 435–439.
Turpeenniemi-Hujanen M, Puistola U, Kivirikko K I 1980 Isolation of lysyl hydroxylase, an enzyme of collagen synthesis, from chick embryos as a homogeneous protein. Biochemistry Journal 189: 247–253.
Young J S and Burns PE 1981 Pressure sores and the spinal cord injured. SCI Digest 3(3): 9–17.
Ibid, 1981 SCI Digest 3(4): 11–23.
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Rodriguez, G., Claus-Walker, J. Biochemical changes in skin composition in spinal cord injury: a possible contribution to decubitus ulcers. Spinal Cord 26, 302–309 (1988). https://doi.org/10.1038/sc.1988.45
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DOI: https://doi.org/10.1038/sc.1988.45