الفهرس 
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Abstract
Non-specific LBP is one of the most prevalentmusculoskeletal disorders involving any age group. It is the leading cause of disability and socioeconomic burden. Most people will have at least one episode of LBP in their life. There is a growing evidence have demonstrated that non-specific chronic LBP is a multifactorial problem involving a complex interaction of biopsychosocial factors in addition to structural and physiological abnormalities in the lumbar region and play a prominent role in its pathophysiology.
Vitamin D plays a significant role in the regulation of calcium and phosphorus homeostasis which is essential for bone formation, maintenance and remodeling in addition to regulation of the neuromuscular function. Furthermore, maintenance of adequate levels of vitamin D is essential to exert skeletal and extra-skeletal functions. It has been established that mild vitamin D deficiency has been linked to various non-specific musculoskeletal complaints such as myopathy, myalgia, paraesthesia and bone tenderness as well as prolonged chronic vitamin D deficiency lead to osteomalacia.
It has been documented that low vitamin D levels are able to exert anatomic, hormonal, neurological and immunological impacts on these musculoskeletal manifestations. Thus low levels of vitamin D have been implicated as one of the underlying factors in the development of chronic non-specific musculoskeletal pain states such as non-specific LBP before clinical manifestations of osteomalacia become evident.
Our study was designed to measure the serum level of vitamin D in patients with non-specific LBP in order to correlate it with the pain and to determine its role in the disease.
The study included 30 patients complaining of non-specific chronic LBP aged between 18-40 years old compared to 10 age and sex matched healthy controls; they were subjected to full history taking with functional assessment for LBP related functional disability through self-reported questionnaire, clinical assessment of the back through clinical examination and back range of motion (ROM) examination, pain assessment by visual analogue scale (VAS) and Likert pain scale to evaluate severity of LBP, radiological assessment by plain x-rays anteroposterior and lateral views of the lumbosacral spine to confirm the diagnosis of non-specific chronic LBP after exclusion of all causes of specific LBP and laboratory investigations included serum calcium, phosphorus, alkaline phosphatase (ALP) and fasting blood sugar. Serum level of 25(OH) vitamin D was measured by ELISA using kits.
Our study has highlighted on the measurement of the serum level and status of 25(OH) vitamin D. By comparing its levels between patient and control groups, we found that the level of vitamin D in non-specific chronic LBP patients was highly significantly lower than the control group. The best cut-off value of serum 25(OH) vitamin D related to presence of non-specific chronic LBP between patients and controls, defined by ROC curve was ≤33.5ng/ml in 93.33% of patients compared with none of controls with highly statistically significant difference. We found thatthe serum level of 25(OH) vitamin D is deficient in 60% of patients, insufficient in 26.7% of patients and sufficient in 13% of patients and 100% of controls.
As regards the comparison of serum 25(OH) vitamin D levels among our patients, we found that the patients with straightening of lumbar spine denoting paraspinal muscles spasm through clinical examination had lower serum 25(OH) vitamin D with statistical significant difference compared to other patients who didn’t.
In our study, there are highly significant negative correlations between serum level of 25(OH) vitamin D and BMI, level of tenderness over the lumbar spine and VAS score and highly significant positive correlation with serum calcium level. Moreover, we found significant negative correlations between serum level of 25(OH) vitamin D and weight, functional assessment of LBP related disability and Likert pain scale score and significant positive correlations with forward flexion and extension by modified schober’s tests through back ROM examination.
Recent studies have not only revealed the high prevalence of vitamin Ddeficiency in non-specific chronic LBP patients but also showed that those patients with low vitamin D levels had lower functional capacity and more pain intensity. Therefore reduced serum vitamin D levels play as a contributing factor for develop¬ment of the non-specific chronic LBP. Several follow-up studies have shown that vitamin D replacementtherapy in patients presenting with non-specific chronic LBPcan be crucial inimproving LBP related functional disability and pain intensity in addition to normalization of the levels.
In conclusion, vitamin D deficiency is highly prevalent in the majority of our patients and should be consid¬ered a contributing factor in the etiology of non-specific chronic LBP. Vitamin D deficiency results in more LBP related functional disability and more pain intensity, so the assessment of vitamin D levels should be checked in non-specific musculoskeletal pain patients especially those presented with non-specific LBP and any deficiency must be treated for alleviation of symptoms and to improve the functional capacity.