ISSN 0972-978X 

  About COAA








Tuberculous Osteomyelitis and Vitamin D deficiency


Professor of Medicine, Calicut Medical College, Calicut, Kerala, India.
Address for Correspondence

PK Sasidharan,
Prof of Medicine, Medical College, Calicut, Kerala, India.

Key words: Tuberculosis, Vitamin D, Osteomyelitis,

J.Orthopaedics 2004;1(2)e3


Tuberculosis is very common in developing countries, and therefore we see all the manifestations including Tuberculous Osteomyelitis. But little is known about its association with vitamin D deficiency(1). The following is a case of Tuberculous Osteomyelitis with severe vitamin D deficiency the response to treatment was inadequate prior to the addition of vitamin D and calcium to antituberculous treatment.    

Case report

30 year old house wife presented with pain and swelling in left ankle region of ten days duration, initially diagnosed and treated as filarial cellulitis. There was no relief with DEC and Ampicillin+Cloxacillin from elsewhere.  She had no fever weight loss or any other constitutional symptoms at the time of presentation. There was no history of arthritis in any other joints, no history of rash or oral or genital ulcers. She was of average build and nourishment with no pallor, clubbing, lymphadenopathy or jaundice. There was no significant illness in the past. Her physical examination was unremarkable except for the swelling and redness at the left ankle and the lower end of tibia and permitted reasonable amount of passive movements and she could walk though there was pain. Except for the arthritis involving the left ankle she looked perfectly normal.  Hemoglobin was 12gm/dl, Total Count 8300, Polymorphs 60,Lymphocytes 37, Eosinophils 2, Monocytes 1; ESR 60mm, Uric acid 5mg/dl, RBS 100mg/dL. Mantaoux test was strongly positive. Serum Ca 9.9mg/dL, SerumPO4 was3.2mg/dL. ALP was not elevated. X-ray showed a suspicious lytic lesion in the lower end of tibia. With this she was started on ATT, there was partial response to ATT but developed skin rash due to PZA which was discontinued. After a week there was high fever and her ESR was 120mm.Ofloxacin was added, investigations were reviewed. CXR was normal. Osteomyelitis suspected and referred  to orthopedic surgeon who did a biopsy which showed granuloma and epitheloid cells suggestive of Koch’s.  ATT continued but the response was very slow and inadequate. Meanwhile since the study on “Vitamin D deficiency  and Tuberculosis” was going on, we took a sample for serum 25(OH) vitamin D and the value came as 1ng/ml (normal being  9-30ng/ml). She was not improving as expected with ATT but after adding Vitamin D and calcium to the ATT she made a steady recovery. ATT was continued for a total of one year. 



Vitamin- D can be considered as a hormone rather than a vitamin, which regulates Calcium homeostasis, but the effects of vitamin-D deficiency are not confined to bone alone(2). Accumulating data give evidence that Vitamin-D is an important effector of macrophage functions and thus has a crucial role in limiting infections like Tuberculosis(3). Tuberculostatic functions are activated in human macrophages by stimulation with 1,25-dihydroxyvitamin-D3, the most active metabolite of Vitamin D. (4)

The author had observed Vitamin D deficiency since 1993, in cases of tuberculosis, and hypothesized that Vitamin D deficiency may be common in patients with tuberculosis, and that it could have a causal role. This is in view of its role in Cell Mediated Immunity (CMI), and also because of the well-known association of tuberculosis with malnutrition(5,6). The study done subsequently had documented vitamin D deficiency in patients with Tuberculosis unequivocally(7). The case presented is a prototype of such a situation. Vitamin D deficiency may not be symptomatic and even Calcium Phosphorus values are not always suggestive. Sunlight exposure alone is not enough to give adequate vitamin to the body, diet rich in vitamin D should be regularly consumed or there should be vitamin D supplementation.


1. Sasidharan PK, Rajeev E, Vijayakumari “Vitamin D deficiency and Tuberculosis” Journal of Association of Physicians of India” April 2002, volume 50, 554
2. Bar-Shavit Z, Noff D, Eldstein S, et al. 1,25- dihydroxyvitamin D3 and the regulation of macrophage function. Calcif Tissue Int. 1981; 33(6): 673-6.
3. Thomas MK, Lloyd-Jones DM, Thadani RJ, et al. Hypovitaminosis-D in medical inpatients. N Engl. J Med. 1998; 338; 777-83.
4. Awumey EM, Mitra DA, et al. Vitamin D metabolism is altered in Asian Indians in the southern United States: a clinical research center study. J Clin Endocrinol Metab 1998 Jan; 83(1): 169-73.
5. Rook GAW. The role of vitamin-D in tuberculosis. Am Rev Of Res. Dis. 1989; 138; 768-770.
6. Rook GAW, Steele J, Fraher L. Vitamin D3, gamma interferon and control of proliferation of mycobacterium tuberculosis by human monocytes. Immunology 1986; 57: 159-183.
7. The need for more vitamin D, New Eng. J Of Med. 1998. 334: 828-9.



 This is a peer reviewed paper 

Please cite as :

PK Sasidharan,
Tuberculous Osteomyelitis and Vitamin D deficiency
J.Orthopaedics 2004;1(2)e3





Arthrocon 2014


13th Summer Meet,16th March,2014

At Malabar Palace,
Calicut, Kerala, India

Download Registration Form

For Details
Dr Anwar Marthya,
Ph:+91 9961303044



Powered by



© Copyright of articles belongs to the respective authors unless otherwise specified.Verbatim copying, redistribution and storage of this article permitted provided no restrictions are imposed on the access and a hyperlink to the original article in Journal of Orthopaedics maintained. All opinion stated are exclusively that of the author(s).
Journal of Orthopaedics upholds the policy of Open Access to Scientific literature.