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P.K.Sasidharan
Professor of Medicine, Calicut Medical College, Calicut, Kerala,
India.
Address for Correspondence
PK Sasidharan,
Prof of Medicine, Medical College, Calicut, Kerala, India. |
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Key words:
Tuberculosis, Vitamin D, Osteomyelitis,
J.Orthopaedics 2004;1(2)e3
Introduction
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.
Discussion
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.
REFERENCES:
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.
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