TB andLeprosy are both strongly associated with poor Vitamin D receptor - which results in less vitamin D in blood from getting to tissues
- Leprosy 28 X more likely if a newly found Vitamin D Receptor modification (A61894G) – Dec 2017
- Vitamin D is treating and preventing Leprosy in Myanmar (Burma) - April 2019
- Includes many studies looking at Leprosy and Vitamin D Receptor
Items in both categories TB and Vitamin D Receptor gene are listed here:
- Certain types of Tuberculosis are 2X more likely with a poor Vitamin D Receptor – April 2019
- Tuberculosis increased risk if poor Vitamin D receptor varies by race – meta-analysis Feb 2019
- Pulmonary Tuberculosis 2X more likely if poor Vitamin D Receptor (Mexico) – April 2018
- TB risk in Blacks increased 20 percent having poor Vitamin D Receptors – Sept 2017
- Tuberculosis 1.3 times more likely if poor Vitamin D Receptor – meta-analysis Oct 2016
- Tuberculosis, genes and vitamin D – Meta-Analysis Dec 2013
Dermatol Clin. 2015 Jul;33(3):541-62. doi: 10.1016/j.det.2015.03.016.
Scollard DM1, Dacso MM2, Abad-Venida ML3.
- 1 National Hansen's Disease Programs, 1770 Physician Park Drive, Baton Rouge, LA 70816, USA. Electronic address: dscollard at hrsa.gov.
- 2 Center for Dermatology and Cosmetic Laser Surgery, 5026 Tennyson Parkway, Plano, TX 75024, USA; Department of Dermatology, University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, TX 75390-9069, USA.
- 3 Department of Dermatology, Jose R. Reyes Memorial Medical Center, Rizal Avenue, Manila 1008, Philippines.
Leprosy and tuberculosis are chronic mycobacterial infections that elicit granulomatous inflammation. Both infections are curable, but granulomatous injury to cutaneous structures, including cutaneous nerves in leprosy, may cause permanent damage. Both diseases are major global concerns: tuberculosis for its high prevalence and mortality, and leprosy for its persistent global presence and high rate of neuropathic disability. Cutaneous manifestations of both leprosy and tuberculosis are frequently subtle and challenging in dermatologic practice and often require a careful travel and social history and a high index of suspicion.
Mamm Genome. 2018 Aug;29(7-8):523-538. doi: 10.1007/s00335-018-9765-4. Epub 2018 Aug 16.
Dallmann-Sauer M1,2,3, Correa-Macedo W1,2,4, Schurr E5,6,7,8.
Mycobacterial diseases are caused by members of the genus Mycobacterium, acid-fast bacteria characterized by the presence of mycolic acids within their cell walls. Claiming almost 2 million lives every year, tuberculosis (TB) is the most common mycobacterial disease and is caused by infection with M. tuberculosis and, in rare cases, by M. bovis or M. africanum.
The second and third most common mycobacterial diseases are leprosy and buruli ulcer (BU), respectively. Both diseases affect the skin and can lead to permanent sequelae and deformities. Leprosy is caused by the uncultivable M. leprae while the etiological agent of BU is the environmental bacterium M. ulcerans. After exposure to these mycobacterial species, a majority of individuals will not progress to clinical disease and, among those who do, inter-individual variability in disease manifestation and outcome can be observed. Susceptibility to mycobacterial diseases carries a human genetic component and intense efforts have been applied over the past decades to decipher the exact nature of the genetic factors controlling disease susceptibility. While for BU this search was mostly conducted on the basis of candidate genes association studies, genome-wide approaches have been widely applied for TB and leprosy. In this review, we summarize some of the findings achieved by genome-wide linkage, association and transcriptome analyses in TB disease and leprosy and the recent genetic findings for BU susceptibility.