In a subset of patients with the tt genotype of the TaqI vitamin D receptor and who are vitamin D deficient, vitamin D supplementation appears to hasten sputum culture conversion. There are no studies of vitamin D using the gold standard outcome of relapse, so the true benefit of vitamin D is not at present known.It was noted as early as the mid-19th century that cod liver oil (which is rich in vitamin D) improved patients with tuberculosis, and the mechanism for this is probably an enhancement of immune responses to tuberculosis.The addition of vitamin D appears to enhance the ability of monocytes and macrophages to kill M. tuberculosis in vitro as well as ameliorating potentially harmful effects of the human immune system. Another reason Vitamin D can be used as a treatment for mycobacterial infections like tuberculosis is because of pro-anti-inflammatory cytokines that are influenced by vitamin D. Vitamin D has a post-anti-inflammatory effect on tuberculosis. Other
arginine has some clinical evidence as an adjuvant. Mycobacterium vaccae has been completed in Phase III trials by Anhui Zhifei Longcom Biologic Pharmacy Co., Ltd., injectable Vaccae(TM) and Immunitor LLC., oral tablet Tubivac (V7). Latent tuberculosis
The treatment of latent tuberculosis infection (LTBI) is essential to controlling and eliminating TB by reducing the risk that TB infection will progress to disease.
Tracheobronchomalacia or TBM is a condition characterized by flaccidity of the tracheal support cartilage which leads to tracheal collapse. This condition can also affect the bronchi. There are two forms of this condition: primary TBM and secondary TBM. Primary TBM is congenital and starts as early as birth. It is mainly linked to genetic causes. Secondary TBM is acquired and starts in adulthood. It is mainly developed after an accident or chronic inflammation.Tracheobronchomalacia may also occur in people who have normal cartliginous structure of the trachea, but significant atrophy of the posterior wall, causing significant invagination of the trachea on expiration. In these cases it is more commonly known as Excessive Dynamic Airway Collapse (EDAC). Signs and symptoms
Initially TBM may be asymptomatic or some patients do not experience symptoms at all. In a progressive TBM case symptoms include:

shortness of breath
a cough
mucus build up
stridor (a wheeze-like sound on breathing out)
difficulty in breathing
bluish coloration to skin around the nose and mouth
Chronic coughSymptoms may become worse if the patient is stressed, sick, lying down, or forcing a cough. Cause
Congenital TBM is present from birth. Acquired TBM often has no clear cause but is frequently found together with other pulmonary diseases like asthma and Chronic obstructive pulmonary disease, as well as Gastroesophageal reflux disease. TBM can be caused by damage to the support cartilage or membranous wall of the trachea, this can be the result of physical trauma (such as from prolonged Tracheal intubation) or pathological changes caused by inflammatory diseases like Relapsing polychondritis.