The study identified and confirmed two independent susceptibility loci within the HLA region (r2 < 0.2): HLA-B/MICA (rs12524487, OR = 3.29, p = 5.57 × 10-16) and HLA-DQB1/HLA-DRB1 (rs113452171, OR = 2.34, p = 3.74 × 10-9; and rs189754752, OR = 2.47, p = 4.22 × 10-9). In addition, a genetic association was identified and confirmed between Takayasus arteritis and the FCGR2A/FCGR3A locus on chromosome 1 (rs10919543, OR = 1.81, p = 5.89 × 10-12). The risk allele at this locus results in increased mRNA expression of FCGR2A. In addition, a genetic association between IL12B and Takayasu arteritis was established (rs56167332, OR = 1.54, p = 2.18 × 10-8). A fifth genetic locus for the disease in an intergenic region on chromosome 21q22 downstream of PSMG1 was revealed (P=4.39X10-7). A recent genome-wide association study (GWAS) identified genetic susceptibility loci for Takayasu arteritis with a genome-wide level of significance in IL6 (rs2069837) (odds ratio [OR] 2.07, P = 6.70 × 10(-9)), RPS9/LILRB3 (rs11666543) (OR 1.65, P = 2.34 × 10(-8)), and the intergenic locus on chromosome 21q22 (rs2836878) (OR 1.79, P = 3.62 × 10(-10)). The genetic susceptibility locus in RPS9/LILRB3 lies within the leukocyte receptor complex gene cluster on chromosome 19q13.4, and the disease risk variant in this locus correlates with reduced expression of multiple genes including the inhibitory leukocyte immunoglobulin-like receptor gene LILRB3 (P = 2.29 × 10(-8)).
Respiratory distress – this could present in the form of stridor, use or reliance on accessory muscles of respiratory, nasal flaring, or wheeze. These signs may develop if glandular swelling is significant enough, resulting in airway obstruction. 3. Cranial nerve palsy – swelling increases the risk of compression of cranial nerves VII, IX and XII. Other diagnostic factors which are less common
1. Connective tissue disorder or Sjogren’s syndrome – history of Sjogren’s syndrome, or a concomitant connect tissue disorder such as systemic lupus erythematosus, rheumatoid arthritis, or scleroderma. 2. Recurrent painless swellings – indicative of underlying autoimmune aetiology. 3. Displacement of earlobe – may be present when swelling of the parotid gland is present. 4. Prodrome of tingling in the affected gland
5. Swelling on hard palate

Diagnostic tests
Tests available as part of diagnosing sialadenitis include:

Culture and sensitivity testing of exudate from salivary duct. Culturing of purulent discharge is advisable in acute presentations of sialadenitis to allow targeted antibiotic therapy. Full blood count if infection is suspected. Facial radiographs such as dental radiographic views should be taken to exclude an obstructive element due to presence of sialolith or evolving abscess. However, sialoliths with low calcium phosphate content may not be visible. Treatment
In chronic recurrent sialadenitis or chronic sclerosing sialadenitis, acute attacks are managed with conservative therapies such as hydration, analgesics (mainly NSAIDs), sialogogues to stimulate salivary secretion, and regular, gentle gland massage. If infection is present, appropriate cultures should be obtained, followed by empirical antibiotic therapy initially, for example amoxicillin/clavulanate or clindamycin which cover oral flora.