Disease relevance of Parotitis

• The changes of Lf in parotitis parallel recent findings in mastitis and pancreatitis [1].
• The adverse effects of the IRX-2 protocol were negligible except for an allergic skin rash (n = 1) and parotiditis (n = 1) [2].
• Neonatal suppurative parotitis possibly associated with congenital cytomegalovirus infection and maternal methyldopa administration [3].
• Hyperglycemia and acute parotitis related to L-asparaginase therapy [4].
• Just as in chronic recurrent parotitis, increased activity of salivary glandular kallikrein in radio-iodine sialadenitis was measured [5].

High impact information on Parotitis

• Nifedipine-induced parotitis [6].
• Recurrent parotitis with H2 receptor antagonists [7].
• Of the nine patients included in this study, five with proven unilateral parotitis initially had diffuse high uptake of 99mTc-pertechnetate in the affected glands with adequate washout following vitamin C stimulation [8].
• Acute pancreatitis and parotitis induced by methimazole in a patient with Graves' disease [9].
• The presence of CEA could be demonstrated at the border of the acinar cells and the intercalated duct cells as well as in the undifferentiated duct cells as observed in chronic obstructive parotitis [10].

Chemical compound and disease context of Parotitis

• During the active phase of chronic recurrent parotitis there is a marked elevation in the parotid concentration of lactoferrin (Lf), and iron-binding glycoprotein with antibacterial properties [1].
• Acute suppurative parotitis in a patient on total parenteral nutrition [11].
• There is inadequate literature on the histamine (H2) receptor blockers, interferon-alpha, doxycycline, trimipramine, nifedipine, methyldopa, nitrofurantoin, nicardipine, isoproterenol or ritodrine to link them as aetiological agents in the development of parotitis [12].
• Antipsychotics, particularly thioridazine, have been associated with parotitis [12].
• Phenylbutazone and oxyphenbutazone have a significant number of reports suggesting that these drugs may be implicated in causing parotitis [12].

Gene context of Parotitis

• AIM: We inquired about the possibility of a familial trend in juvenile parotitis and evaluated the role of SPINK1 mutations in juvenile parotitis [13].
• In our present study, seven patients with acute exacerbated chronic recurrent parotitis were treated with the kallikrein inhibitor aprotinin (Trasylol, Bayer AG, Leverkusen) [14].
• This variant was designated C2 and it was associated with parotitis [15].
• METHODS: During an epidemic outbreak of parotiditis 48 clinical samples (saliva swabs and CSF) were studied [16].
• RESULTS: Brain stem microglial nodules and lymphocytic infiltrates in liver and kidneys are strongly associated with CMV parotitis; their incidence diminishes with increasing age [17].

Analytical, diagnostic and therapeutic context of Parotitis

• Occlusion of Stenon's duct by prolamine: a possible treatment of chronic parotitis? Preliminary experience from animal experiments [18].
• Immunosuppression and withdrawal of sulphasalazine resulted in rapid resolution of the parotitis and disappearance of autoantibodies [19].

References