Primary parotid tuberculosis mimicking parotid neoplasm: a case report

<p>Abstract</p> <p>Introduction</p> <p>Tuberculosis of the parotid gland is a rare clinical entity which causes some difficulties in diagnosis because of the similarities in presentation to that of a neoplasm. Diagnosis mainly relies in the treating physician having a high index of suspicion. The diagnosis is generally overlooked by otolaryngologists and most cases are undergoing unnecessary surgery.</p> <p>Case presentation</p> <p>A 20-year-old male presented with a mass in the right parotid region. The mass had been present for one year. Physical examination revealed a mobile, non-tender mass occupying the superficial lobe of the right parotid gland. Radiologic investigations revealed a well-defined, solid, mass lesion located in the posterior part of the superficial lobe of the right parotid gland. A provisional diagnosis of a neoplasm of the parotid gland was made and a right superficial parotidectomy was performed. Histopathologic examination of the specimen was reported as tuberculosis of the parotid gland. The patient was commenced on antitubercular chemotherapy.</p> <p>Conclusion</p> <p>Although rare, tuberculosis should be kept in mind and considered in the differential diagnosis of patients presenting with a solitary tumor in the parotid gland in order to avoid unnecessary surgery.</p

Curcumin ameliorates impaired insulin/IGF signalling and memory deficit in a streptozotocin-treated rat model

Increased serum insulin levels and reduced peripheral insulin activities seen in insulin resistance syndrome are associated with age-dependent cognitive impairment and Sporadic Alzheimer’s Disease (SAD), suggesting a disturbance in the insulin signalling system in the brain and possibly being one of the causes of dementia. Therefore, the streptozotocin (STZ)-induced animal may be an appropriate model for the investigation of SAD and related dementia. This study was designed to investigate the beneficial effect of Curcumin (CUR), a neuroprotective agent, on intracerebroventricular (ICV) STZ-induced cognitive impairment in rats. For this purpose, adult male Wistar rats were bilaterally ICV injected with STZ (3 mg/kg). An artificial cerebrospinal fluid (aCSF) was given to the control group (SHAM) instead of STZ on days 1 and 3. Learning and memory performance were assessed using the “passive avoidance task” and the “Morris water maze test”. After confirmation of acquisition impairment with these tests, the STZ group was divided into two subgroups: STZ + vehicle (Vh) and STZ + CUR. The rats in the SHAM and STZ + Vh groups were administered intraperitoneally with 0.5 ml Vh and the rats in the STZ + CUR group were treated intraperitoneally with CUR (300 mg kg−1 day−1 in Vh) for 10 days starting from the 25th day after STZ injection. The Morris water maze test was reapplied on the 35th day after STZ injection and all of the rats were sacrificed on day 36 for quantitation of IGF-1 and for histopathological evaluation. Rats in the STZ + CUR group were found to have a higher performance in cognitive tests than rats in the STZ + Vh group (P < 0.01). In parallel with the cognitive tests, IGF-1 levels were decreased in all of the STZ-injected groups (1.78 ± 0.34) compared to the SHAM group (3.46 ± 0.41). In contrast, CUR treatment significantly increased IGF-1 levels (P < 0.001). The degree of neuronal loss decreased after CUR treatment compared to the SHAM group (P < 0.02). These results clearly indicate that CUR treatment is effective in reducing the cognitive impairment caused by STZ in rats, and may be a potential therapeutic agent for altering neurodegeneration in SAD