Salivary Gland Dysfunction and Its Association with Hepatitis C Infection

We hypothesized that there was a difference in the unstimulated whole salivary flow rate (UWSR) in chronic HCV subjects compared to those with chronic liver disease (CLD) due to other causes.Purposes of this study:1. To compare UWSR and the prevalence of salivary hypofunction (UWSR<0.1mL/min) in chronic HCV and non-HCV subjects with CLD.2. To examine possible factors that may affect UWSR in subjects with CLD.3. To compare the correlation between UWSR and patient's subjective assessment of oral dryness, oral discomfort, difficulty in swallowing dry food and any food without additional liquids, difficulty in speaking and lip dryness, in patients with CLD.Methods: A case-control study examined 76 chronic HCV and 52 non-HCV subjects from a tertiary-referral liver clinic (n=128). None had known predisposing factors for salivary hypofunction. UWSR was measured and a 6-item visual analog scale (VAS) questionnaire was used to assess subjective symptoms of salivary gland dysfunction. An oral examination was done to identify lichenoid lesions. The Student's t-test and Pearson's correlation tests were used to compare groups and linear regression was used to identify predictors of salivary flow. Results: Mean age, proportion of male subjects and proportion with cirrhosis were comparable in chronic HCV and non-HCV groups. Mean UWSR (mL/min±S.D) and prevalence of salivary hypofunction were lower in the HCV versus non-HCV group (0.26±0.15 versus 0.30±0.21, p=0.22 and 10% versus 17%, p = 0.17). HCV status was associated with lower UWSR but in multivariate analysis only female gender, use of anticholinergic medication and presence of cirrhosis were statistically significant predictors of UWSR. All VAS scores were significantly higher in the HCV than non-HCV group (p<0.05). A moderately strong correlation between UWSR and VAS scores was shown amongst HCV subjects (r values -0.45 to -0.30). Conclusions: Reduced salivary flow is frequent in CLD patients and associated with cirrhosis, using anticholinergic medication and being female. Amongst patients with HCV, the moderately strong correlation between UWSR and VAS scores suggest the VAS questionnaire maybe a useful tool to screen for salivary hypofunction and lead to early implementation of preventive measures to avoid dental complications

Somatosensory profile of a patient with mixed connective tissue disease and Sjögren syndrome

BACKGROUND AND OVERVIEW: The authors report the case of a patient with mixed connective tissue disease (MCTD) and Sjögren syndrome, showing signs and symptoms of bilateral trigeminal neuropathy and aseptic meningitis. The patient was assessed by means of quantitative sensory testing (QST) according to the German Research Network on Neuropathic Pain standards, in both the gingiva and forearm, and the results were compared with those of healthy control participants. CASE DESCRIPTION: A 27-year-old woman, who had received a diagnosis of MCTD and Sjögren syndrome from a rheumatologist, sought treatment at an orofacial pain clinic for bilateral electriclike pain in the maxillary anterior gingiva, eyelids, and cheeks. QST indicated allodynia and hyperalgesia in response to mechanical and thermal stimuli in both her gingiva and forearm, and cold hyperalgesia in her forearm only. She had been prescribed an oral corticosteroid (prednisone, 7 milligrams per day) by the rheumatologist, and was given lidocaine gel and systemic pregabalin (400 mg/d) at the clinic. CONCLUSIONS AND PRACTICAL IMPLICATIONS: The cause of trigeminal neuropathy in MCTD and Sjögren syndrome (SS) is unknown. The QST data in this case showed that the somatosensory disturbance severity was higher in the gingiva than in the forearm, suggesting that the trigeminal nerve may be more susceptible than other parts of the nervous system in patients with MCTD. If reproducible in future studies, the finding of greater hypersensitivity in the gingiva than in the forearm may provide an opportunity for dentists to play a role in the detection, diagnosis, or both of MCTD and SS. Dentists must be sufficiently familiar with MCTD and SS to include them in their differential diagnoses and should consider performing simple neurosensory testing such as via intraoral cotton swab or pinprick test

Somatosensory profile of a patient with mixed connective tissue disease and Sjögren syndrome

BACKGROUND AND OVERVIEW: The authors report the case of a patient with mixed connective tissue disease (MCTD) and Sjögren syndrome, showing signs and symptoms of bilateral trigeminal neuropathy and aseptic meningitis. The patient was assessed by means of quantitative sensory testing (QST) according to the German Research Network on Neuropathic Pain standards, in both the gingiva and forearm, and the results were compared with those of healthy control participants. CASE DESCRIPTION: A 27-year-old woman, who had received a diagnosis of MCTD and Sjögren syndrome from a rheumatologist, sought treatment at an orofacial pain clinic for bilateral electriclike pain in the maxillary anterior gingiva, eyelids, and cheeks. QST indicated allodynia and hyperalgesia in response to mechanical and thermal stimuli in both her gingiva and forearm, and cold hyperalgesia in her forearm only. She had been prescribed an oral corticosteroid (prednisone, 7 milligrams per day) by the rheumatologist, and was given lidocaine gel and systemic pregabalin (400 mg/d) at the clinic. CONCLUSIONS AND PRACTICAL IMPLICATIONS: The cause of trigeminal neuropathy in MCTD and Sjögren syndrome (SS) is unknown. The QST data in this case showed that the somatosensory disturbance severity was higher in the gingiva than in the forearm, suggesting that the trigeminal nerve may be more susceptible than other parts of the nervous system in patients with MCTD. If reproducible in future studies, the finding of greater hypersensitivity in the gingiva than in the forearm may provide an opportunity for dentists to play a role in the detection, diagnosis, or both of MCTD and SS. Dentists must be sufficiently familiar with MCTD and SS to include them in their differential diagnoses and should consider performing simple neurosensory testing such as via intraoral cotton swab or pinprick test

Empagliflozin in Patients with Chronic Kidney Disease

Background The effects of empagliflozin in patients with chronic kidney disease who are at risk for disease progression are not well understood. The EMPA-KIDNEY trial was designed to assess the effects of treatment with empagliflozin in a broad range of such patients. Methods We enrolled patients with chronic kidney disease who had an estimated glomerular filtration rate (eGFR) of at least 20 but less than 45 ml per minute per 1.73 m(2) of body-surface area, or who had an eGFR of at least 45 but less than 90 ml per minute per 1.73 m(2) with a urinary albumin-to-creatinine ratio (with albumin measured in milligrams and creatinine measured in grams) of at least 200. Patients were randomly assigned to receive empagliflozin (10 mg once daily) or matching placebo. The primary outcome was a composite of progression of kidney disease (defined as end-stage kidney disease, a sustained decrease in eGFR to < 10 ml per minute per 1.73 m(2), a sustained decrease in eGFR of & GE;40% from baseline, or death from renal causes) or death from cardiovascular causes. Results A total of 6609 patients underwent randomization. During a median of 2.0 years of follow-up, progression of kidney disease or death from cardiovascular causes occurred in 432 of 3304 patients (13.1%) in the empagliflozin group and in 558 of 3305 patients (16.9%) in the placebo group (hazard ratio, 0.72; 95% confidence interval [CI], 0.64 to 0.82; P < 0.001). Results were consistent among patients with or without diabetes and across subgroups defined according to eGFR ranges. The rate of hospitalization from any cause was lower in the empagliflozin group than in the placebo group (hazard ratio, 0.86; 95% CI, 0.78 to 0.95; P=0.003), but there were no significant between-group differences with respect to the composite outcome of hospitalization for heart failure or death from cardiovascular causes (which occurred in 4.0% in the empagliflozin group and 4.6% in the placebo group) or death from any cause (in 4.5% and 5.1%, respectively). The rates of serious adverse events were similar in the two groups. Conclusions Among a wide range of patients with chronic kidney disease who were at risk for disease progression, empagliflozin therapy led to a lower risk of progression of kidney disease or death from cardiovascular causes than placebo