Medicina clinica (English ed.)最新文献

Background and objective

Temporomandibular disorders (TMDs) are a common pathology, associated with pain in the facial territory and with associated psychological disorders, such as anxiety and depression. The aim of this study was to evaluate the efficacy of antidepressants in the treatment of pain associated with TMD.

Materials and methods

Sixty four patients suffering from chronic orofacial pain, randomly distributed in 3 groups: control group treated with night splint, group treated with 10 mg/day of citalopram and group treated with 25 mg/day of amitriptyline. Pain intensity was assessed, randomly, by a single blinded evaluator, according to the VAS at baseline and after one, three, six and nine weeks.

Results

All groups showed a reduction of pain throughout the period of time evaluated, however, the group treated with amitriptyline showed the best pain reduction results 3.3 ± 1.5, 1.5 ± 1.4 and 0.9 ± 1.3 at 3, 6 and 9 weeks, respectively.

Conclusions

Low doses of amitriptyline appear to be a good therapeutic option in patients with TMDs suffering from chronic orofacial pain.

Background

Diabetic peripheral neuropathy (DPN) is the most dominant cause of neuropathy worldwide, and there has been no specific treatment until now. The aim of the current study was to assess the probable protective effect of empagliflozin in type 2 diabetics who are suffering from DPN.

Methods

Fifty eligible type 2 diabetes mellitus (T2DM) cases with diabetic peripheral neuropathy were recruited in this study and classified into 2 groups. Group I (n = 25) (control group) received placebo tablets once daily. Group II (n = 25) (empagliflozin group) received empagliflozin 25 mg once daily for three months. Empagliflozin efficacy was evaluated using electrophysiological studies, and HbA1c levels, the brief pain inventory short-form item (BPI-SF) score, the diabetic neuropathy symptom (DNS) score, the atherosclerotic cardiovascular disease (ASCVD) risk score, and the serum levels of neuron-specific enolase (NSE), malondialdehyde (MDA) and calprotectin (Calpro), lipid profile, and random blood glucose level (RBG).

Results

After three months, comparing the results of the empagliflozin arm to the control arm showed a significant improvement in the electrophysiological studies and a significant decrease in the BPI-SF score and the mean serum levels of NSE and MDA. However, no significant difference was determined in HbA1c, Calpro, lipid profile, and RBG levels. In addition, the DNS and ASCVD risk scores were not significantly different. The NSE and MDA levels were significantly negatively correlated with the electrophysiological parameters. However, the BPI-SF score showed a non-significant difference.

Conclusions

Empagliflozin may be a promising neuroprotective and therapeutic agent for diabetic peripheral neuropathy.

Trial registration Identifier: NCT05977465.

Introduction

The presence of cortical atrophy (focal or diffuse) prior to the development of symptoms of cognitive impairment could predict the earliest cases of neurodegenerative disease in patients with CRSD. We reviewed the usefulness of cranial CT and MRI as early markers of cortical atrophy in patients with RSBD at our center.

Patients and methods

Retrospective observational descriptive analysis of patients diagnosed with RSBD from October 2012 to October 2022. All with cranial CT or MRI, evaluated by a neuroradiologist.

Results

54 patients were included, 21 women (38.88%), 33 men (61.12%), mean age at diagnosis of TCSR: 69.04 ± 12.625. Of the 54 patients, 44 (81.48%) had imaging tests consistent with their age, and 10 had atrophy greater than expected for their age. Of the 54 patients, 21 (38.88%) with a diagnosis of neurodegenerative disease, 33 (61.12%) persist as idiopathic, almost all with more than 5 years of evolution (range of 1 to 10 years of evolution without diagnosis). Of the 10 (18.52%) patients with greater atrophy, all were diagnosed with neurodegenerative disease (8 in 1 year, 2 in 8 years).

Conclusions

Almost half of our series have developed a neurodegenerative disease in the first 10 years of evolution. The majority of them presented global cortical atrophy measured by the GCA scale in the first year of diagnosis, without other neurological symptoms. Patients who did not show cortical atrophy at diagnosis have not yet developed the neurodegenerative disease in 10 years of evolution. In our experience, the absence of cortical atrophy on cranial MRI or CT (measured by scales such as GCA) at the diagnosis of CRST seems to predict slower progression cases. These data should be corroborated with larger series.

Bronchiectasis is a clinical-radiological condition composed of irreversible bronchial dilation due to inflammation and infection of the airways, which causes respiratory symptoms, usually productive cough and infectious exacerbations. Bronchiectasis can have multiple causes, both pulmonary and extrapulmonary, and its clinical presentation is very heterogenous. Its prevalence is unknown, although up to 35%–50% of severe COPD and 25% of severe asthma present them, so their underdiagnosis is evident. Chronic bacterial bronchial infection is common, and Pseudomonas aeruginosa is the pathogen that has been found to imply a worse prognosis. Treatment of bronchiectasis has three fundamental characteristics: it must be multidisciplinary (involvement of several specialties), pyramidal (from primary care to the most specialized units) and multidimensional (management of all aspects that make up the disease).