Etiology Of Syndrome Research Articles

Traumatic and Non-traumatic Etiology of Complex Regional Pain Syndrome

Traumatic and Non-traumatic Etiology of Complex Regional Pain Syndrome

The Latest Data Concerning the Etiology and Pathogenesis of Irritable Bowel Syndrome.

Globally, irritable bowel syndrome (IBS) is present in approximately 10% of the population. While this condition does not pose a risk of complications, it has a substantial impact on the patient's quality of life. Moreover, this disease has a significant financial impact on healthcare systems. This includes the direct costs associated with the diagnosis and treatment of these patients, as well as the indirect costs that arise from work absenteeism and reduced productivity. In light of these data, recent research has focused on elucidating the pathophysiological basis of this condition in order to improve the quality of life for affected individuals. Despite extensive research to date, we still do not fully understand the precise mechanisms underlying IBS. Numerous studies have demonstrated the involvement of the gut-brain axis, visceral hypersensitivity, gastrointestinal dysmotility, gut microbiota dysbiosis, food allergies and intolerances, low-grade mucosal inflammation, genetic factors, and psychosocial factors. The acquisition of new data is crucial for the advancement of optimal therapeutic approaches aimed at enhancing the general health of these patients while simultaneously reducing the financial burden associated with this ailment.

Cochlear implantation in syndromic patients: difficulties and lessons learnt.

Identify the prevalence of syndromes in a cohort of patients who underwent cochlear implantation, to report on the presence of inner and middle ear malformations and highlight the surgical difficulties encountered. Observational, retrospective study. Tertiary referral children's hospital pediatric cochlear implant program. An IRB-approved retrospective chart review of children undergoing cochlear implantation at a tertiary academic medical center, from 2018 to 2023. Preoperative imaging data of syndromic patients in that cohort with special attention to the presence of inner ear or middle ear malformations were collected. Abnormal intraoperative findings and difficulties reported by the surgeons were also noted. 1024 children were unilaterally implanted for bilateral profound hearing loss. There were 45 cases diagnosed with associated syndromes (4.3%). The commonest syndromes were Jervell and Lange Nielsen (JLN) syndrome followed by Waardenberg syndrome (WS), in a prevalence of 34% and 32% respectively. These syndromes had no associated inner ear malformations (IEM). Less common syndromes included Branchio-oto-renal (BOR) syndrome, CHARGE association and Treacher Collins syndrome, 3 cases each, and keratosis icthyosis deafness syndrome (KID), Usher syndrome and Albino, 2 cases each and an H syndrome case. There were 9 cases (20%) with IEM, with 6 cases of perilymph gusher. Two cases had middle ear anomalies and one case had a facial nerve course abnormality. The outcome of these cases was similar to non-syndromic cases. Children with syndromic HL should be dealt with on a case by case scenario to diagnose inner and middle ear malformations. Additional disabilities can affect the rehabilitation procedures. All children with congenital hearing loss should undergo pediatric, cardiologic, ophthalmologic and nephrologic examination in order to exclude the syndromic etiology of hearing loss.

Proprotein convertase subtilisin/kexin type 9 and apelin in fibromyalgia syndrome.

This study aimed to investigate the potential roles of proprotein convertase subtilisin/ kexin type 9 (PCSK9) and apelin in the etiology of fibromyalgia syndrome (FS). The retrospective study was conducted between May 2022 and February 2023. Fifty-eight female FS patients (mean age: 45.2±9.9 years; range, 25 to 66 years) and 30 age- and body mass index-matched control subjects (mean age: 43.1±9.9 years; range, 26 to 67 years) were included in the study. Apelin and PCSK9 levels of all individuals were measured using appropriate methods. The levels of PCSK9 (173.2±62.2 vs. 75.1±44.1, p<0.001) and apelin (354.6±195.5 vs. 229.0±83.2, p<0.001) were significantly higher in patients with FS compared to the control group. A positive correlation was found between PCSK9 and apelin levels and various measures, including the Fibromyalgia Impact Questionnaire (FIQ), Symptom Severity Scale (SSS), Pittsburgh Sleep Quality Index (PSQI), and Beck Depression Inventory (BDI). Additionally, there was a positive correlation between apelin levels and FIQ, SSS, PSQI, Beck Anxiety Inventory, and BDI scores. The optimal cutoff value for PCSK9 in predicting FS was 110.0 ng/mL, with a sensitivity of 84.5% and specificity of 83.9% (area under the curve [AUC]=0.920, 95% confidence interval [CI]: 0.852-0.987, p<0.001). For apelin, the optimal cutoff value for predicting FS was 258.8 ng/L, with a sensitivity of 63.8% and specificity of 64.5% (AUC=0.732, 95% CI: 0.623-0.840, p<0.001). Our findings suggest that PCSK9 may play a role in FS etiology and potentially contribute to oxidative stress. Increased apelin levels may be a compensatory response to high oxidative stress, possibly leading to hyperalgesia. Both PCSK9 and apelin can be predictive markers for FS.

Etiologies of non-traumatic extremity compartment syndrome: A multi-center retrospective review

Determine the etiologies of non-traumatic extremity compartment syndrome (NTECS), understand the demographics of NTECS patients, describe their diagnostic workup and treatment, and establish their rate and cause of in-hospital mortality.This is a retrospective cohort study of all patients diagnosed with NTECS at two level 1 trauma centers between January 2006 and December 2019. Data pertaining to the etiology of NTECS, patient demographics, diagnostic and treatment modalities, and in-hospital mortality were collected from electronic medical records.A total of 572 patients were included in this study with an average age of 54±18 years. The etiologies of NTECS were categorized into one of seven groups: 233 hypercoagulable state, 113 found-down secondary to substance use, 68 hypocoaguable state, 58 perioperative positioning, 55 shock, 30 infection, and 15 intravenous/intraosseous (IV/IO) infiltration. Approximately 13 % of patients underwent a skin graft or flap procedures, while 13 % of patients required an extremity amputation. The in-hospital mortality was highest in patients who developed NTECS due to shock (58 %). The average in hospital-mortality for all NTECS etiologies was 20 %.While uncommon, many etiologies of NTECS exist and often manifest insidiously. 13% of patients who develop NTECS will require a skin graft / flap, or extremity amputation. 20 % of patients who develop NTECS die during their hospitalization. High clinical suspicion and future research in this field are necessary to improve clinical outcomes for these patients.Level IV: Retrospective review

Role of blood flow in intracanal pressure: a novel theory of carpal tunnel syndrome etiology

Carpal tunnel syndrome is the most common compressive neuropathy of the upper extremity. It is believed that the cause of carpal tunnel syndrome is an increase in intracanal pressure, which leads to disruption of the blood supply to the median nerve and the occurrence of neurological disorders. The level of interstitial pressure is an indicator that describes the state of the microvasculature of the surrounding tissues. However, the question of the influence of changes in blood flow on the development of carpal tunnel syndrome still remains open. Purpose: to study the role of blood flow in the formation of intracanal pressure and the development of carpal tunnel syndrome. Objectives of the study: 1. To evaluate pressure levels in the carpal tunnel in patients with carpal tunnel syndrome and in healthy volunteers; 2. To study changes in pressure in the carpal tunnel in the absence of blood circulation in the limb in patients with carpal tunnel syndrome and in healthy volunteers; 3. To assess changes in carpal tunnel pressure before and after median nerve decompression in patients with carpal tunnel syndrome. We studied 40 people of both sexes aged from 21 to 82 years (mean age 50.1 years), divided into 2 groups. Group I included 20 patients with an established diagnosis of primary carpal tunnel syndrome. Group II, the control group, included 20 healthy volunteers. All participants had interstitial pressure measured in the carpal tunnel. In group I, the patients with carpal tunnel syndrome, 4 measurements were performed: before the start of surgery before a tourniquet was applied, 5 minutes after the tourniquet was applied (in the absence of blood circulation), then intraoperatively after decompression was performed in the conditions of a tourniquet applied and 5 minutes after its removal and restoration of blood circulation. In group II, 2 measurements were taken: before applying the tourniquet and after removing it. It was revealed that with carpal tunnel syndrome, the pressure inside the tunnel increased from 8 mm Hg normally to 24.5 mm Hg. When decompression is performed in patients with primary compressive neuropathy of the median nerve, a significant decrease in pressure in the carpal tunnel is observed from 24.5 mm Hg to 8 mm Hg. Even a short-term cessation of blood circulation in the upper limb leads to an increase in pressure inside the carpal tunnel.

LEP rs7799039 and LEPR rs1137101 gene variants are not associated with clinical features in patients with metabolic syndrome in the Turkish population.

Genetic predisposition plays a role in the etiology of metabolic syndrome (MetS), an important health problem worldwide. Leptin (LEP), produced by adipose tissue, plays a crucial role in the development of MetS. In this study, we evaluated the effects of LEP and LEP receptor (LEPR) variants on clinical findings and risk of developing MetS in the Turkish population. A total of 320 patients were included in the study, of whom 150 were patients with MetS and 170 were healthy controls. DNA was extracted from blood samples. LEP rs7799039 and LEPR rs1137101 variants were genotyped using the polymerase chain reaction-based restriction fragment length polymorphism method. The genotype distributions of these variants and clinical and laboratory findings were compared. The LEP rs7799039 GA and AA genotypes and A allele frequencies were higher in participants with MetS than in the control group. For LEP rs7799039, the genotype AA-GA was higher in males, and the GG genotype was higher in females. On analyzing the clinical outcomes associated with these variants, it was observed that individuals possessing LEP rs7799039 GA and AA genotypes displayed elevated levels of triglycerides. In addition, those with the AG-GG genotype of LEPR rs1137101 had lower mean hemoglobin levels. Our results showed that the LEP rs7799039 and LEPR rs1137101 variants may be associated with both the risk of MetS development and clinical findings. Among the various contributors to MetS, a genetic predisposition is commonly recognized as the primary cause.

Early-onset palatal myoclonus in Wernekinck commissure syndrome secondary to caudal paramedian midbrain infarction: A case report and a mini review of the literature

IntroductionWernekinck commissure syndrome (WCS) is an extremely rare midbrain syndrome, which selectively destroys the decussation of the superior cerebellar peduncle and the central tegmental tract, which commonly presents with bilateral cerebellar ataxia, dysarthria, and internuclear ophthalmoplegia. Palatal myoclonus in Wernekinck commissure syndrome is uncommon and often occurs as a late phenomenon due to hypertrophic degeneration of bilateral inferior olivary nuclei. Material and methodA patient with WCS, admitted to our hospital from December 2023, was chosen for this study, and the syndrome's clinical manifestations, imaging features, and etiology were retrospectively analyzed based on the literature. A 68-year-old right-handed East Asian man presented with dizziness, slurred speech, difficulty with swallowing and walking, and rhythmic contractions of the soft palate. He had several risk factors for ischemic cerebrovascular diseases (age, sex, dyslipidemia, hypertension and smoking history). Brain magnetic resonance imaging showed hyperintensity of DWI and hypointensity of ADC at the caudal midbrain which was around the paramedian mesencephalic tegmentum anterior to the aqueduct of midbrain. ResultsHe was diagnosed with Wernekinck commissure syndrome (WCS) secondary to caudal paramedian midbrain infarction. He was started on dual antiplatelet therapy (aspirin and clopidogrel) and intensive statin therapy. Blood pressure and glucose were also adjusted. His symptoms improved rapidly, and he walked steadily and speak clearly after 7 days of treatment. ConclusionsPalatal myoclonus is known to occur as a late phenomenon due to hypertrophic degeneration of bilateral inferior olivary nuclei. However, Our case suggests that palatal myoclonus can occur in the early stages in WCS.

Etiology, Clinical Characteristics and Prognosis of Secondary Hemophagocytic Syndrome

To understand the etiology, clinical characteristics and prognosis of secondary hemophagocytic syndrome (HLH), so as to improve the understanding of HLH and reduce the rates of misdiagnosis and missed diagnosis of HLH. A retrospective study was conducted to analyze the cause, clinical characteristics, laboratory findings, therapy and outcomes of 75 adult patients with secondary HLH admitted to our hospital from January 2015 to December 2021. Follow-up continued until the last discharge time. Among 75 patients, infection-related HLH was the most common (45.33%), followed by lymphoma-related HLH (17.33%). Fever was the most common clinical manifestation (97.67%). Laboratory indicators such as NK cell activity (98.31% low or absent), sCD25 (93.22% increased), and serum ferritin (94.44% elevated) had higher sensitivity in diagnosis. By comparing the clinical manifestations and laboratory indicators of HLH patients with different causes, sex, lymph node enlargement and bone marrow morphology were more valuable for the diagnosis of primary disease (all P <0.05). By comparing the treatment and clinical outcomes of HLH patients with different causes, the highest clinical remission rate (83.3%) was achieved in patients with autoimmune disease-related HLH treated with hormone+cyclosporine (P <0.05). The overall 12-month survival rate of all patients was 26.7%, in which the infection-related HLH was the lowest (14.7%) while autoimmune disease-related HLH was the highest (63.6%). The causes and clinical characteristics of adult secondary HLH are varied, with poor prognosis and heterogeneity in disease severity. It is important to identify HLH cause early for diagnosis and needed to further understand HLH.

Clinical Utility of Plasma Microbial Cell-Free DNA Sequencing Among Immunocompromised Patients With Pneumonia.

Plasma microbial cell-free DNA (mcfDNA) sequencing can establish the etiology of multiple infectious syndromes by identifying microbial DNA in plasma. However, data are needed to define the clinical scenarios where this tool offers the highest clinical benefit. We conducted a prospective multicenter observational study that evaluated the impact of plasma mcfDNA sequencing compared with usual care testing among adults with hematologic malignancies. This is a secondary analysis of an expanded cohort that evaluated the clinical utility of plasma mcfDNA sequencing across prespecified and adjudicated outcomes. We examined the percentage of participants for whom plasma mcfDNA sequencing identified a probable cause of pneumonia or clinically relevant nonpneumonia infection. We then assessed potential changes in antimicrobial therapy based on plasma mcfDNA sequencing results and the potential for early mcfDNA testing to avoid bronchoscopy and its associated adverse events. Of 223 participants, at least 1 microbial detection by plasma mcfDNA sequencing was adjudicated as a probable cause of pneumonia in 57 (25.6%) and a clinically relevant nonpneumonia infection in 88 (39.5%). A probable cause of pneumonia was exclusively identified by plasma mcfDNA sequencing in 23 (10.3%) participants. Antimicrobial therapy would have changed for 41 (18.4%) participants had plasma mcfDNA results been available in real time. Among the 57 participants with a probable cause of pneumonia identified by plasma mcfDNA sequencing, bronchoscopy identified no additional probable cause of pneumonia in 52 (91.2%). Plasma mcfDNA sequencing could improve management of both pneumonia and other concurrent infections in immunocompromised patients with suspected pneumonia.

Neurocognitive Profile in Pediatric Kidney Transplant Candidates: Effects of Medical and Sociodemographic Factors.

We evaluated the effects of kidney failure etiology, dialysis, and sociodemographic factors on the subdomains of intellectual functioning in pediatric kidney transplant candidates. This retrospective study included 78 pediatric kidney transplant candidates who completed a Wechsler Intelligence Scale assessment during pre-transplant neuropsychological evaluation between 1/1/2010 and 10/31/2022. Linear regression models were employed to examine the effects of kidney failure etiology, dialysis status, neighborhood area deprivation, and race on subdomains of intellectual functioning. The mean scores of various intellectual functioning domains in pediatric kidney transplant candidates were significantly lower than in the general population (ps <0.001). After adjusting for covariates, patients with congenital anomalies of the kidney and urinary tract had significantly lower processing speed (M=85; 95% CI: 79-91) compared to patients with nephrotic syndrome (M=99; 95% CI: 90-107) and other etiologies (M=84; 95% CI: 78-90) (p=0.003). Patients living in high-level deprivation neighborhoods showed lower working memory performance (M=84, 95% CI: 77-91) than patients living in median-level (M=91, 95% CI: 87-95) and low-level (M=98, 95% CI: 92-104) neighborhood area deprivation (p=0.03). Patients from marginalized racial groups demonstrated lower verbal skills (M=80, 95% CI: 74-87) than White patients (M=92, 95% CI: 88-97) (p=0.02). Additionally, patients receiving dialysis showed higher reasoning skills (M=98, 95% CI: 90-104) than patients without dialysis (M= 90, 95% CI: 86-95) (p=0.04). Neurocognitive development in pediatric kidney transplant candidates is associated with medical and sociodemographic factors. Strategies to monitor, treat, and accommodate neurocognitive concerns need to be considered to optimize long-term medical and social outcomes.

Case presentation: a severe case of cobalamin c deficiency presenting with nephrotic syndrome, malignant hypertension and hemolytic anemia

BackgroundThe etiology of nephrotic syndrome can vary, with underlying metabolic diseases being a potential factor. Cobalamin C (cblC) defect is an autosomal recessive inborn error of metabolism caused by mutations in the MMACHC gene, resulting in impaired vitamin B12 processing. While cblC defect typically manifests with hematological and neurological symptoms, renal involvement is increasingly recognized but remains rare.Case PresentationWe describe a 7-month-old male patient presenting with fatigue and edema. His initial laboratory findings showed anemia, thrombocytopenia, hypoalbuminemia and proteinuria. Further examinations reveals hemolysis in peripheral blood smear. During his follow up respiratory distress due to pleural effusion in the right hemithorax was noticed. And fluid leakage to the third spaces supported a diagnosis of nephrotic syndrome. The patient’s condition deteriorated, leading to intensive care admission due to, hypertensive crisis, and respiratory distress. High total plasma homocysteine and low methionine levels raised suspicion of cobalamin metabolism disorders. Genetic testing confirmed biallelic MMACHC gene mutations, establishing the diagnosis of cblC defect. Treatment with hydroxycobalamin, folic acid, and betaine led to remarkable clinical improvement.Discussion/ConclusionThis case underscores the significance of recognizing metabolic disorders like cblC defect in atypical presentations of nephrotic syndrome. Early diagnosis and comprehensive management are vital to prevent irreversible renal damage. While cblC defects are more commonly associated with atypical hemolytic uremic syndrome, this case highlights the importance of considering cobalamin defects in the differential diagnosis of nephrotic syndrome, especially when associated with accompanying findings such as hemolysis. Our case, which has one of the highest homocysteine levels reported in the literature, emphasizes this situation again.

Las Bolitas Syndrome in Penaeus vannamei Hatcheries in Latin America.

In September 2023, several hatcheries in Latin America experienced significant mortality rates, up to 90%, in zoea stage 2 of Penaeus vannamei. Observations of fresh mounts revealed structures resembling lipid droplets, similar to those seen in a condition known as "las bolitas syndrome". Routine histopathological examinations identified detached cells and tissues in the digestive tracts of affected zoea, contrasting with the typical algal cell contents seen in healthy zoea. Polymerase chain reaction (PCR) testing for over 20 known shrimp pathogens indicated minimal differences between diseased and healthy batches. Both groups tested negative for acute hepatopancreatic necrosis disease (AHPND) but positive for Vibrio species and Rickettsia-like bacteria in the diseased samples. Histological analyses of the affected zoea revealed characteristic tissue degeneration in the hepatopancreas, forming spheres that eventually migrated into the upper gut, midgut, and midgut caeca, a pathology identified as bolitas syndrome (BS). Microbiological assessments revealed Vibrio species at concentrations of 106 CFU zoea/g in affected zoea, approximately two orders of magnitude higher than in healthy zoea. Bacterial isolation from both healthy and BS-affected zoea on thiosulphate-citrate-bile salts-sucrose (TCBS) agar and CHROMagar™ (Paris, France), followed by identification using API 20E, identified six strains of Vibrio alginolyticus. Despite similarities to "las bolitas syndrome" in fresh mounts, distinct histopathological differences were noted, particularly the presence of sloughed cells in the intestines and variations in hepatopancreatic lobes. This study highlights the critical need for further research to fully understand the etiology and pathology of bolitas syndrome in zoea stage 2 of P. vannamei to develop effective mitigation strategies for hatchery operations.

Clinical value of adding Dapagliflozin in patients with nephrotic syndrome.

Sodium-glucose cotransporter 2 (SGLT2) inhibitors in nephrotic patients on immunosuppression are underexplored. We evaluated dapagliflozin's impact in non-diabetic primary nephrotic syndrome. Randomized controlled clinical trial was conducted on 60 non-diabetic primary nephrotic syndrome patients, equally assigned to dapagliflozin and control groups. All patients received the standard of care medication and the Dapagliflozin group received 10mg dapagliflozin in addition. Demographic data, nephrotic syndrome etiology, proteinuria levels, eGFR, and immunosuppression doses, were well-matched. After 6months of follow up primary outcomes included changes in and eGFR. Both groups exhibited significant reductions in proteinuria after 6months, with the dapagliflozin group achieving a mean UPCR reduction of - 94.7%, and the control group - 86.7% (p < 0.001). However, the comparative change in proteinuria between both groups did not reach statistical significance (p = 0.158). Dapagliflozin initially led to a transient eGFR decline. Dapagliflozin also resulted in a significant mean body weight reduction (p < 0.001) and notable improvements in triglyceride levels compared to the control group (p = 0.045). In primary nephrotic syndrome patients, adjunct dapagliflozin may enhance the standard of care. While notable, the reduction in proteinuria was comparable to that of the control group by the study's end. Furthermore, after 6months, eGFR remained stable in both groups. However, significant weight loss and serum triglyceride reduction were particularly pronounced in the dapagliflozin group. Further long-term investigations are necessary to address potential immunosuppression-related confounding effects in patients with primary glomerular disease.

Exhaustive clinical examination of etiology and initial response to first-line treatment in 577 children with infantile epileptic spasm syndrome children: A 5-year retrospective observational study.

Employing whole-exome sequencing (WES) technology to investigate the etiology of infantile epileptic spasm syndrome (IESS), and determining whether different etiologies exhibit phenotypic variations, while elucidating the potential associated factors, might improve short-term responses to first-line treatment. We retrospectively evaluated patients with IESS admitted for treatment between January 2018 and June 2023. Clinical phenotypic differences among etiological classifications and clinical manifestations were analyzed. Variable selection using the best subset method was performed, followed by logistic regression analysis to identify the factors influencing treatment response. A total of 577 patients were included; 412 completed trio-WES. Magnetic resonance imaging abnormalities were detected in 387 patients (67.1%). Patients with etiology as structural abnormalities were likelier to have non-spasms at the initial seizure onset. A total of 532 patients completed the first-line treatment; 273 patients received it for the first time at our hospital (initial response rates: 30.1% and 42.1%, respectively). The response group had a lower proportion of early-onset seizures (≤3 months) than the no-response group (11.3% vs. 23.7%, p < 0.01 and 11.3% vs. 21.5%, p = 0.03, respectively). Logistic regression analysis indicated that earlier initiation of first-line treatment was associated with a higher likelihood of an initial response. However, the etiological classification did not have a significant impact on the initial response. IESS patients with structural abnormalities are more likely to present with non-spasm seizures at initial onset. Early initiation of first-line treatment is crucial; however, initial responses may be less favorable when seizures occur in early infancy.

Modern pharmacotherapy for cholestasis syndrome

Diseases of the hepatobiliary system today remain an urgent health problem worldwide. A significant percentage of gastroenterological patients are people suffering from cholestasis syndrome. In gastroenterology, there are a number of nosological forms accompanied by the development of cholestasis syndrome. This pathological condition has many etiological factors, but in general, the mechanisms of its formation for various reasons are largely similar. When working with this group of patients, it is necessary to take into account the peculiarities of the clinical picture, which may vary depending on the etiology of the cholestatic syndrome. The fact of the economic burden in this pathology is also important, because sometimes it is necessary to resort to high-tech examination methods and expensive laboratory screening to perform high-quality differential diagnosis. As for the treatment of cholestatic syndrome, at the moment there are many drugs with different mechanisms of action, the predominant part of which, according to randomized clinical trials and meta-analyses, has proven effectiveness. In this article, based on literature sources taken from foreign and domestic databases, the etiology and pathogenesis of the development of cholestasis syndrome, the clinical picture and approaches to the diagnosis of this condition are considered. When considering the treatment of cholestatic syndrome, this article focuses on therapy with ursodeoxycholic acid drugs, in particular Ecurochol. A clinical case is also considered on the example of a patient with cholestasis syndrome who was prescribed treatment with Ecurochol and who showed positive dynamics due to improvements in the ultrasound picture of the abdominal organs.

Determine The Risk Of Long-Term Complications In Patients With Acute Coronary Syndrome

The article is devoted to one of the current topics of modern healthcare - acute coronary syndrome (ACS). Most patients had associated and comorbid diseases, primarily such as stable angina, chronic heart failure, broncho-obstructive diseases and diabetes mellitus, which in some cases required treatment adjustments [1]. The article provides information on the etiology of acute coronary syndrome, clinical symptoms and risk factors that may develop in patients.

Coronary Plaque Erosion: Epidemiology, Diagnosis, and Treatment.

Plaque erosion (PE), a distinct etiology of acute coronary syndromes (ACSs), is often overshadowed by plaque ruptures (PRs). Concerning its epidemiology, PE has garnered increasing recognition, with recent studies revealing its prevalence to be approximately 40% among ACS patients, challenging earlier assumptions based on autopsy data. Notably, PE exhibits distinct epidemiological features, preferentially affecting younger demographics, particularly women, and often manifesting as a non-ST-segment elevation myocardial infarction. There are seasonal variations, with PE events being less common in winter, potentially linked to physiological changes and cholesterol solidification, while peaking in summer, warranting further investigation. Moving to molecular mechanisms, PE presents a unique profile characterized by a lesser degree of inflammation compared to PR, with endothelial shear stress emerging as a plausible molecular mechanism. Neutrophil activation, toll-like receptor-2 pathways, and hyaluronidase 2 expression are among the factors implicated in PE pathophysiology, underscoring its multifactorial nature. Advancements in intravascular imaging diagnostics, particularly optical coherence tomography and near-infrared spectroscopy coupled with intravascular ultrasound, offer unprecedented insights into plaque composition and morphology. Artificial intelligence algorithms show promise in enhancing diagnostic accuracy and streamlining image interpretation, augmenting clinician decision-making. Therapeutically, the management of PE evolves, with studies exploring less invasive approaches such as antithrombotic therapy without stenting, particularly in cases identified early through intravascular imaging. Additionally, the potential role of drug-coated balloons in reducing thrombus burden and minimizing future major adverse cardiovascular events warrants further investigation. Looking ahead, the integration of advanced imaging modalities, biomarkers, and artificial intelligence promises to revolutionize the diagnosis and treatment of coronary PE, ushering in a new era of personalized and precise cardiovascular care.

Aetiology of vaginal discharge, urethral discharge, and genital ulcer in sub-Saharan Africa: A systematic review and meta-regression.

Syndromic management is widely used to treat symptomatic sexually transmitted infections in settings without aetiologic diagnostics. However, underlying aetiologies and consequent treatment suitability are uncertain without regular assessment. This systematic review estimated the distribution, trends, and determinants of aetiologies for vaginal discharge, urethral discharge, and genital ulcer in sub-Saharan Africa (SSA). We searched Embase, MEDLINE, Global Health, Web of Science, and grey literature from inception until December 20, 2023, for observational studies reporting aetiologic diagnoses among symptomatic populations in SSA. We adjusted observations for diagnostic test performance, used generalised linear mixed-effects meta-regressions to generate estimates, and critically appraised studies using an adapted Joanna Briggs Institute checklist. Of 4,418 identified records, 206 reports were included from 190 studies in 32 countries conducted between 1969 and 2022. In 2015, estimated primary aetiologies for vaginal discharge were candidiasis (69.4% [95% confidence interval (CI): 44.3% to 86.6%], n = 50), bacterial vaginosis (50.0% [95% CI: 32.3% to 67.8%], n = 39), chlamydia (16.2% [95% CI: 8.6% to 28.5%], n = 50), and trichomoniasis (12.9% [95% CI: 7.7% to 20.7%], n = 80); for urethral discharge were gonorrhoea (77.1% [95% CI: 68.1% to 84.1%], n = 68) and chlamydia (21.9% [95% CI: 15.4% to 30.3%], n = 48); and for genital ulcer were herpes simplex virus type 2 (HSV-2) (48.3% [95% CI: 32.9% to 64.1%], n = 47) and syphilis (9.3% [95% CI: 6.4% to 13.4%], n = 117). Temporal variation was substantial, particularly for genital ulcer where HSV-2 replaced chancroid as the primary cause. Aetiologic distributions for each symptom were largely the same across regions and population strata, despite HIV status and age being significantly associated with several infection diagnoses. Limitations of the review include the absence of studies in 16 of 48 SSA countries, substantial heterogeneity in study observations, and impeded assessment of this variability due to incomplete or inconsistent reporting across studies. In our study, syndrome aetiologies in SSA aligned with World Health Organization guidelines without strong evidence of geographic or demographic variation, supporting broad guideline applicability. Temporal changes underscore the importance of regular aetiologic re-assessment for effective syndromic management. CRD42022348045.

Mental fatigue and chronic fatigue syndrome in clinical practice

Fatigue is an extremely disabling symptom both in healthy people and in various diseases. Physical fatigue is characterized by limitations in physical functioning, while mental/cognitive fatigue involves difficulties in concentrating and performing cognitive tasks. Mental and physical fatigue exist in both pathological and physiological fatigue. Fatigue is primarily an adaptive physiological process. It is a signal to have a rest and helps conserve energy to prevent injury, which can be useful after intense work, or when the body’s defenses need to be redistributed, for example, during infectious disease. It is important to distinguish between fatigue or tiredness and chronic fatigue syndrome in clinical practice. Chronic fatigue syndrome has multisystem manifestations and affects millions of people globally. Although the exact aetiology of chronic fatigue syndrome is uncertain, the studies point to neurological, immunological, autonomic and energy disorders. The main sings of chronic fatigue syndrome are debilitating fatigue that is worsened by activity, poor exercise tolerance, unrefreshing sleep and cognitive impairment. Reduced information processing speed is the most common cognitive impairment in chronic fatigue syndrome. Other manifestations include decreased reaction time, working memory, and attention. These symptoms must persist for at least 3–6 months for a diagnosis to be made. As there are no specific tests for chronic fatigue syndrome, a diagnosis can be established on the basis of a medical history and physical examination.Although there are no standards-based methods specific to chronic fatigue syndrome, clinicians can reduce the severity of symptoms using pharmacological and non-pharmacological treatment approaches that have proved their efficacy in clinical practice. In particular, nootropics are widely used in asthenic conditions and chronic fatigue syndrome. Fonturacetam is a nootropic drug that directly activates brain integration activities, promotes memory consolidation, and improves concentration and mental activity.