Idiopathic (primary) achalasia

Idiopathic achalasia is a primary esophageal motor disorder characterized by esophageal aperistalsis and abnormal lower esophageal sphincter (LES) relaxation in response to deglutition. It is a rare disease with an annual incidence of approximately 1/100,000 and a prevalence rate of 1/10,000. The disease can occur at any age, with a similar rate in men and women, but is usually diagnosed between 25 and 60 years. It is characterized predominantly by dysphagia to solids and liquids, bland regurgitation, and chest pain. Weight loss (usually between 5 to 10 kg) is present in most but not in all patients. Heartburn occurs in 27%–42% of achalasia patients. Etiology is unknown. Some familial cases have been reported, but the rarity of familial occurrence does not support the hypothesis that genetic inheritance is a significant etiologic factor. Association of achalasia with viral infections and auto-antibodies against myenteric plexus has been reported, but the causal relationship remains unclear. The diagnosis is based on history of the disease, radiography (barium esophagogram), and esophageal motility testing (esophageal manometry). Endoscopic examination is important to rule out malignancy as the cause of achalasia. Treatment is strictly palliative. Current medical and surgical therapeutic options (pneumatic dilation, surgical myotomy, and pharmacologic agents) aimed at reducing the LES pressure and facilitating esophageal emptying by gravity and hydrostatic pressure of retained food and liquids. Although it cannot be permanently cured, excellent palliation is available in over 90% of patients

Gender effect on clinical features of achalasia: a prospective study

BACKGROUND: Achalasia is a well-characterized esophageal motor disorder but the rarity of the disease limits performing large studies on its demographic and clinical features. METHODS: Prospectively, 213 achalasia patients (110 men and 103 women) were enrolled in the study. The diagnosis established by clinical, radiographic, and endoscopic as well as manometry criteria. All patients underwent a pre-designed clinical evaluation before and within 6 months after the treatment. RESULTS: Solid dysphagia was the most common clinical symptom in men and women. Chest pain was the only symptom which was significantly different between two groups and was more complained by women than men (70.9% vs. 54.5% P value= 0.03). Although the occurrence of chest pain significantly reduced after treatment in both groups (P < 0.001), it was still higher among women (32% vs. 20.9% P value= 0.04). In both sexes, chest pain did not relate to the symptom duration, LES pressure and type of treatment patients received. Also no significant relation was found between chest pain and other symptoms expressed by men and women before and after treatment. Chest pain was less frequently reported by patients over 56 yrs of age in comparison to those less than 56 yrs (p < 0.05). CONCLUSION: It seems that chest pain is the distinct symptom of achalasia which is affected by sex as well as age and does not relate to the duration of illness, LESP and the type of treatment achalasia patients receive

The Role of Dysregulated Neuroinflammatory Molecular Pathways in Parkinson Disease: A Systematic Review

Background: Parkinson disease (PD) is a prevalent neurodegenerative disorder affecting dopaminergic neurons in the substantia nigra (SN). Neuroinflammation has a vital role in PD pathophysiology. Objectives: This study assesses whether the neuroinflammatory molecular and signaling pathways could be associated with PD’s progression and clinical manifestations. Materials & Methods: PubMed, Web of Science, Embase, and Scopus databases were investigated from 2006 until December 2023 to find relevant studies. All observational studies written in English and reporting qualitative or quantitative information on the relationship between neuroinflammation and PD were included in this review. Results: Finally, 41 papers were involved in the systematic review. According to the involved studies, it is suggested that tumor necrosis factor-α, C-reactive protein, microsomal prostaglandin E synthase1, toll-like receptor-4 (TLR-4), CCL23, CCL25, TNF-receptor superfamily member 9, EV-derived cytokines, transforming growth factor alpha, vascular endothelial growth factor A, SH-SY5Y, TLR 2/4, miR-485-3p, leucine-rich repeat kinase 2, and α-synuclein may be upregulated in the PD patients. Also, the activity of astrocytes and microglial cells was reported to be increased in PD patients through different mechanisms.  Conclusion: This study demonstrated that the neurodegeneration in PD could be initiated by α-synuclein protein aggregation and the activation of astrocytes and microglial cells, which leads to neuroinflammation characterized by inflammatory responses in neurons. Finally, chronic neuroinflammation could be the cause of dopaminergic neuronal death in SN. The impact of both single and all factors involved in neuroinflammation was assessed to plan further studies in a particular pathway to intercept the onset of inflammatory pathways in favor of therapeutic purposes