Gastrointestinal (GI) involvement in the pathogenesis of Parkinson’s Disease (PD) has been widely recognized and supported in recent literature. Prospective and retrospective studies found non-motor symptoms within the GI, specifically constipation, precede cardinal signs and cognitive decline by almost 20 years. In 2002, Braak et al. were the first to propose that PD is a six-stage propagating neuropathological process originating from the GI tract (GIT). Aggregated α-synuclein (α-syn) protein from the GIT is pathognomonic for the development of PD. This article reviews the current literature from the past 10 years as well as original research found in PubMed on the combined effects of enteric glial cells and lectins on the development of Parkinson’s Disease. Studies have found that these aggregated and phosphorylated proteins gain access to the brain via retrograde transport through fast and slow fibers of intestinal neurons. Plant lectins, commonly found within plant-based diets, have been found to induce Leaky Gut Syndrome and can activate enteric glial cells, causing the release of pro-inflammatory cytokines. Oxidative stress on the enteric neurons, caused by a chronic neuro-inflammatory state, can cause a-syn aggregation and lead to Lewy Body formation, a hallmark finding in PD. Although the current literature provides a connection between the consumption of plant lectins and the pathophysiology of PD, further research is required to evaluate confounding variables such as food antigen mimicry and other harmful substances found in our diets.
Diffuse alveolar hemorrhage (DAH) is a potentially life-threatening pulmonary pathology which results in intra-alveolar hemorrhage secondary to disruption of the alveolar capillary basement membrane. Most commonly, these patients present with hemoptysis, hypoxemia and pulmonary infiltrates. Although rare, sevoflurane, an inhalational anesthetic used as a rapid induction agent for anesthesia may be implicated in the etiology of DAH. We report a case of a 21-year-old otherwise healthy male found to have postoperative diffuse alveolar hemorrhage secondary to sevoflurane inhalation. Thus far, only five documented cases describing sevoflurane induced diffuse alveolar hemorrhage have been described in the literature, with prior cases also showing a clear temporal association between sevoflurane administration and symptom onset. Although uncommon, we must take sevoflurane into consideration as a possible etiology of diffuse alveolar hemorrhage when encountering signs of respiratory distress and hemoptysis in postoperative patients.
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