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Neurofeedback in an Integrative Medical Practice
Published in Hanno W. Kirk, Restoring the Brain, 2020
20-year-old woman presented with 5-month history of nausea and vomiting spells that occurred at least daily. Associated symptoms included chronic fatigue, palpitations, flushing, diaphoresis, urgent need to defecate, syncope or near-syncope, anorexia, and 20 lb. weight loss. Medical work up included normal pelvic ultrasound, normal head and abdominal CT scans, normal colonoscopy, and unremarkable stool analysis. Upper endoscopy showed “reactive gastropathy.” Gastric emptying test was significant for markedly prolonged gastric emptying time and established a diagnosis of gastroparesis. Dynamic defecography demonstrated pelvic floor laxity with cystocele and rectocele. Blood work confirmed mild malnutrition with low albumin and vitamin D levels but had no signs of inflammation, hormonal dysfunction, or liver problems.
Environmental and Exposure-Related Deaths
Published in John M. Wayne, Cynthia A. Schandl, S. Erin Presnell, Forensic Pathology Review, 2017
John M. Wayne, Cynthia A. Schandl, S. Erin Presnell
Answer E is incorrect. Nonsteroidal anti-inflammatory drugs (NSAIDs) may also lead to gastric mucosal injury, but these changes, which may range from normal appearance to mucosal erosion, are characteristically at the gastroduodenal region, while these pictured lesions appear to affect the gastric body. In addition, if this was suspected, histological examination in this case would exclude ulceration and reactive gastropathy secondary to NSAID use.
Clinical pharmacology and therapeutics: nonopioids
Published in Nigel Sykes, Michael I Bennett, Chun-Su Yuan, Clinical Pain Management, 2008
The topical theory166 suggests that phosphatidylcholine and other zwitterionic phospholipids in gastric mucus and bile help protect mucosa from hydrochloric acid and bile salts. Acidic NSAIDs given orally combine with these molecules and neutralize their effect, also explaining why enterohepatic recirculation could have a significant effect. There is recent evidence of changes in mucin in reactive gastropathy from NSAIDs or bile reflux.167
The clinical toxicity of imidacloprid self-poisoning following the introduction of newer formulations
Published in Clinical Toxicology, 2021
Varan Perananthan, Fahim Mohamed, Seyed Shahmy, Indika Gawarammana, Andrew Dawson, Nicholas Buckley
Worse clinical outcomes in imidacloprid toxicity could be due to the higher dose seen in the latter cohort but also could be due to solvents, stabilisers and surfactants present in newer formulations of imidacloprid [22,23]. Stabilisers and surfactants in imidacloprid products vary between brands but are not generally disclosed. Common solvents in pesticide formulations vary from low toxicity substances (water, glycerol, propylene glycol, propylene carbonate) to more toxic hydrocarbons. Some formulations of imidacloprid contain N-methyl-2-pyrrolidone (NMP) and dimethylsulfoxide. NMP causes developmental toxicity in rat studies including decreased foetal body weight, incomplete ossification of skulls and malformations [24]. NMP may also cause central nervous depression, gastrointestinal irritation and hyperglycemia [15]. Features of gastrointestinal toxicity were common prior to 2007 and post 2010. Non-specific gastrointestinal symptoms can occur in large volumes of glycerol intake. Furthermore, NMP present in most formulations is corrosive and in large volumes can induce a reactive gastropathy causing abdominal pain [15].
Hyperplastic polyps arising in autoimmune metaplastic atrophic gastritis patients: is this a distinct clinicopathological entity?
Published in Scandinavian Journal of Gastroenterology, 2018
Hejun Zhang, Xueqiong Nie, Zhiqiang Song, Rongli Cui, Zhu Jin
The exact pathogenesis of GHPs is not known. In addition to H. pylori infection, AMAG and chemical/reactive gastropathy, GHPs could arise in association with diverse other forms of gastric diseases, such as lymphocytic gastritis or cytomegalovirus gastritis [8]. Regardless of the etiology, the GHP is a result of a prominent, reparative, or regenerative phenomenon following chronic mucosal injury. According to the hyperplasia–dysplasia–carcinoma sequence, the polyp grows larger and becomes pedunculated or sub-pedunculated in association with the underlying genetic changes, such as p53 gene mutation [3,4,19], and a dysplastic lesion appears, followed by the cancerous lesion. Animal models [31] and clinical observation [32] supported that hypergastrinemia promoted carcinogenesis in gastric corpus, and hypergastrinemia, secondary to AMAG or proton pump inhibitor therapy, has also been implicated in the causation and carcinogenesis of GHPs [19,23,29,33]. Binding to the cholecystokinin-2 receptor, which located on the ECL cells in corpus mucosa [34], gastrin promotes hyperplasia and carcinogenesis in the gastric corpus. In this study, all A-GHPs with carcinomatous transformation were located in the upper third of the stomach. A subset of antral mucosa of A-GHP patients in this study were examined by gastrin-immunohistochemical staining, showed the G-cell hyperplasia (>140/mm [35]) (Figure 2(F)).
A novel APOA1 frameshift mutation Glu120Glyfs*60 with upper gastrointestinal involvement and an indolent course
Published in Amyloid, 2023
Eli Muchtar, Surendra Dasari, Jason D. Theis, Laura Ongie, Huong T. Cabral, Ellen D. McPhail, Angela Dispenzieri, Morie A. Gertz, Karen L. Rech
The proband was a 22-year-old male presenting with reduced performance as a cross-country runner. Blood count was normal with haemoglobin of 13.6 g/dL and a normal mean corpuscular volume. Iron deficiency, however, was detected (ferritin 7.4 mcg/L, normal 22–275). He reported infrequent episodes of melena, usually after strenuous activity. Bowel movements were normal. The patient reported epigastric discomfort with meals. Weight was stable. The patient denied bleeding tendency. An oral ferrous sulfate was started, and ferritin mildly increased (26 mcg/L). Given possible melena history, esophagogastroduodenoscopy (EGD) was pursued. There were pigmented nonbleeding linear superficial gastric ulcers in the gastric body. Duodenum examination was unremarkable. Gastric biopsies from the ulcerative tissue demonstrated H-pylori-negative reactive gastropathy. A random duodenal biopsy demonstrated small bowel mucosa with sub-epithelial closely-packed Congo-red positive amyloid nodules (Figure 1(A,B)). Liquid chromatography tandem mass spectrometry (LC-MS/MS) was performed on peptides extracted from the Congo red-positive area, detecting increased apolipoprotein AI (APOAI) peptide spectral counts (Figure 1(C)), but peptide profile consistent with a known APOA1 gene variant was not found. There were no proteomic features suggestive of other amyloidosis types. As an APOA1 mutation was suspected, APOA1 gene sequencing was performed, revealing heterozygous thymidine duplication (c.428dupT), leading to a frameshift variant with glutamic acid at position 144 as the first amino acid changed, shifting the reading frame and replacing it for Glycine (Glu120Glyfs*60; p.Glu144Glyfs*60) (Supplementary Figure 1). The product of this DNA mutation was a truncated protein, shorter by 65 amino acid residues compared to the wild-type protein. With this frameshift data, the variant protein was subsequently confirmed by mass spectrometry (Figure 1(D,E); Supplementary Figure 2).