Ultrastructural differences between diabetic and idiopathic gastroparesis (original) (raw)
Related papers
Similarities and Differences Between Diabetic and Idiopathic Gastroparesis
Clinical Gastroenterology and Hepatology, 2011
Background & Aims-Gastroparesis can be diabetic or idiopathic, yet little is known about differences in their presentation. We compared clinical characteristics, symptoms, and gastric emptying in patients with type-1 or -2 diabetic (DG) or idiopathic (IG) gastroparesis.
Pathophysiology of Diabetic Gastroparesis
Diabetes, 1997
Our understanding of the nature of diabetic gastroparesis has advanced in the last decade due to new investigational procedures (electrogastrography, visceral evoked potential recording), and transferring these insights into clinical routine will be our task in the future. Meanwhile, the clinical relevance of gastroparesis—whether overt or silent—remains unquestioned: proper gastric emptying is a prerequisite for adequate metabolic control, and its disturbance may result not only in further progression of the chronic complications of the disease, but also in the false assumption that these patients are not compliant with their doctor's management—the patients just may have delayed emptying of their stomach without noticing it.
clinical practice Diabetic Gastroparesis
A 36-year-old man with a 20-year history of type 1 diabetes mellitus, background retinopathy, peripheral sensory neuropathy, and nephropathy presents with a history of several months of nausea and vomiting of undigested food and bile, during which time he lost 4 kg. On physical examination (performed 1 hour after the patient has eaten), his blood pressure is 130/80 mm Hg while he is lying down and 110/60 mm Hg while he is standing. His abdomen is not tender. There is epigastric distention, but no splash is audible when the upper abdomen is shaken. How should the gastrointestinal symptoms of this patient be evaluated and treated?
The Investigation and Treatment of Diabetic Gastroparesis
Clinical therapeutics, 2018
This review provides an update on the investigations and treatment options for gastroparesis. A comprehensive literature search of Medline, PubMed, Embase and OVID was conducted which included all systematic reviews and research articles that focused on the diagnosis, investigations and management diabetic gastroparesis. Dietary modifications and pharmacologic treatment with prokinetics to increase gastric motility form the mainstay of treatment. However, the use of prokinetics is limited by adverse effects and serious adverse effects, leaving metoclopramide as the only drug approved by the US Food and Drug Administration for the treatment of gastroparesis. Newer therapies, including motilin receptor agonists, ghrelin receptor agonists, and neurokinin receptor antagonists, are currently being investigated. Transpyloric stenting, gastric electrical stimulation, and gastric per-oral endoscopic myotomy provide mechanical options for intervention, and surgical interventions in severe in...
Pathophysiology of idiopathic gastroparesis and implications for therapy
Scandinavian Journal of Gastroenterology, 2019
Idiopathic gastroparesis is a gastric motility disorder characterized by chronic upper gastrointestinal symptoms and delayed gastric emptying without an identifiable underlying condition. This review summarizes recent understanding of the pathophysiology and treatment of idiopathic gastroparesis Materials and methods Structured literature search in the PubMed, Embase and ClinicalTrials.gov databases Results Idiopathic gastroparesis involves several alterations in gastric motility and sensation, including delayed gastric emptying, altered myoelectrical activity, impaired fundic accommodation, visceral hypersensitivity and disturbances in antropyloroduodenal motility and coordination. Multiple cellular changes have been identified, including depletion of interstitial cells of Cajal (ICC) and enteric nerves, as well as stromal fibrosis. The underlying cause of these changes is not fully understood, but may be an immune imbalance, including loss of anti-inflammatory heme-oxygenase-1 positive (HO-1) macrophages. There is currently no causal therapy for idiopathic gastroparesis. The treatment ladder consists of dietary measures, prokinetic and antiemetic medications, and varying surgical or endoscopic interventions, including the promising pyloric therapies. There are ongoing trials with several novel medications, raising hopes for future treatment. Conclusions Patients with idiopathic gastroparesis presents several pathophysiological alterations in the stomach, where depletion of ICC is of special importance. Treatment is currently focused on alleviating symptoms through dietary adjustments, medication or surgical or endoscopic interventions.
2008
Evidence suggests that distinct mechanisms underlie diabetic and idiopathic gastroparesis. Differences in gastric acid in gastroparesis of different etiologies and varying degrees of gastric stasis are uninvestigated. We tested the hypotheses that (i) gastric pH profiles show differential alteration in diabetic vs. idiopathic gastroparesis and (ii) abnormal pH profiles relate to the severity of gastric stasis. Sixty-four healthy controls and 44 gastroparesis patients (20 diabetic, 24 idiopathic) swallowed wireless transmitting capsules then consumed 99m Tcsulfur colloid-labeled meals for gastric scintigraphy. Gastric pH from the capsule was recorded every 5 seconds. Basal pH was higher in diabetics (3.64+0.41) versus controls (1.90+ 0.18) and idiopathics (2.41+0.42)(P<0.05). Meals evoked initial pH increases that were greater in diabetics (4.98+0.32) than idiopathics (3.89+0.39)(P=0.03) but not controls (4.48+0.14). pH nadirs prior to gastric capsule evacuation were higher in diabetics (1.50+0.23) than controls (0.58+0.11)(P=0.003). Four hour gastric retention was similar in diabetic (18.3+0.5%) and idiopathic (19.4+0.5%) patients but higher than controls (2.2+0.5%)(P<0.001). Compared to controls, those with moderate-severe stasis (>20% retention at 4 hours) had higher basal (3.91+0.55) and nadir pH (2.23+0.42) values (P<0.05). In subgroup analyses, both diabetics and idiopathics with moderate-severe gastroparesis exhibited increased pH parameters versus those with mild gastroparesis. In conclusion, diabetics with gastroparesis exhibit reduced gastric acid, an effect more pronounced in those with severely delayed gastric emptying. Idiopathic gastroparetics exhibit nearly normal acid profiles, although those with severely delayed emptying show reduced acid versus those with mild delays. Thus, both etiology and degree of gastric stasis determine gastric acidity in gastroparesis.
Risk factors and early detection of gastroparesis in patients with type 2 diabetes mellitus
Regulatory mechanisms in biosystems, 2019
Nowadays, diabetes mellitus is considered as one of the greatest global problems in internal medicine as it results in multiple organ damage and irreversible changes in the vital functional systems of the body. Unfortunately, there are no statistical data on the prevalence of gastrointestinal autonomic neuropathy in patients with type 2 diabetes mellitus in the Ukrainian population; making an early accurate diagnosis can be a clinical challenge since its manifestations are often considered as the manifestations of other diseases. Multifaceted clinical manifestations of gastroparesis cause difficulties in making a timely diagnosis, which can lead to an unfavourable prognosis. Diabetic gastroparesis symptoms were found in 45.5% of patients with type 2 diabetes mellitus: mild gastroparesis was observed in 29 (18.6%) patients; moderate gastroparesis was seen in 32 (20.5%) subjects; the signs of severe diabetic gastroparesis were present in 10 (6.4%) patients only. According to the assessment of the Neuropathy Disability Score, in patients with type 2 diabetes mellitus (disease duration of more than 10 years) and severe manifestations of polyneuropathy, the presence of risk factors for hypoglycemia as well as cigarette smoking are predictors of the development and progression of diabetic gastroparesis symptoms. They include a positive family history of diabetes mellitus, chronic microvascular complications of diabetes mellitus, concomitant cardiovascular diseases. Diabetes mellitus duration of more than 10 years, severe manifestations of polyneuropathy, increase in the incidence of hypoglycemic episodes as well as cigarette smoking should be considered as risk factors for gastroparesis in type 2 diabetes mellitus. We developed a mathematical model to assess the risk of developing gastroparesis in patients with type 2 diabetes mellitus using the results of a questionnaire (the Gastroparesis Cardinal Symptom Index, the Hypoglycemia Fear Survey-Total), and the Neuropathy Disability Score. For future research into diabetic gastroparesis, we recommend that a multicenter study is performed with an increased sample size because the early detection of delayed gastric emptying in this study was as high as we expected. Importantly, a case study of the complete disease history and questionnaires for the early diagnosis of delayed gastric emptying are required for studying the exact risk factors of autonomic neuropathy of the stomach in patients with type 2 diabetes mellitus.
AJP: Gastrointestinal and Liver Physiology, 2008
Evidence suggests that distinct mechanisms underlie diabetic and idiopathic gastroparesis. Differences in gastric acid in gastroparesis of different etiologies and varying degrees of gastric stasis are uninvestigated. We tested the hypotheses that (i) gastric pH profiles show differential alteration in diabetic vs. idiopathic gastroparesis and (ii) abnormal pH profiles relate to the severity of gastric stasis. Sixty-four healthy controls and 44 gastroparesis patients (20 diabetic, 24 idiopathic) swallowed wireless transmitting capsules then consumed 99m Tcsulfur colloid-labeled meals for gastric scintigraphy. Gastric pH from the capsule was recorded every 5 seconds. Basal pH was higher in diabetics (3.64+0.41) versus controls (1.90+ 0.18) and idiopathics (2.41+0.42)(P<0.05). Meals evoked initial pH increases that were greater in diabetics (4.98+0.32) than idiopathics (3.89+0.39)(P=0.03) but not controls (4.48+0.14). pH nadirs prior to gastric capsule evacuation were higher in diabetics (1.50+0.23) than controls (0.58+0.11)(P=0.003). Four hour gastric retention was similar in diabetic (18.3+0.5%) and idiopathic (19.4+0.5%) patients but higher than controls (2.2+0.5%)(P<0.001). Compared to controls, those with moderate-severe stasis (>20% retention at 4 hours) had higher basal (3.91+0.55) and nadir pH (2.23+0.42) values (P<0.05). In subgroup analyses, both diabetics and idiopathics with moderate-severe gastroparesis exhibited increased pH parameters versus those with mild gastroparesis. In conclusion, diabetics with gastroparesis exhibit reduced gastric acid, an effect more pronounced in those with severely delayed gastric emptying. Idiopathic gastroparetics exhibit nearly normal acid profiles, although those with severely delayed emptying show reduced acid versus those with mild delays. Thus, both etiology and degree of gastric stasis determine gastric acidity in gastroparesis.