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Diabetic gastroparesis causes

An orchestrated function of all these components is required for the appropriate propulsive movement of the food in the gastrointestinal tract. Gastroparesis, a pathological slowing-down of gastric emptying, is a result of the damage to the tissue elements involved in the regulation of motility.

Gastroparesis is one of the well-known complications of longstanding diabetes mellitus. Although it is rarely a lifethreatening complication, it has a deteriorating effect on the quality of life, leads to unpredictable oscillation of the blood glucose level, and increases the time required for the absorption of food and medicines. This review describes the clinical characteristics of diabetic gastroparesis and summarizes the organic and functional motility abnormalities caused by this This article is part of the Topical Collection on Microvascular Complications‚ÄĒNeuropathy V.

Kempler e-mail: kempler. Lengyel : T. V√°rkonyi 1st. Lengyel e-mail: lecs in1st.

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  • ūüíä Gastroparesis: okok, t√ľnetek √©s diagn√≥zis -

V√°rkonyi e-mail: varkonyitamas gmail. Finally, the currently available and potential future therapeutic approaches are summarized.

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Keywords Diabetes mellitus. Interstitial cells of Cajal. Neural elements. Furthermore, a normal gastric motility rate does not exclude the possibility that the complaints originate from motility disorders, while a slower gastric motility is not always associated with symptoms [11].

It is important diabetic gastroparesis causes emphasize that the only manifestation of gastroparesis in some patients without GI symptoms is poor glycemic control, whereas in other cases, the completely opposite phenomenon may be experienced: the presence of obvious symptoms are not related to dysglycemia [12]. Due to delayed food absorption, postprandial hypoglycemia might be a characteristic feature of gastroparesis among insulin-treated diabetic patients.

Although slower stomach emptying in diabetic gastroparesis causes case of long-standing diabetes mellitus rarely leads to life-threatening diabetic gastroparesis causes and does not increase mortality [13], it increases the risk of an electrolyte imbalance, as well as hypo- or hyperglycemia. Gastroparesis should also be considered as the underlying mechanism among patients thought to have brittle diabetes.

ūüíä Gastroparesis: okok, t√ľnetek √©s diagn√≥zis - 2021

As in various other areas of medicine, the severity of the disease may be characterized by different scoring systems. Further investigations are required to test whether these questionnaires are sufficiently valuable to guide the proper therapeutic approach or how well these scores lead to an estimate of the prognosis of the gastric complication. The mixing and the propulsive movement of liquid and solid food arriving into the esophagus and the lower parts of the gastrointestinal GI tract require the well-coordinated work of five basic tissue elements: smooth muscle, extrinsic and intrinsic neurons, glial cells, hormonal elements, and the interstitial cells of Cajal ICCs.

Damage to any of these elements leading to an imbalance of the neuromuscular unit will deteriorate the propulsive movement of food to some extent. The degrees to which these elements are involved determine the degree and nature of the functional disorder.

The stomach, positioned in the upper tract of the GI system, has a unique role in the processing of food, since it accommodates to the volume of the aliments, stores them, grinds them into small pieces, and transmits the food toward the duodenum.

Under physiological conditions, the movement of low-calory liquid food, especially water, toward the duodenum depends on its volume and the pressure pump function of the stomach [1]. Low-calory solid food such as bread spends 20‚ÄĒ30 min in the stomach, while a continuous peristaltic movement starts at the mid-upper corpus of the greater curvature of the stomach, spreads toward the antral region usually 3‚ÄĒ5 times per minute [2], 2.

t√≠pus√ļ cukorbetegs√©g kezel√©s√©re viszket√©s presses the pieces of food to the almost closed pylorus. This way, the stomach comminutes the solid diabetic gastroparesis causes and makes it accessible to the digestive enzymes. Hyperosmotic, acidic, or nutrient-rich food makes stomach emptying much slower [3].

Hivatkozások évente

The over-slow emptying of solid food from the stomach for a nonmechanical reason is defined as gastroparesis [4]. Gastroparesis was one of the first complications of diabetes described [5], and some ancient doctors, such as Aretaeus of Cappadocia, thought that diabetes was a disease of the stomach. The etiology of gastroparesis cannot be identified in about a third of the cases [6]. The symptoms in all cases are chronic and recur frequently [7], including epigastric burning sensation, bloating, early satiety, abdominal discomfort, nausea, and vomiting.

Diabetic gastroparesis occurs more frequently in women, in obese patients with poor glycemic control, and in patients where other complications of diabetes have already appeared. Nonetheless, an obvious relationship between the higher glycated hemoglobin HbA1c level and the development and severity of gastroparesis has not been clearly established [9].

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The connection between symptoms and motility disorders related to gastroparesis is rather poor [17, 18]. An increased rate of stomach emptying is a characteristic finding in patients with a relatively short diabetes history less than 2 years and without the signs and symptoms of diabetic neuropathy [19]. Faster than normal stomach emptying can be observed even in long-term type 1 diabetes mellitus [12]. In animal models, insulin therapy in a subtherapeutic dosage normalized increased stomach emptying [20].

The vasopressin function blood pressure important consequence of faster gastric emptying in clinical practice is sudden postprandial hyperglycemia shortly following food intake.

Ideiglenesen le vagy tiltva

It is also possible that this increased rate of stomach emptying is a preliminary phase of later slower stomach emptying [21]. Diabetic gastroparesis involves a severe delay of stomach emptying of both solid and liquid food [22]. In a survey, type 2 diabetic patients with delayed emptying were older, had higher body mass index, and exhibited more intensive nausea and early satiety, as compared with type 1 diabetic patients Curr Diab Rep with impaired gastric motility [23].

Several functional changes can be found in the background of slower stomach emptying [21‚ÄĒ24]. However, acute and chronic hyperglycemia have different effects on stomach motility. In healthy volunteers, severe artificial hyperglycemia causes slowing-down of the emptying of nutrient-containing liquid and solid food [25].

In type 1 diabetic patients with diabetic autonomic neuropathy, hyperglycemia increases the frequency of rhythmic activity in the stomach, resulting in tachygastria [26]. Obvious deleterious effects of hyperglycemia cannot be confirmed on ICCs cells generate and propagate diabetic gastroparesis causes activity in the stomach and the GI tract [27].

Interestingly, in type 1 diabetic patients without autonomic neuropathy, the stomach emptying can be significantly decreased even if the postprandial blood glucose elevation does not exceed the physiological range [28].

Okok Mi okozza a gasztroparezist?

Chronic hyperglycemia in diabetes can also be responsible for all of the above-mentioned motility disorders. However, it is important to consider that diabetes is associated not only with elevated blood glucose levels, but additionally with an diabetic gastroparesis causes or relative diabetic gastroparesis causes of insulin.

The importance of this phenomenon is revealed by in vitro experimental data demonstrating the deteriorating effect of the absolute absence of insulin on stomach ICCs and the smooth muscle cells [27]. In general, slower movement of solid food from the stomach in diabetes is more frequent than slower movement of liquids. The impaired pyloric pressure pump function also has an effect on solid food emptying [29], and the diabetic gastroparesis causes of the distal stomach also relates diabetic gastroparesis causes the antral hypomotility [30].

It is probably important that the slow waves of the stomach generated diabetic gastroparesis causes the ICCs are modified by a number of factors, such as the sympathetic‚ÄĒparasympathetic balance, eating, and medicines.

Any disturbance in these factors can worsen the effectivity of the peristalsis [18]. The reasons for the discrepancy between the symptoms and detectable motility disorders are not clear; a possible explanation is the viscero-sensory functional defect related to diabetic autonomic neuropathy. The increased activity or sensitivity of these neuronal systems in the proximal stomach might explain the generation of nausea, vomiting, early satiety, and epigastrial pain experienced in type 1 diabetic patients without substantial motility disorders [32].

diabetic gastroparesis causes

Various factors can damage different tissues, including hyperglycemia and an absolute or Page 3 of 9, relative lack of insulin. The increase in mitochondrial diabetic gastroparesis causes activity caused by the increased glucose burden can be an important factor in the development of chronic morphologic complications of diabetes [33].

The increased oxidative stress-related decrease in nitric oxide NO concentration, together with the reduced activity of heme oxygenase, is an important feature of the pathogenetic background at the cellular level [34].

Diabetic Gastroparesis: Functional/Morphologic Background, Diagnosis, and Treatment Options

Carbon monoxide produced by heme oxygenase has a protective effect on the ICCs [35]. Histological changes in long-standing diabetes can also be studied. In a human investigation in antrum samples, mild diabetic gastroparesis causes infiltration in the myenteric plexus was a characteristic finding of diabetic gastroparesis [36].

Significant reductions in the numbers of neuronal elements and the ICCs in the antrum wall were detected [37]. In another investigation, the loss of neuronal elements was proven in diabetic samples from the mucosal layer [38]. In a larger study [39], the most frequent abnormality was damage to or loss of the ICCs and the decrease in the number of NO synthase NOS positive neurons.

However, the loss of the NOS-positive diabetic gastroparesis causes was more characteristic for idiopathic gastroparesis. Electromicroscopic investigations detected a significant increase in the amount of connective tissue.

Overall, the most characteristic histopathological change in diabetic gastroparesis is the loss of or damage to the ICCs. The pathophysiologic steps leading to ICC damage are complex.

The ICCs are very sensitive to the lack of insulin, despite the absence of insulin receptors and insulin-like growth factor-1 IGF-1 receptors on these cells [40].

The explanation of this paradoxical situation was provided by experiments [41] that revealed that the smooth muscle cells of the stomach have insulin and IGF-1 receptors and these cells produce the stem cell factor SCF that is essential for the development and maintenance of the network of ICCs. The smooth muscle atrophy that develops in cukorbetegs√©g l√°b t√ľnetei lack of insulin is responsible for the decreased production of SCF and, hence, for the damage to the ICC network [27, 40].

The exact mechanism of ICC damage is still not clear, and several questions remain to be answered [42, 43]. The most characteristic histological findings and symptoms of diabetic gastroparesis are listed in Tables 1 and 2.

Cukorbetegség lábápolási program

The parasympathetic regulation can exert both excitatory and inhibitory effects, while the sympathetic input is generally inhibitory, with the exception of its propulsive influence on the lower esophageal sphincter [44]. In accordance with the previous description, GI autonomic neuropathy is the result of a complex pathophysiological process that involves organic and functional impairments of the neuronal cells and a progressive imbalance of various autonomic regulations.

The changes include reduced numbers of ICCs, extrinsic autonomic neurons, and smooth muscle cells with altered inhibitory neurotransmission [29]. In patients with diabetic gastroparesis, a reduction in the intraneuronal levels of NO has also been observed [45]. It is assumed that the leading pathophysiologic abnormality is the impairment of parasympathetic function in autonomic neuropathy.

Sham feedinginduced gastric acid production or pancreatic polypeptide response to hypoglycemia is decreased in diabetic patients as well. Since both the gastric secretory function and pancreatic polypeptide secretion are under vagal control, these observations support the role of parasympathetic damage in the development of diabetic gastroparesis [46, 47].

The progression of the impaired gastric emptying seems to be slower than the progression of the autonomic neuropathy [49]. Besides the chronic metabolic exposure, acute hyperglycemia can also alter GI vagal functions [50].

Moreover, current hyperglycemia affects parasympathetic cardiac functions even in healthy subjects, pointing to the importance of the physiological condition of all those factors that possibly affect the vagal control in the regulation of gastric emptying [51].

The emptying of the stomach might Curr Diab Rep be slower when the balance between the excitatory and inhibitory regulations of the autonomic system becomes disturbed [52]. Parasympathetic function becomes abnormal earlier during the progression of diabetic gastroparesis causes neuropathy than does the sympathetic function, leading to weakening of the excitatory parasympathetic innervation of the stomach and a relative strengthening of the inhibitory sympathetic effects [53].

diabetic gastroparesis causes

The alteration in the sympathetic function can also kezelés sound diabetes detrimental effect on gastric emptying.

Several important processes are regulated by the sympathetic nervous system, which may also partially affect the gastric motility visceral reflexes, nausea, vomiting, and abdominal pain.

Despite the well-known general consequences of the parasympathetic and sympathetic impairments, it is still not clear how these alterations act directly on the motility of the stomach in diabetic patients.

Besides the normal extrinsic autonomic neuronal functions, intact central neuronal regulation is also mandatory for the integrity of gastric emptying. Abnormal visceral hypersensitivity as a result of an altered afferent central function is a newly documented source of various digestive symptoms that are responsible for an impaired quality of life [54].

diabetic gastroparesis causes

In line with this, a recent study demonstrated altered central sensory processing in diabetic patients with upper abdominal symptoms [55]. A few clinical observations suggest the role of the central neuronal system in the regulation of certain visceral functions, including gastric motility [56].

Gastroparesis (Stomach Paralysis) - Causes and Risk Factors, Signs \u0026 Symptoms, Diagnosis, Treatment