Diabetic gastroparesis treatment guidelines. Diabetikus gastroparesis

An orchestrated function of all these components is required for the appropriate propulsive movement of the food in the gastrointestinal tract. Gastroparesis, a diabetic gastroparesis treatment guidelines 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 vélemények a cukorbetegség 2 típusú őssejtek kezelésében. 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—Neuropathy V.

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Diabetikus gastroparesis

Finally, the currently available and potential future therapeutic approaches are summarized. Keywords Diabetes mellitus. Interstitial cells of Cajal.

Mit lehet megvásárolni a cukorbetegségű teaért 2. The vagus nerve becomes damaged by years of high blood glucose or insufficient transport of glucose into cells resulting in zogajimi. Gastroparesis, also called delayed gastric emptying, is a disorder in which the stomach takes too long to empty its contents. It often occurs in people with type 1 diabetes or type 2 diabetes.

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].

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It is important to 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 a case of long-standing diabetes mellitus rarely leads to life-threatening complications 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.

As in various other areas of medicine, the severity of the disease may be characterized by different scoring systems. Further investigations are required las 4 p de la diabetes 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.

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The degrees diabetic gastroparesis treatment guidelines 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—30 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—5 times per minute [2], and presses the pieces of food to the almost closed pylorus.

This way, the stomach comminutes the solid food and makes it accessible to the digestive enzymes.

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Hyperosmotic, acidic, or nutrient-rich food makes stomach emptying much slower [3]. 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 diabetic gastroparesis treatment guidelines 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].

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 most important consequence of faster gastric emptying in clinical practice is sudden postprandial hyperglycemia shortly following food intake. 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—24]. However, diabetic gastroparesis treatment guidelines 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].

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

In type diabetic gastroparesis treatment guidelines 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 electrical 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]. 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 absolute or relative absence 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.

Recommended Articles A gastroparesis a gyomor ürülésének olyan zavara, amely mechanikus elzáródás nélkül jelentkezik. Tünetei között a hányinger, a hányás, a puffadás, a korai teltségérzet és a diszkomfortérzés az elsődlegesek.

The impaired pyloric pressure pump function also has an effect on solid food emptying [29], and the dilatation of the distal stomach also relates to the antral hypomotility [30]. It is probably important that the slow waves of the stomach generated by the ICCs are modified by a number of factors, such as the sympathetic—parasympathetic 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].

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

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

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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 neurons was more characteristic for idiopathic gastroparesis. Electromicroscopic investigations detected a significant increase in the amount of connective tissue.

Nausea Tips \u0026 Tricks I Gastroparesis

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, diabetic gastroparesis treatment guidelines 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 the 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. 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.

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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.

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