Have been diag. with gastroparesis. The doc has given me 3 choices, 1.do nothing, 2. take reglan (which have irreversible side effects) and 3. gastric pacemaker. I'm off Prilosec, Carafate. Now taking dexilant, Pepcid, reglan. Does anyone know about the pacemakers? Do they work? I am only taking one reglan at bedtime so I can sleep. Otherwise can't really eat anything, have tried nutrition drinks but takes sev. hours to get one can down due to the slow stomach emptying.
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replied September 20th, 2014
Thank you for asking

gstroparesis has many etiologies. Treatment Options

Gastroparesis treatments include dietary measures, medications that accelerate emptying or blunt vomiting, nonmedication interventions, and psychological therapies. Predictors of inadequate therapeutic responses include severe overall symptoms, increased bloating, and significant distention but not gastroparesis cause or emptying rates.

Nonmedication Interventions

Traditional dietary recommendations include consuming frequent small meals and avoiding roughage and high fat foods. However, a recent survey noted that gastroparetics ingested 1.4 meals daily and only 13% complied with fat restrictions.[4] Maintaining euglycemia is advocated as part of managing diabetic gastroparesis. A recent study employing continuous glucose monitoring observed prolonged postprandial hyperglycemia in diabetic gastroparetics compared to diabetics with normal emptying emphasizing impacts of gastric retention on glycemic control.[28] In one preliminary investigation, type 2 diabetics followed 6 months after initiating a regimen to improve diabetic control reduced hemoglobin A1c values from 10.5 0.3 to 9.0 0.5%, however, t1/2 values of emptying showed no change (94 8 versus 96 9 min).Conversely, another study correlated 1.8% hemoglobin A1c reductions after initiating insulin pump therapy with reduced hospitalizations and lengths of stay for diabetic gastroparesis.

Gastrokinetic and Antiemetic Therapies

Prokinetic agents act on diverse receptors to stimulate gastric emptying. Metoclopramide reduces symptoms by gastrokinetic serotonin 5-HT4 agonism and dopamine D2 antagonism and antiemetic brainstem D2 antagonism and vagal and brainstem 5-HT3 antagonism. Side effects limit metoclopramide use in 30%. Tardive dyskinesia is a catastrophic consequence occurring most often in older women a mean of 1.5-2 years after starting metoclopramide. Metoclopramide is the second most common cause of medication-induced tardive dyskinesia after haloperidol. Erythromycin improves symptoms by stimulating antral contractility via motilin receptor agonism. Patients commonly report tolerance to its benefits due to motilin receptor downregulation. Erythromycin may elicit pain, nausea, and vomiting at high doses by inducing spastic gut contractions and increases risks of sudden cardiac death by more than 100%. Intravenous azithromycin evokes more intense and prolonged antral and small bowel responses than erythromycin. The peripheral dopamine D2 antagonist domperidone does not cross the blood-brain barrier, thus, central neural side effects are limited. In a systematic review in diabetic gastroparesis, 64% of patients noted symptom reductions, 67% reported decreased hospitalizations, and 60% exhibited accelerated emptying.A recent study identified single nucleotide polymorphisms in three genes related to cancer and hedgehog signaling that correlated with domperidone efficacy. Domperidone prolongs electrocardiographic QTc intervals and may increase risks of sudden cardiac death. Domperidone is not Food and Drug Administration (FDA) approved, but is available from foreign pharmacies and websites, compounding pharmacies, and an FDA-sanctioned Investigational New Drug process. The acetylcholinesterase inhibitor pyridostigmine decreased symptoms in autoimmune gastroparesis.

Newer prokinetics have theoretical benefits. A recent report of hepatitis C patients with interferon-induced gastroparesis observed emptying acceleration and symptom reductions with the 5-HT4 agonist mosapride.Other agents with stomach stimulating effects but unproved benefits in gastroparesis include new 5-HT4 agonists (prucalopride, velusetrag, naronapride) and acetylcholinesterase inhibitors (acotiamide). Ghrelin, an endogenous mediator of food intake, exhibits gastrokinetic actions. In diabetic gastroparetics, the intravenous ghrelin agonist TZP-101 decreased nausea and vomiting and overall symptoms versus placebo ( A preliminary study reported reductions in overall and individual gastroparesis symptoms using an oral ghrelin analog (TZP-102) in diabetics with gastroparesis.

Antiemetic agents without prokinetic activity are often used; only case reports have been published suggesting efficacy of the dopamine antagonist thiethylperazine, the neurokinin NK1 antagonist aprepitant, and the antidepressant agent mirtazapine. In a retrospective study, tricylic antidepressants reduced nausea and vomiting in 88% of diabetics (29% with delayed emptying). The herbal extract STW5 (iberogast) reportedly is efficacious in functional dyspepsia and gastroparesis.

Endoscopic and Surgical Treatments

Case series of pyloric botulinum toxin injection report improved symptoms and accelerated emptying which persists 3-6 months. In the largest series, more patients responded to 200 unit botulinum toxin doses versus 100 units and women and idiopathics more often benefited.

Pyloric botulinum toxin also was efficacious in children (mean age 9.98 years) with gastroparesis, especially in older boys with vomiting.

Small underpowered, placebo-controlled controlled trials did not note superior responses for botulinum toxin versus placebo. Pneumatic pyloric dilation and venting gastrostomy are other endoscopic techniques that have been promoted.

Several thousand gastric electrical stimulator implantations have been performed, as obtaining FDA Humanitarian Device Exemption for refractory diabetic and idiopathic gastroparesis. Uncontrolled series note up to 80% reductions in nausea and vomiting with extended benefits more than 10 years and improvements in nutritional and metabolic status, quality of life, and healthcare utilization in some reports.[40] Subgroups unlikely to respond include idiopathic patients and those with pain requiring chronic opiates. Two small underpowered trials studied gastric stimulation in sham-controlled fashion. The first trial included an initial 2-month sham stimulation-controlled crossover phase in 33 patients. Weekly vomiting frequencies trended lower with the device ON versus OFF in diabetics but not idiopathics: early satiety, bloating, fullness, and overall symptoms were unimproved. A second trial of 55 diabetics also included a sham-stimulation phase.

After an initial 6-week postoperative period during which the device was ON, patients were randomized to the device ON or OFF for 3 months and then crossed over for 3 more months. During this crossover, vomiting frequencies were identical whether stimulators were ON or OFF. Proposed mechanisms of gastric stimulation include promoting fundic relaxation, reducing luminal hypersensitivity, altering autonomic sympathovagal balance, and modulating central nervous system activity. Most studies show no effect on emptying, although one recent investigation related improved symptoms during stimulation to reduced gastric retention only in diabetic patients.

Research in new stimulation methods is active. Multichannel pacing protocols offer the potential to accelerate emptying through delivering high energy pulses. A recent study of two-channel sequential pacing reported gastrokinetic and symptom benefits in diabetic gastroparetics. Studies using temporary gastric stimulation through endoscopically placed electrodes have not proven conclusive to predict treatment responses to surgically implanted stimulators. Most recently, feasibility of miniature wireless gastric stimulators positioned during endoscopy was demonstrated

Other Measures

Additional measures sometimes are considered. Jejunostomy feedings improve overall health and show trends to reduced healthcare utilitization in diabetic gastroparetics. Total parenteral nutrition (TPN) can reverse rapid weight loss and ensure adequate sustenance, but usually is needed only for associated intestinal dysmotility. Psychological dysfunction may complicate gastroparesis care. In a recent investigation, depression, and anxiety scores correlated with gastroparesis severity. Medication use and hospitalizations paralleled depression and anxiety intensity. The role of mental health specialists in gastroparesis is undefined.

I hope it helps. Seek a gastroenterologist for further management.

take care
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