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PubMed2006

Botulinum toxin for gastrointestinal disorders: therapy and mechanisms.

Botulinum toxin has gained widespread acceptance as a treatment option for various spastic gastrointestinal disorders such as achalasia, gastroparesis, sphincter of Oddi dysfunction, chronic anal fissures, and pelvic floor dyssnergia, despite the lack of strong evidence supporting its use in many of these diseases. This review summarizes the trials investigating the use of BoNT since it was first utilized as a treatment in achalasia. BoNT has proven to be safe, but long-term efficacy in many disorders has not been observed, primarily due to is relatively short duration of action. BoNT may be most useful in confirming a diagnosis which can lead to a more definitive treatment modality. Furthermore, its safety profile allows it to be a useful alternative in patients who are at high risk for invasive procedures.

Animals↗
PubMedDate not supplied

The influence of some disease states on drug disposition.

The course of action of a drug is dependent upon the normal functioning of a number of organs which combine to absorb, distribute, metabolise and excrete the drug at a characteristic rate. A pathological condition of any of these organs may disturb not only their individual contribution to the course of the drug action, but as a secondary effect, those of other organs. Numerous studies of the effect of diseases of the cardiovascular system, gastrointestinal tract, liver and kidney have shown that organ dysfunction may be reflected in a changed rate and/or extent of absorption, apparent volume of distribution, plasma protein binding, plasma half-life and plasma and hepatic clearance. Moreover, from a clinical point of view, an important observation has been that for a given pathology, the pharmacokinetic consequence is not necessarily the same for all drugs. At the present time it is not always possible to predict the effect of a given disease on the effectiveness of therapy or to correlate changed kinetics with conventional organ function tests. In some disease states there is a strong argument for the monitoring of each individual patient's plasma drug level especially in the case of drugs with a low therapeutic index. It is also evident that further carefully controlled pharmacokinetic studies need to be carried out to elucidate the underlying mechanisms responsible for observed changes in kinetic constants. A greater understanding of the nature of these mechanisms may eventually help in the design and development of new drugs and in the more effective use of existing ones.

Cardiovascular Diseases↗
PubMed1986

Diabetic autonomic neuropathy.

The incidence of autonomic dysfunction as a complication of diabetes mellitus is reported to be as high as 20% to 40%. Symptoms of diabetic autonomic neuropathy (DAN) are often vague, and signs difficult to detect on routine physical examination. The early diagnosis of DAN is possible by utilizing several simple noninvasive tests, which may also be helpful in localizing the lesion(s) to specific autonomic pathways. DAN may affect multiple organ systems, to include cardiovascular, gastrointestinal, genitourinary and/or neuroendocrine, and may, in fact, be life-threatening. The same metabolic disturbances of somatic peripheral nerve may also be responsible for DAN. Like somatosensory neuropathy, definitive therapy for DAN is not yet satisfactory, although multiple chemotherapeutic agents have been tried and warrant further investigation.

Autonomic Nervous System Diseases↗
PubMed1991

Neuromuscular disease of the gastrointestinal tract.

Gastrointestinal motility is the function of gastrointestinal smooth muscle. It is controlled by both the intrinsic and extrinsic nerves of the gastrointestinal tract and, to a lesser degree, the gastrointestinal hormones. Therefore, any abnormality of the above factors, theoretically, can cause gastrointestinal dysmotility. In a clinical situation, commonly seen is gastrointestinal dysmotility caused by either smooth muscle or intrinsic and extrinsic nerves dysfunction. Diseases that cause smooth muscle dysfunction include familial visceral myopathies, nonfamilial visceral myopathies, collagen disease, muscular dystrophies, amyloidosis, thyroid disease, and so on. Diseases that cause enteric nerve dysfunction include familial visceral neuropathies, nonfamilial visceral neuropathies, diabetes mellitus, Chagas' disease, ganglioneuromatosis of the intestine, visceral neuropathy of carcinomatosis, Parkinson's disease, and so on. The patients with neuromuscular disease of the gastrointestinal tract have a wide range of clinical manifestations regardless of the underlying cause. At one end of the spectrum, the patients may be asymptomatic, and at the other end of the spectrum, the patients may have functional obstruction of the gastrointestinal tract. Plain abdominal x-rays, upper gastrointestinal (UGI) and small bowel x-rays, enteroclysis, barium enema, and manometric studies are useful for the work-up of these patients. Enteroclysis is especially helpful in ruling out mechanical obstruction of the small intestine in patients with chronic intestinal pseudo-obstruction. Treatment is mainly symptomatic and supportive. There is no effective drug to improve gastrointestinal motility. Surgery may be helpful in selected cases of severe gastrointestinal dysmotility.

Gastrointestinal Diseases↗
PubMed2003

Chronic idiopathic slow transit constipation: pathophysiology and management.

OBJECTIVE: Patients with idiopathic slow-transit constipation comprise a small proportion of the total population complaining of constipation. The purpose of this review is to present an update of pathophysiology of this disorder and its application in clinical management. METHODS: Medline was used to search English language articles published up to the end of September 2002 on the subject of slow-transit constipation. RESULTS AND CONCLUSIONS: Patients with idiopathic slow-transit constipation can be divided into 2 subgroups: 1. patients with normal proximal gastrointestinal motility and with onset of constipation in connection with childbirth or pelvic surgery. This subgroup may benefit from consideration of surgical treatment; 2. patients who have a dysfunctional enteric nervous/neuroendocrine system and exhibit colonic dysmotility as part of a generalised gastrointestinal dysmotility. Surgical approach in this subgroup seems to be unhelpful and medical treatment appears to be a better approach.

Autonomic Nervous System↗
PubMed2006

Autonomic dysfunction in spinal cord injury: clinical presentation of symptoms and signs.

Spinal cord injury and especially cervical spinal cord injury implies serious disturbances in autonomic nervous system function. The clinical effects of these disturbances are striking. In the acute phase, the autonomic imbalance and its effect on cardiovascular, respiratory system and temperature regulation may be life threatening. Serious complications such as over-hydration with the risk of pulmonary edema or hyponatremia are seen. The cord-injured person suffers from autonomic nervous system dysfunction also affecting bladder and bowel control, renal and sexual function. Paralytic ileus may cause vomiting and aspiration, which in turn interferes with respiratory function in those with cervical spinal cord injury. The cord-injured person is at risk to develop pressure sores from the moment of the accident. Two to three months post-injury the cord-injured person with a lesion level above the fifth thoracic segment may develop autonomic dysreflexia, characterised by sympathetically mediated vasoconstriction in muscular, skin, renal and presumably gastrointestinal vascular beds induced by an afferent peripheral stimulation below lesion level. The reaction might cause cerebrovascular complications and has effects on metabolism. Some of the autonomic disturbances are transient and a new balance is reached months post-injury, while others persist for life.

Autonomic Dysreflexia↗
PubMed2003

Non erectile dysfunction application of sildenafil.

Sildenafil has proven effective in the therapy of male erectile dysfunction. However, little is known about other potential beneficial effects of sildenafil. Meanwhile, first observations have been made in numerous medical disciplines and disorders. Small doses of sildenafil may be a useful adjunct to inhaled iloprost in the management of pulmonary hypertension. In female sexual dysfunction and infertility, genital blood flow and endometrial thickening are enhanced after application of the compound. In gastrointestinal disorders, sildenafil also exerts several effects which might be of clinical relevance. In patients with heart failure, endothelial dysfunction is influenced by the phosphodiesterase-5 (PDE 5) inhibitor and exercise capacity might be improved. Moreover, in the treatment of Raynaud's phenomenon, a disease without highly effective medical treatment option yet, first observations with sildenafil seem to be promising.

Female↗
PubMed2006

NSAID-analgesia, pain control and morbidity in cardiothoracic surgery.

OBJECTIVE: While narcotics remain the backbone of perioperative analgesia, the adjunctive role of other analgesics, including non-steroidal anti-inflammatory drugs (NSAIDs), is being recognized increasingly. This meta-analysis sought to determine whether adjunctive NSAIDs improve postoperative analgesia and reduce cumulative narcotic requirements. METHODS: A comprehensive search was undertaken to identify all randomized trials, in cardiothoracic patients, of NSAIDs plus narcotics vs narcotics without NSAIDs. Medline, Cochrane Library, EMBASE, and abstract databases were searched up to September 2005. The primary outcome was visual analogue scale (VAS) pain score. Secondary outcomes included 24-hr cumulative morphine-equivalents, rescue medications required, mortality, myocardial infarction, atrial fibrillation, stroke, renal failure, hospital readmissions, and in-hospital costs. RESULTS: Twenty randomized trials involving 1,065 patients were included. A significant reduction in 24-hr VAS pain score was found in patients receiving NSAIDs [weighted mean difference (WMD) -0.91 points, 95% confidence interval (CI) -1.48 to -0.34 points]. In addition, patients required significantly less morphine-equivalents in the first 24 hr (WMD -7.67 mg, 95% CI -8.97 to -6.38 mg). No significant difference was found with respect to mortality [odds ratio (OR) 0.19, 95% CI 0.01 to 4.22], myocardial infarction (OR 0.71, 95% CI 0.09 to 5.71), renal dysfunction (OR 0.95, 95% CI 0.37 to 2.46), or gastrointestinal bleeding (OR 0.96, 95% CI 0.13 to 7.09). CONCLUSION: In patients less than 70 yr of age undergoing cardiothoracic surgery, the adjunctive use of NSAIDs with narcotic analgesia reduces 24-hr VAS pain score and narcotic requirements.

Age Factors↗
PubMed1988

Neurourological implications of the changing approach in management of occult spinal lesions.

Occult lesions of the spine in children are a rare but recognizable cause of neurogenic dysfunction involving the lower extremities, and lower urinary and gastrointestinal tracts. We report the preoperative and postoperative urodynamic findings in 40 children with varying spinal abnormalities. Of these patients 28 were neonates or infants (average age 8.7 months) and 12 were older children (average age 11.7 years). Preoperative urodynamic testing revealed normal function in 18 of 28 children (64 per cent) in the younger age group in contrast to 1 of 12 (8 per cent) in the older age group. Of the 10 infants with abnormal studies postoperative urodynamic findings returned to normal in 6, while 2 others remained abnormal but were improved. In contrast, of 11 older children with abnormal preoperative evaluations 3 (27 per cent) reverted to normal postoperatively. The neurourological changes seen in these occult lesions are variable, may occur at any age, are progressive and are potentially reversible by surgical correction but this reversibility diminishes with age.

Adolescent↗
PubMed1984

Cardiologic perspectives of chest pain in childhood: a referral problem? To whom?

Discussed are the diagnostic and therapeutic issues of cardiac disease in the pediatric age group that have the potential to result in ischemic ventricular dysfunction. The discussion then turns to the nontraumatic thoracic, gastrointestinal, and psychogenic disturbances that are likely to produce symptoms of chest pain. In this context, the question of when to refer, when to reassure, when to begin a diagnostic evaluation, and when to institute longitudinal follow-up are addressed.

Arrhythmias, Cardiac↗
PubMed2026

Ivonescimab plus chemotherapy versus placebo plus chemotherapy in patients with advanced EGFR-mutated non-small-cell lung cancer after disease progression on EGFR tyrosine kinase inhibitor therapy (HARMONi): a multicentre, randomised, double-blind, phase 3 trial.

BACKGROUND: Ivonescimab has shown clinical efficacy in non-small-cell lung cancer (NSCLC). We aimed to assess the efficacy and safety of ivonescimab plus chemotherapy versus placebo plus chemotherapy in patients with advanced EGFR-mutated NSCLC whose disease progressed after third-generation EGFR tyrosine kinase inhibitor (TKI) therapy. METHODS: HARMONi is a randomised, placebo-controlled, double-blind, phase 3 trial done at 114 cancer centres and hospitals across Asia, Europe, and North America. Eligible patients were aged at least 18 years (upper limit: 75 years in Asia) with stage IIIB/IIIC or IV non-squamous EGFR-mutated NSCLC, disease progression after treatment with a third-generation EGFR-TKI, and an Eastern Cooperative Oncology Group performance status score of 0 or 1. Patients were randomly assigned (1:1) via a centralised interactive voice response system or interactive web response system to receive ivonescimab (20 mg/kg) or placebo plus pemetrexed (500 mg/m2) and carboplatin (target area under the curve 5 mg/mL per min) intravenously every 3 weeks. Randomisation was stratified by brain metastases status at enrolment and geographical region. The primary endpoints were progression-free survival by blinded independent radiology review committee and overall survival in the intention-to-treat population. Safety was assessed in patients who received at least one dose of trial treatment. This study is registered with ClinicalTrials.gov (NCT06396065), has completed enrolment, and is ongoing for treatment and follow-up. FINDINGS: From Jan 25, 2022, to Oct 1, 2024, 660 individuals were screened for eligibility; of these, 438 were enrolled and randomly assigned to receive ivonescimab plus chemotherapy or placebo plus chemotherapy (219 per group). Of enrolled patients, 257 (59%) were female and 181 (41%) were male; 306 (70%) reported race as Asian, and 105 (24%) as White. At a median follow-up of 22&#xb7;3 months (95% CI 21&#xb7;5-23&#xb7;0), 275 progression or death events had occurred in 345 patients (129 events among 172 patients in the ivonescimab plus chemotherapy group and 146 events among 173 patients in the placebo plus chemotherapy group). Median progression-free survival was 6&#xb7;8 months (95% CI 5&#xb7;7-7&#xb7;1) in the ivonescimab plus chemotherapy group versus 4&#xb7;4 months (4&#xb7;1-5&#xb7;5) in the placebo plus chemotherapy group (hazard ratio [HR] 0&#xb7;52; 95% CI 0&#xb7;41-0&#xb7;66; p<0&#xb7;0001). At a median follow-up of 29&#xb7;7 months (95% CI 27&#xb7;7-31&#xb7;0), 262 deaths occurred in 438 patients (122 in the ivonescimab plus chemotherapy group and 140 in the placebo plus chemotherapy group). Median overall survival was 16&#xb7;8 months (14&#xb7;3-19&#xb7;0) in the ivonescimab plus chemotherapy group versus 14&#xb7;0 months (12&#xb7;8-15&#xb7;7) in the placebo plus chemotherapy group (HR 0&#xb7;79; 0&#xb7;62-1&#xb7;01). The most common grade 3-4 treatment-related adverse events in the ivonescimab plus chemotherapy versus the placebo plus chemotherapy group were decreased neutrophil count (42 [19%] of 218 vs 36 [17%] of 218), decreased white blood cell count (28 [13%] vs 24 [11%]), decreased platelet count (27 [12%] vs 14 [6%]), and anaemia (22 [10%] vs 27 [12%]). Serious treatment-related adverse events occurred in 61 (28%) patients in the ivonescimab plus chemotherapy group and 33 (15%) patients in the placebo plus chemotherapy group. Treatment-related adverse events led to death in four patients (disease progression, multiple organ dysfunction syndrome, and hepatic failure, each in one patient; gastrointestinal haemorrhage and pulmonary embolism in one patient) in the ivonescimab plus chemotherapy group and five patients (pneumonitis, myocardial infarction, cerebrovascular accident, cognitive disorder, and embolic stroke, each in one patient) in the placebo plus chemotherapy group. INTERPRETATION: Ivonescimab plus chemotherapy showed a clinically meaningful and statistically significant progression-free survival benefit in patients with EGFR-mutated NSCLC after progression on EGFR-TKI therapy. The clinical benefit and lack of new safety signals of ivonescimab with chemotherapy support the potential for the combination as a new treatment option in this patient population. FUNDING: Summit Therapeutics.

Humans↗
PubMed2001

Myasthenia gravis with autoimmune autonomic neuropathy.

The autoantibodies that impair neuromuscular junction transmission in myasthenia gravis are specific for the nicotinic acetylcholine receptor (AChR) of muscle. Antibodies specific for AChRs in ganglionic neurons are found in a majority of patients with subacute autonomic neuropathy. Dysautonomia is not a recognized feature of myasthenia gravis, but there have been rare reports of myasthenia gravis coexisting with autonomic failure, usually in association with thymoma. Here we report seven patients who had myasthenia gravis with subacute autonomic failure. Their autonomic dysfunction ranged from isolated gastroparesis to severe panautonomic failure. Gastrointestinal dysmotility was a common feature. All had antibodies against muscle AChR, and three (all of whom had thymoma) had antibodies against neuronal ganglionic AChRs. In several patients, gastrointestinal function improved clinically after administration of an acetylcholinesterase inhibitor. These observations support a rare but definite clinical association between myasthenia gravis and autonomic failure and strengthen the concept that subacute autonomic neuropathy is an autoimmune disorder.

Adult↗
PubMed1997

Effects of cholecystectomy on gastric emptying and myoelectrical activity in man.

To investigate the effects of cholecystectomy on gastric motor function, 13 patients with symptomatic gallstones were studied before and 8-12 months after surgery. Twelve healthy subjects entered the study as control group. The cutaneous electrogastrography and ultrasound examination of gastric emptying were simultaneously performed at pre- and post-prandial states. The dominant gastric frequency and its coefficient of variation were not affected by surgery. After cholecystectomy, an increase in normal 3 cpm wave percentage and a decrease in power ratio were found (P < 0.05 and P < 0.01, respectively). Gastric emptying recorded after cholecystectomy was faster than before surgery (306.9 +/- 15.9 min vs 336.9 +/- 11.8 min, respectively; P < 0.05). Such changes were associated with the relief of symptoms, and the comparison between patients and controls showed a normalization of the gastric electrical activity and gastric emptying after surgery. In conclusion, in symptomatic patients, gallstones are associated with motor dysfunctions, and cholecystectomy seems to induce a normalization of gastrointestinal motility.

Adult↗
PubMed2005

Intestinal perception: mechanisms and assessment.

Physiological stimuli in the gut induce regulatory reflexes to accomplish the digestive process, but are normally not perceived. However, under some circumstances, gut stimuli may activate perception pathways and induce conscious sensations. Experimental evidence gathered during the past decade suggests that patients with functional gut disorders and unexplained abdominal symptoms may have a sensory dysfunction of the gut, so that physiological stimuli would induce symptoms. Assessment of visceral sensitivity is still poorly developed, but in analogy to somatosensory testing, differential stimulation of visceral afferents may be achieved by a combination of stimulation techniques, which may help to characterize sensory dysfunctions. Visceral afferent input is modulated by a series of mechanisms at different levels of the brain-gut axis, and conceivably, a dysfunction of these regulatory mechanisms could cause hyperalgesia. The sensory dysfunction in functional patients seems to be associated with altered reflex activity, and both mechanisms may interact to produce the symptoms. Evidence of a gut sensory-reflex dysfunction as a common pathophysiological mechanism in different functional gastrointestinal disorders would suggest that they are different forms of the same process, and that the clinical manifestations depend on the specific pathways affected.

Afferent Pathways↗
PubMed2004

Diabetic neuropathy: an intensive review.

PURPOSE: The epidemiology, classification, pathology, and treatment of diabetic neuropathy are reviewed. SUMMARY: Diabetic peripheral neuropathy is a common complication of diabetes that can cause significant morbidity and mortality. Some 30% of hospitalized and 20% of community-dwelling diabetes patients have peripheral neuropathy; the annual incidence rate is approximately 2%. The primary risk factor is hyperglycemia. Sensorimotor neuropathy is marked by pain, paresthesia, and sensory loss. Cardiac autonomic neuropathy (CAN) may contribute to myocardial infarction, malignant arrhythmia, and sudden death. Gastroparesis is the most debilitating complication of gastrointestinal autonomic neuropathy. Genitourinary autonomic neuropathy can cause sexual dysfunction and neurogenic bladder. The pathology of diabetic neuropathy involves oxidative stress, advanced glycation end products, polyol pathway flux, and protein kinase C activation; all contribute to microvascular disease and nerve dysfunction. For symptom management current evidence from clinical trials supports the use of desipramine, amitriptyline, capsaicin, tramadol, gabapentin, bupropion, and venlafaxine as preferred medications. Citalopram, nonsteroidal antiinflammatory drugs, and opioid analgesics may be used as adjuvant agents. Lamotrigine, oxcarbazepine, paroxetine, levodopa, and alpha-lipoic acid are alternative considerations. Evidence supporting the use of zonisamide, fluoxetine, mexiletine, dextromethorphan, and phenytoin is considered equivocal. Complementary therapies have also shown efficacy. The symptoms of CAN may be ameliorated with fludrocortisone, clonidine, midodrine, dihydroergotamine or caffeine, octreotide, and beta-blockers. Gastroparesis may be treated with metoclopramide or erythromycin. The most promising disease-modifying therapy is ruboxistaurin, which is in Phase III trials. Glycemic control remains the foundation of prevention and the prerequisite of adequate treatment. CONCLUSION: Diabetic neuropathy is a many-faceted complication of diabetes that can be managed symptomatically with an array of drugs.

Analgesics, Opioid↗
PubMed2006

The cellular, metabolic, and systemic consequences of aggressive fluid resuscitation strategies.

Increasing evidence has demonstrated that aggressive crystalloid-based resuscitation strategies are associated with cardiac and pulmonary complications, gastrointestinal dysmotility, coagulation disturbances, and immunological and inflammatory mediator dysfunction. As large volumes of fluids are administered, imbalances in intracellular and extracellular osmolarity occur. Disturbances in cell volume disrupt numerous regulatory mechanisms responsible for keeping the inflammatory cascade under control. Several authors have demonstrated the detrimental effects of large, crystalloid-based resuscitation strategies on pulmonary complications in specific surgical populations. Additionally, fluid-restrictive strategies have been associated with a decreased frequency of and shorter time to recovery from acute respiratory distress syndrome and trends toward shorter lengths of stay and lower mortality. Early resuscitation of hemorrhagic shock with predominately saline-based regimens has been associated with cardiac dysfunction and lower cardiac output, as well as higher mortality. Numerous investigators have evaluated potential risk factors for developing abdominal compartment syndrome and have universally noted the excessive use of crystalloids as the primary determinant. Resuscitation regimens that cause early increases in blood flow and pressure may result in greater hemorrhage and mortality than those regimens that yield comparable flow and pressure increases late in resuscitation. Future resuscitation research is likely to focus on improvements in fluid composition and adjuncts to administration of large volume of fluid.

Abdominal Cavity↗