Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Celiac axis compression syndrome has generated much controversy since its original description in 1963. The main symptoms are postprandial epigastric abdominal pain, regurgitation of undigested food, and weight loss, all of which are caused by gastric ischemia from impingement of the celiac axis by the median arcuate ligament of the diaphragm. These symptoms are seen in other common disorders such as chronic mesenteric ischemia and gastroparesis. This makes the diagnosis of celiac axis compression syndrome a true challenge for the clinician. We present data on three patients successfully treated. The pre- and postoperative studies clearly demonstrate a resolution of the condition. The duplex ultrasound images clearly show variable compression on the celiac axis. The angiogram presented shows a classic image of the disease. A review of the data has enabled us to develop an algorithm for the diagnosis of this disease.
 ...
PMID:Reversible gastroparesis: functional documentation of celiac axis compression syndrome and postoperative improvement. 1667 60

Nitric oxide (NO), produced by the neural nitric oxide synthase enzyme (nNOS) is a transmitter of inhibitory neurons supplying the muscle of the gastrointestinal tract. Transmission from these neurons is necessary for sphincter relaxation that allows the passage of gut contents, and also for relaxation of muscle during propulsive activity in the colon. There are deficiencies of transmission from NOS neurons to the lower esophageal sphincter in esophageal achalasia, to the pyloric sphincter in hypertrophic pyloric stenosis and to the internal anal sphincter in colonic achalasia. Deficits in NOS neurons are observed in two disorders in which colonic propulsion fails, Hirschsprung's disease and Chagas' disease. In addition, damage to NOS neurons occurs when there is stress to cells, in diabetes, resulting in gastroparesis, and following ischemia and reperfusion. A number of factors may contribute to the propensity of NOS neurons to be involved in enteric neuropathies. One of these is the failure of the neurons to maintain Ca(2+) homeostasis. In neurons in general, stress can increase cytoplasmic Ca(2+), causing a Ca(2+) toxicity. NOS neurons face the additional problem that NOS is activated by Ca(2+). This is hypothesized to produce an excess of NO, whose free radical properties can cause cell damage, which is exacerbated by peroxynitrite formed when NO reacts with oxygen free radicals.
 ...
PMID:The involvement of nitric oxide synthase neurons in enteric neuropathies. 2189 78

Autonomic neuropathy, once considered to be the Cinderella of diabetes complications, has come of age. The autonomic nervous system innervates the entire human body, and is involved in the regulation of every single organ in the body. Thus, perturbations in autonomic function account for everything from abnormalities in pupillary function to gastroparesis, intestinal dysmotility, diabetic diarrhea, genitourinary dysfunction, amongst others. "Know autonomic function and one knows the whole of medicine!" It is now becoming apparent that before the advent of severe pathological damage to the autonomic nervous system there may be an imbalance between the two major arms, namely the sympathetic and parasympathetic nerve fibers that innervate the heart and blood vessels, resulting in abnormalities in heart rate control and vascular dynamics. Cardiac autonomic neuropathy (CAN) has been linked to resting tachycardia, postural hypotension, orthostatic bradycardia and orthostatic tachycardia (POTTS), exercise intolerance, decreased hypoxia-induced respiratory drive, loss of baroreceptor sensitivity, enhanced intraoperative or perioperative cardiovascular lability, increased incidence of asymptomatic ischemia, myocardial infarction, and decreased rate of survival after myocardial infarction and congestive heart failure. Autonomic dysfunction can affect daily activities of individuals with diabetes and may invoke potentially life-threatening outcomes. Intensification of glycemic control in the presence of autonomic dysfunction (more so if combined with peripheral neuropathy) increases the likelihood of sudden death and is a caveat for aggressive glycemic control. Advances in technology, built on decades of research and clinical testing, now make it possible to objectively identify early stages of CAN with the use of careful measurement of time and frequency domain analyses of autonomic function. Fifteen studies using different end points report prevalence rates of 1% to 90%. CAN may be present at diagnosis, and prevalence increases with age, duration of diabetes, obesity, smoking, and poor glycemic control. CAN also cosegregates with distal symmetric polyneuropathy, microangiopathy, and macroangiopathy. It now appears that autonomic imbalance may precede the development of the inflammatory cascade in type 2 diabetes and there is a role for central loss of dopaminergic restraint on sympathetic overactivity. Restoration of dopaminergic tone suppresses the sympathetic dominance and reduces cardiovascular events and mortality by close to 50%. Cinderella's slipper can now be worn!
...
PMID:Diabetic autonomic neuropathy. 2409 32

Gastroparesis (GP) is a chronic neuromuscular disorder of the upper gastrointestinal tract. The incidence of GP is not well described; however, the number of individuals affected by symptoms of GP in the United States is estimated to be over 4 million. The etiology of GP is diverse. Approximately 25% of cases are associated with diabetes, whereas nearly 50% are classified as idiopathic; many of these latter cases likely represent a postinfectious process. Connective tissue disorders, autoimmune disorders, prior gastric surgery, ischemia, and medications make up the vast majority of the remaining cases. The pathophysiology of GP is also diverse. Abnormalities in fundic tone, antroduodenal dyscoordination, a weak antral pump, gastric dysrhythmias, and abnormal duodenal feedback all contribute to delays in gastric emptying and symptom expression. Characteristic symptoms of GP include nausea, vomiting, epigastric pain, early satiety, and weight loss. The diagnosis of GP is made using a combination of characteristic symptoms in conjunction with objective evidence of delayed gastric emptying in the absence of mechanical obstruction. Once the diagnosis is made, treatment options include dietary modification, medications to accelerate gastric emptying, antiemetic agents, gastric electrical stimulation, and surgery. In the following sections we will provide an overview of the health care impact of GP, describe the underlying pathophysiology, and review treatment options using an evidence-based approach.
...
PMID:Gastroparesis: A Review of Current Diagnosis and Treatment Options. 2587 55

Gastroparesis is a chronic, bothersome, and often disabling neuromuscular disorder of the upper gastrointestinal tract. The most frequently reported symptoms of gastroparesis include nausea, vomiting, epigastric pain, early satiety, and unintentional weight loss. Etiologies of gastroparesis include diabetes, connective tissue disorders, prior infection, mesenteric ischemia, and post-surgical complications. The largest category of gastroparesis patients is comprised of those in whom no definitive cause can be identified (idiopathic gastroparesis). The individual and societal burden of gastroparesis is substantial. It considerably reduces patients' quality of life accompanied by a significant negative impact to the healthcare system. The current treatments of gastroparesis are less than ideal. Dietary modification may improve symptoms in patients with mild disease. Metoclopramide is the only medication currently approved for the treatment of gastroparesis; however, it is associated with adverse effects in a sizable proportion of patients. Other medications are frequently employed to treat symptoms of nausea and vomiting, although technically all are used off-label since they are not FDA approved for the treatment of gastroparesis. These data highlight the need to identify novel, more effective treatment options for this disabling disease. This review will provide a brief synopsis on the epidemiology, etiology, and impact of gastroparesis, discussing new therapeutic advances.
 ...
PMID:Gastroparesis: Medical and Therapeutic Advances. 2950 99

The growing population of intestinal transplant recipients present a unique challenge to the gastroenterologists responsible for their support and evaluation. Improvements in patient and graft survival are largely attributed to surgical advancements, refined antirejection therapy, and enhanced endoscopic surveillance protocols that better perceive rejection and other complications. This article reviews the endoscopic management and interventions provided for transplant recipients at the University of Illinois Hospital with complications, such as acute rejection, ischemia, bleeding, fistula, post-transplant lymphoproliferative disorder, and gastroparesis. Further research is needed on promising strategies currently used for related diseases to treat and sustain the intestinal graft.
 ...
PMID:Endoscopic Follow-up of Intestinal Transplant Recipients. 2973 31

IN BRIEF Distal symmetric polyneuropathy (DSPN) and diabetic autonomic neuropathies, particularly cardiovascular autonomic neuropathy (CAN), are prevalent diabetes complications with high morbidity, mortality, and amputation risks. The diagnosis of DSPN is principally a clinical one based on the presence of typical symptoms combined with symmetrical, distal-to-proximal stocking-glove sensory loss. CAN is an independent risk factor for cardiovascular mortality, arrhythmia, silent ischemia, major cardiovascular events, and myocardial dysfunction. Screening for CAN in high-risk patients is recommended. Symptoms of gastroparesis are nonspecific and do not correspond with its severity. Diagnosis of gastroparesis should exclude other factors well documented to affect gastric emptying such as hyperglycemia, hypoglycemia, and certain medications. There is a lack of treatment options targeting the neuropathic disease state. Managing neuropathic pain also remains a challenge. Given the high risk of addiction, abuse, psychosocial issues, and mortality, opioids are not recommended as first-, second-, or third-line agents for treating painful DSPN.
 ...
PMID:Update on the Management of Diabetic Neuropathy. 3014 Jan 38


<< Previous 1 2