Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0000737 (abdominal pain)
 31,184 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 21-year-old Black male with painful neuropathy, abdominal pain, tachycardia and encephalopathy developed striking scalp alopecia 1 week after admission. Thallium poisoning was suspected and confirmed by urinalysis. The clinical course, investigations and management are presented.
 ...
PMID:Thallium poisoning. A case report. 687 93

Twenty-seven cases of chronic intestinal pseudo-obstruction are reported. The causes of pseudo-obstruction were progressive systemic sclerosis in 14, hollow visceral myopathy in 4, visceral neuropathy in 2, sclerosing mesenteritis in 1, and jejunal diverticulosis in 1. No identifiable cause was found in five. Chronic pseudo-obstruction is a long-term illness characterized by vomiting, abdominal distention, abdominal pain and weight loss. Involvement is often present throughout the intestine so that patients may present with a variety of symptoms deriving from the esophagus, stomach, small intestine, and colon. Hollow visceral myopathy and visceral neuropathy are usually familial and urologic involvement is sometimes present in the former. Abnormalities of smooth muscle function can be discerned by radiography and esophageal manometry. The pattern and distribution of the abnormalities are helpful in differentiating pseudo-obstruction from true mechanical obstruction. They may also be helpful in differentiating one form of pseudo-obstruction from another. The majority of cases have identifiable pathology within either the smooth muscle or myenteric plexus of the bowel wall. The natural history of pseudo-obstruction is variable. Remissions and exacerbations occur and may be unrelated to anything that is done therapeutically. The illness is unresponsive to any drug known to have an effect on intestinal motility. Antibiotic treatment of small intestinal bacterial overgrowth and selected surgical procedures may occasionally be palliative. Many patients develop malnutrition and require home parenteral nutrition in order to survive.
 ...
PMID:Chronic intestinal pseudo-obstruction. A report of 27 cases and review of the literature. 689 76

The clinical features of acute intermittent porphyria (AIP) are described in this chapter. AIP is inherited as an autosomal dominant pattern of inheritance. Prevalence in Japan is 1.5 in 100,000. Attacks are more frequent in women of 20s to 40s. The common clinical pattern of symptom involves acute abdominal pain, psychiatric disturbances, and acute neuropathy. The nerve biopsy shows segmental demyelination and axonal degeneration. Many small vacuolations are distinctively seen in all of the cell components of the nerve. Clinical diagnosis is not difficult when doctors keep the possibility of AIP in their minds in cases of abdominal pain, weakness and mental symptoms. The major trust of treatment is avoidance of acute attacks which is almost entirely dependent upon avoidance of porphyrogenic drugs. The intravenous administration of heme and glucose is important and effective therapy for acute attacks of porphyria.
 ...
PMID:[Acute intermittent porphyria]. 761 56

The clinical picture of lead neuropathy was classically described as a painless progressive motor neuropathy with axonal loss. The literature review fails to demonstrate a consensus on the site of axonal loss. This is an EMG report of a patient who developed a late lead neuropathy after a shotgun injury. A 69-year-old Filipino, healthy, male nondrinker sustained a shotgun injury to his left elbow. Nineteen years later he developed abdominal pain, followed by generalized weakness, distal greater than proximal in the extremities, and impaired pin-prick, proprioception, and two-point discrimination. He became nonambulatory and totally dependent in daily activities. He was lost to follow-up for 2 years until January 1993 when he presented with a blood lead level of 84 micrograms/dL. EMG examination revealed a sensorimotor peripheral polyneuropathy with severe axonal loss. This case demonstrates that axonal loss is the predominant feature in lead neuropathy and the location of pathology is in the peripheral nerves.
 ...
PMID:An EMG case report of lead neuropathy 19 years after a shotgun injury. 787 Jan 11

Gastrointestinal motor dysfunction, intestinal pseudo-obstruction syndromes, and hollow visceral neuropathy and myopathy were previously considered functional bowel diseases but are now recognized to be organic disorders. They may alter the muscle of the intestinal wall or the nerves of the myenteric plexus, or both. Their symptoms of chronic unexplained abdominal pain, abdominal distention and bloating, early satiety, nausea, vomiting, and alternating diarrhea and constipation are the most common and perhaps the most difficult problems encountered by gastroenterologists. New intestinal recording devices assess motility and allow objective classification of neuromuscular disease, permitting accurate diagnosis and better treatment.
 ...
PMID:Neuromuscular diseases of the gastrointestinal tract. Specific disorders that often get a nonspecific diagnosis. 787 32

A 23-year-old man with epilepsy and a past history of abdominal pain and ileus, developed hypertension and arm and bulbar weakness when valproic acid and carbamazepine were reinitiated. Electrophysiologic studies demonstrated a peripheral neuropathy with features of axonal degeneration and demyelination. Axonal degeneration was documented by sural nerve biopsy. Markedly elevated urinary delta-aminolevulinic acid and porphobilinogen indicated a diagnosis of acute porphyria. Other laboratory studies were most consistent with hereditary coproporphyria. Motor function improved considerably but incompletely over 1 year. An acute, primarily motor neuropathy can occur in several forms of porphyria, including acute intermittent porphyria, variegate porphyria, and hereditary coproporphyria, sometimes even in the absence of concomitant gastrointestinal symptoms.
 ...
PMID:Acute peripheral neuropathy due to hereditary coproporphyria. 800 8

First, it is important to find out whether the patient is complaining of infrequent defaecation, excessive straining at defaecation, abdominal pain or bloating, a general sense of malaise attributed to constipation, soiling, or a combination of more than one symptom. Second, one must decide if there is a definable abnormality as a cause of the symptom(s). Is the colon apparently normal or is its lumen widened (megacolon)? Is the upper gut normal or is there evidence of neuropathy or myopathy? Is the ano-rectum normal or is there evidence of a weak pelvic floor, mucosal prolapse, major rectocele, an internal intussusception or solitary rectal ulcer? Is there any systemic component such as hypothyroidism, hypercalcaemia, neurological or psychiatric disorder or relevant drug therapy? Choice of treatment will depend on this clinical evaluation. The range of treatments available is: Reassurance and stop current treatment: Patients with a bowel obsession may take laxatives or rectal preparations regularly without need. Increase dietary fibre: Most cases of 'simple' constipation respond to increased dietary fibre, possibly with an added supplement of natural bran. Toilet training and altered routine of life: Young people particularly may need to recognise the call to stool and alter their daily routine to permit and encourage regular defaecation. Medicinal bulking agent: Ispaghula, methyl cellulose, concentrated wheat germ or bran, and similar preparations are useful when patients with a normal colon find it difficult to take adequate dietary fibre. These preparations increase the bulk of stool and soften its consistency. They may be useful for those patients with the constipated form of irritable bowel syndrome.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Clinical management of constipation. 823 32

Ormaplatin is a cisplatin analog which has demonstrated activity against cisplatin-resistant tumors in preclinical studies. We delivered 28 cycles to 14 patients in a phase I trial of intraperitoneal ormaplatin given every 28 days. The maximum tolerated dose was 88.4 mg/m2 and acute dose-limiting toxicity was abdominal pain. Other toxicities include nausea, emisis, fever, and severe neuropathy seen in 1 patient at a cumulative dose of 399 mg/m2. No objective responses were observed. Hematologic toxicity was mild. The dose recommended for future trials of intraperitoneal ormaplatin is 66.5 mg/m2. Pharmacokinetic analysis performed at a dose of 66.5 mg/m2 demonstrated that the initial phase of elimination from the peritoneal cavity follows first-order kinetics with k = 0.69 hr-1 and half-life of 1.4 hr. Plasma pharmacokinetic behavior is best described by biexponential model with k1 = 0.369 hr-1, k2 = 0.107 hr-1, and first half-life of 2.9 hr and second half-life of 8.4 hr. Pharmacologic advantage, calculated by ratio of peritoneal to plasma AUC, is 17.1. If site-specific activity is demonstrated, then the intraperitoneal route of administration of ormaplatin at 66.5 mg/m2 may be beneficial.
 ...
PMID:Phase I and pharmacokinetic study of intraperitoneal ormaplatin. 824 79

"Hyperlipidemic crisis" is a term used to describe episodic abdominal pain in patients with hyperlipidemia. The morphologic correlates of this phenomenon have not been investigated and the etiology of the disorder is uncertain. We report a unique histologic finding in the pancreas of a 34-year-old woman with a 17-year history of episodic abdominal pain, sometimes accompanied by hyperamylasemia. At the age of 18 years, grossly elevated cholesterol and triglyceride levels were documented and type V hyperlipidemia was diagnosed. At the age of 34 years, subtotal pancreatectomy was performed for intractable abdominal pain. Histologic examination identified an increased number of enlarged pancreatic nerves that were infiltrated by foamy macrophages and encircled by fibrous tissue; endoneurial infiltration with macrophages occasionally split nerves into individual fascicles. Otherwise, the pancreas had only minimal fibrosis, nesidioblastosis, mucinous metaplasia of some pancreatic ducts, and scattered small collections of chronic inflammatory cells, subtle features suggesting very mild chronic pancreatitis. We propose that this novel xanthomatous neuropathy mimicked pancreatitis and was one of the underlying pathophysiologic mechanisms of abdominal pain in this patient. Further studies are necessary to document the prevalence of this new entity in patients with hyperlipidemia and to correlate its occurrence with "hyperlipidemic crisis" in those individuals.
 ...
PMID:Pancreatic xanthomatous neuropathy associated with hyperlipidemia: a cause of abdominal pain mimicking chronic pancreatitis. 811 25

The porphyrias are a group of disorders of haem metabolism. A knowledge of which anaesthetic can precipitate an acute attack of porphyria is important, since an accumulation of metabolites can result in life threatening symptoms, such as abdominal pain, vomiting, photophobia, neuropathy, bulbar paresis and respiratory failure. Treatment consists primarily of adequate calorie intake e.g. glucose, but is otherwise symptomatic. Anaesthetic drug recommendations are based both on animal experiments and patient experience, primarily case histories. An array of local anaesthetics, hypnotics, sedatives, neuroleptics, analgesics, muscle relaxants, inhalation anaesthetics and some antibiotics are reviewed. Patients with a history of porphyria should be in an optimal condition and maintain a high calorie intake perioperatively. The pre-operative fast should be a minimum and iv-glucose is advisable while fasting. There are anaesthetic agents that are safe for both regional and general anaesthesia.
 ...
PMID:[Anesthesia and porphyria]. 831 98


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>