Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0152169 (renal colic)
 811 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Intermittent incomplete intestinal obstruction was proven by sonography in 25 male and 48 female patients with an age range of 10 to 88 years. All of them suffered from intermittent colicky pain, nausea and meteorism followed by liquid stools. Only 52 patients had undergone a total of 69 abdominal operations. The pertinent symptoms could be traced back for 6 months to 10 years (4 +/- 3 years). In 47 patients, intake of bulky food during the last 12 to 48 hours triggered the onset of disorders. The preadmission diagnoses were: incomplete intestinal obstruction (only 21), gastroenteritis (15), biliary colic (13), peptic ulcer (10), renal colic (4), food intoxication (4), appendicitis (3), adnexitis (3). Sonographic findings were: inconstant lumen distension, visible bowel wall movements with contractions of 3 to 6 mm, food bolus, enhanced paradoxical peristalsis, proof of distended and collapsed gut segments, bowel wall edema and free peritoneal fluid. Based on these ultrasonic findings and trend observation, conservative treatment was successfully instituted. All patients were discharged symptom-free with no subsequent attacks for 12 months. 20 patients, subsequently suffering from complete intestinal obstruction after 1 to 3 years, were operated on, comprising 8 cases of intestinal resection, 7 cases of adhesiolysis and intestinal tube splinting, 3 cases of band dissection and 2 cases of palliative bypass procedures. The diagnostic accuracy of abdominal ultrasonography is clearly demonstrated by the fact, that 11 of these patients with intermittent incomplete intestinal obstruction and now suffering from complete obstruction had no previous abdominal surgery.
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PMID:[Intermittent incomplete ileus of the small intestine. Sonographic diagnosis and trends]. 217 61

Analgesic nephropathy is a unique drug-induced kidney disease characterized pathologically by renal papillary necrosis and chronic interstitial nephritis, and is the result of excessive consumption of combination antipyretic analgesics. The clinical features of the disorder relate mainly to the papillary necrosis, renal colic, and obstructive uropathy and the development of chronic renal failure in a small percentage of patients. There are significant geographic variations in the clinical features that may be related to the differing combinations of analgesics. The pathogenesis of the disease is in part related to the kidneys' ability to concentrate drugs in the papillae. The following sequence of events presents a plausible explanation for the evolution of the disease. If a combination of phenacetin and aspirin is ingested, the following steps occur. Phenacetin is converted in the gut and liver to acetaminophen by first-pass metabolism. Acetaminophen is then taken up by the kidney and excreted. During its excretion, acetaminophen becomes concentrated in the papillae of the kidney during physiologic degrees of antidiuresis, the concentration being up to five times the intracellular concentration of other tissues. Acetaminophen undergoes oxidative metabolism by prostaglandin H synthase to a reactive quinoneimine that is conjugated to glutathione. If acetaminophen is present alone, there is sufficient glutathione generated in the papillae to detoxify the reactive intermediate. If the acetaminophen is ingested with aspirin, the aspirin is converted to salicylate and salicylate becomes highly concentrated in both the cortex and papillae of the kidney. Salicylate is a potent depletor of glutathione. The mechanism is not completely understood; however, the inhibition of the production of NADPH via the pentose shunt is a possible explanation. With the cellular glutathione depleted, the reactive metabolite of acetaminophen then produces lipid peroxides and arylation of tissue proteins, ultimately resulting in necrosis of the papillae.
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PMID:Combination analgesic-induced kidney disease: the Australian experience. 866 29

Extracorporeal shock wave lithotripsy (ESWL) is considered a very safe and noninvasive procedure for the treatment of urolithiasis. Achievements in the technical development of recent decades resulted in a continuous reduction of side effects. One of our patients, a woman with cystinuria, developed a temporary ureteral stricture after several sessions of ESWL. Encouraged by this observation we set out to explore--based on a MEDLINE literature search--published reports of more severe side effects observed in modern ESWL therapy. Besides hydronephrosis and renal colic the most common side effects were renal and perirenal hematomas in up to 4% in the larger series. Uncommon extrarenal complications are described mostly in case reports, which are also outlined in this report. The injury of visceral organs (liver, spleen, gut, pancreas) was published most frequently. A rupture or dissection of an abdominal aortic aneurysm as an outstanding serious complication was also reported several times. Taking obvious and well-known contraindications into consideration and carefully preparing the patients for the therapy (i.e., checking hemostasis, drug history), ESWL is a very safe procedure with a low risk of serious complications. Yet, postoperative clinical and ultrasound monitoring seems to be essential especially with respect to the increasing numbers of outpatient procedures.
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PMID:[Ureteral stricture after extracorporeal shock wave lithotripsy. Case report and overview of the spectrum of rare side effects of modern ESWL treatment]. 1745 33

In this review, evidence is presented to support the hypothesis that mechanosensory transduction occurs in tubes and sacs and can initiate visceral pain. Experimental evidence for this mechanism in urinary bladder, ureter, gut, lung, uterus, tooth-pulp and tongue is reviewed. Potential therapeutic strategies are considered for the treatment of visceral pain in such conditions as renal colic, interstitial cystitis and inflammatory bowel disease by agents that interfere with mechanosensory transduction in the organs considered, including P2X3 and P2X2/3 receptor antagonists that are orally bioavailable and stable in vivo and agents that inhibit or enhance ATP release and breakdown.
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PMID:Purinergic mechanosensory transduction and visceral pain. 1994 30

Experimental evidence is presented to support the hypothesis that purinergic mechanosensory transduction can initiate visceral pain in urinary bladder, ureter, gut and uterus. In general, physiological reflexes are mediated via P2X3 and P2X2/3 receptors on low threshold sensory fibres, while these receptors on high threshold sensory fibres mediate pain. Potential therapeutic strategies are considered for the treatment of visceral pain in such conditions as renal colic, interstitial cystitis and inflammatory bowel disease by purinergic agents, including P2X3 and P2X2/3 receptor antagonists that are orally bioavailable and stable in vivo and agents that modulate ATP release and breakdown.
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PMID:Targeting the visceral purinergic system for pain control. 2203 85