Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0016199 (flank pain)
 2,189 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Experience with chemodissolution of uric acid stones in 30 patients is presented. Chemodissolution was achieved either with infusion of 0.16 M i.v. lactate or oral sodium bicarbonate, in addition to liberal fluid intake and allopurinol wherever indicated. In some cases direct chemodissolution by in situ irrigation with sodium bicarbonate solution was done after an initial percutaneous nephrostomy. Seven patients presented with acute obstructive anuria. In this group, 5 of them had bilateral obstructive calculi, while 2 had unilateral obstruction in a solitary kidney. The latter 2 had complete recovery following intravenous lactate therapy. Of the 5 presenting with bilateral obstruction, 2 patients had complete response to chemodissolution, whereas the remaining 3 had only a partial response requiring surgery for ultimate salvage. In this group I, 6 patients are doing well with a normal serum creatinine at 3 months to 4 years follow-up, while 1 patient has a serum creatinine, stabilised at 3.2 mg%. In the second group, 23 patients presented with non-obstructing urinary stones. Flank pain was the commonest complaint and a concomitant history of gout was present in 6 patients. Hyperuricaemia was detected in 12 and hyperuricosuria in 19. All cases were managed by high fluid intake and oral sodium bicarbonate, with self-monitoring of urine pH, which was kept between 6.5 and 7.0. Allopurinol was administered in cases having hyperuricaemia and/or hyperuricosuria. Systemic alkali therapy in the form of intravenous molar lactate or sodium bicarbonate is effective and safe both in obstructive anuria and non-obstructive urinary uric acid stones.
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PMID:Chemodissolution of urinary uric acid stones by alkali therapy. 131 80

Rheumatic manifestations are common and varied in infective endocarditis. We performed a retrospective case analysis on 87 patients with 93 episodes of infective endocarditis admitted to Flinders Medical Centre over an 11 year period (1980-1990). Disabling musculoskeletal symptoms and signs were documented in 22 (25%) of the patients. Thirteen patients developed severe or moderately severe low back pain during their illness, two with radiological evidence of a septic discitis or vertebral osteomyelitis. Two patients developed polyarthralgia/arthritis, four had septic arthritis (all with acute Staphylococcus aureus endocarditis), three developed severe loin pain, two acute gout, two had severe buttock pain and sacroiliac joint tenderness and two each developed disabling jaw/facial pain, neck/scapular pain and flank pain respectively. Five patients presented initially to the orthopaedic or rheumatological unit for management of their musculoskeletal symptoms. Four of seven patients with Streptococcus bovis endocarditis demonstrated prominent low back pain supporting a previously noted association between this organism and back symptoms. Furthermore, in one patient who had three separate episodes of endocarditis involving three different organisms, florid back symptoms were only seen in the infective episode involving Streptococcus bovis.
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PMID:Rheumatic manifestations of infective endocarditis. 141 Oct 84

Suprofen, a new nonsteroidal anti-inflammatory drug, was marketed in early 1986 as an analgesic agent. Until physicians began reporting an unusual acute flank pain syndrome to the spontaneous reporting system, 700,000 persons used the drug in the United States. Through August 1986, a total of 163 cases of this syndrome were reported. To elucidate the epidemiology of the syndrome, a case-control study was performed, comparing 62 of the case patients who had been reported to the spontaneous reporting system to 185 suprofen-exposed control subjects who did not have the syndrome. Case patients were more likely to be men (odds ratio, 3.8; 95% confidence interval, 1.2-12.1), suffer from hay fever and asthma (odds ratio, 3.4; 95% confidence interval, 1.0-11.9); to participate in regular exercise (odds ratio, 5.9; 95% confidence interval, 1.1-30.7), especially in the use of Nautilus equipment (p = 0.02); and to use alcohol (odds ratio, 4.4; 95% confidence interval, 1.1-17.5). Possible risk factors included young age, concurrent use of other analgesic agents (especially ibuprofen), preexisting renal disease, a history of kidney stones, a history of gout, a recent increase in activity, a recent increase in sun exposure, and residence in the Sunbelt. These were findings that were suggestive but did not reach conventional statistical significance. These findings are consistent with the postulated mechanism for this unusual syndrome: acute diffuse crystallization of uric acid in renal tubules.
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PMID:The epidemiology of the acute flank pain syndrome from suprofen. 259 70

While calcium oxalate and calcium phosphate make up at least 80% of all kidney stones, infection-induced and uric acid stones occur in 10% and 8%, respectively. Although any type of stone may become infected, the term "infection stones" means that stone formation exclusively depends on urease-producing bacteria. The splitting of urea leads to a rise in urinary pH which may induce crystallization of struvite (magnesium-ammonium-phosphate), the major constituent of infection stones, or carbonate apatite. Struvite stones account for the majority of staghorn calculi. They can grow quite large and may fill the entire collecting system. Patients with struvite stones may present with acute flank pain or remain completely asymptomatic. The cure of infection stones requires complete removal of the stone material. For uric acid crystallization and stone formation, low urine pH (below 5.5) is a more important risk factor than increased urinary uric acid excretion. Main causes of low urine pH are tubular disorders (including gout), chronic diarrheal states or severe dehydration. Accordingly, the treatment of uric acid stones consists not only of hydration (urine volume above 2000 ml per day), but mainly of urine alkalinization to pH values between 6.2 and 6.8. Urinary uric acid excretion can be reduced by a low-purine diet as well as--in case of recurrent uric acid stones and/or gout--by allopurinol. Cystinuria is a rare hereditary gene disorders with impaired tubular reabsorption of cystine. Stone formation occurs as a consequence of cystine's relatively low solubility at urine pH levels below 8. Only symptomatic diet and drug treatments are currently available, with urine dilution and urine alkalinization being the most efficient ones. Cystine stones respond poorly to shockwave lithotripsy, so that invasive procedures may regularly be necessary. 2,8-dihydroxy-adenine stones occur as a consequence of an enzyme deficiency that involves purine metabolism. These resulting stones are not visible by fluoroscopy and are therefore often misinterpreted as uric acid stones. Low-purine diet and allopurinol reduce the frequency of stone formation.
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PMID:[Pathophysiology, diagnosis and conservative therapy of non-calcium kidney calculi]. 1264 87

The clinical manifestations of hyperuricosuria (HU) are usually underestimated by the clinician. The aim of this study was to review the clinical spectrum of symptomatology of HU and to evaluate the presence of associated hypercalciuria (HC) and hyperoxaluria (HX). A retrospective review was done on 64 children with HU seen between January 2004 and December 2008. The patients were divided into HU 19, HU + HC 4, HU + HX 21 and HU + HC + HX 20. The mean age at diagnosis was 80 months (range six to 156 months). Duration of follow-up ranged was from six to 66 months. There were 228 symptomatic episodes for 64 patients (males 31, females 33). The relationship of symptomatology to age and gender were not significant. The most common symptoms were abdominal pain 67.2% (in 7/44 it was localized to the right lower quadrant, mimicking appendicitis), flank pain 59.4%, increased urinary frequency 43.4%, urgency 39%, enuresis 31.25%, oliguria 29.7%, dysuria 25%, red urine 20.35%, vaginal itching 15.21%, dribbling 14.06%, orange urine 12.5%, hesitancy 12.5% and penile pain 7.81%. To our knowledge, the vaginal itching and penile pain were not previously described. Family history was positive for stones and/or gout in 62.5%. The presence of a positive family history and red urine were significant (P-value <0.05) for the presence of an underlying HU. In the presence of recurrent abdominal/flank pain, hematuria without proteinuria or edema and urological symptomatology, especially in the presence of red urine, and a positive family history of gout or stones, a search for HU is in order. This will avoid unnecessary and invasive investigations.
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PMID:The clinical spectrum of idiopathic hyperuricosuria in children: isolated and associated with hypercalciuria/hyperoxaluria. 2298 10

Complete deficiency of hypoxanthine-guanine phosphoribosyltransferase (HPRT) activity causes Lesch Nyhan disease (LND), characterized by hyperuricemia, severe action dystonia, choreoathetosis, ballismus, cognitive and attention deficit and self-injurious behavior. Partial HPRT deficiency is present in patients with Lesch-Nyhan variant (LNV), who present with HPRT-related gout and a variable degree of neurological involvement. The diagnosis of HPRT deficiency relies on clinical, biochemical, enzymatic and molecular data. Patients with HPRT deficiency present low or undetectable HPRT activity in hemolysates, with increased adenine phosphoribosyltransferase (APRT) activity. We present a 9-year-old boy who experienced an episode of macroscopic hematuria with dysuria and left flank pain. He presented hyperuricemia and hyperuricosuria. HPRT and APRT activities were both normal in hemolysate; however, HPRT activity assayed in intact erythrocytes was 50% of control levels. A new missense point mutation c.424 A>G (T142A) was found in the HPRT1 gene. The apparent Michaelis constant (Km) for 5-phosphoribosyl-pyrophosphate assayed in patient hemolysate was 20-fold of control levels. In conclusion, we report a patient with HPRT deficiency who presented with both normal HPRT and APRT activity in hemolysate, in which the enzyme activity determined in intact erythrocytes was of diagnostic utility.
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PMID:Unapparent hypoxanthine-guanine phosphoribosyltransferase deficiency. 2878