Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
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

Little information is available regarding the correlation between Prader-Willi syndrome and urolithiasis. We report a patient with Prader-Willi syndrome with a renal uric acid (UA) stone. A 23-year-old male patient was admitted to our department with gross hematuria and left flank pain. The blood and urine examination demonstrated hyperuricemia with the presence of UA crystals in the urine. Excretory urography revealed a radiolucent stone (17 x 27 mm) in the left renal pelvis suggesting a UA stone. The stone was removed successfully using extracorporeal shockwave lithotripsy (ESWL) combined with medication for UA metabolism. The stone was thought to have formed as a result of overeating associated with Prader-Willi syndrome, and accompanying overproduction of purine.
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PMID:[A case of Prader-Willi syndrome accompanied with a renal stone]. 950 7

A 69-year-old man was admitted with right flank pain. The patient was diagnosed with advanced gastric cancer with multiple metastases in the liver and abdominal lymph nodes and underwent chemotherapy. Three days following the initial administration of S-1 plus cisplatin, the patient developed tumor lysis syndrome (TLS) with increased LDH, hyperuricemia, hyperkalemia, and elevated creatinine. Although rare, TLS following chemotherapy for solid tumors is a potentially fatal complication, and high physician awareness is required, especially in patients with risk factors, such as bulky disease.
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PMID:[Acute tumor lysis syndrome in the setting of advanced gastric cancer]. 2286 61

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