Giant prostatic hyperplasia: report of a previously asymptomatic man presenting with gross hematuria and hypovolemic shock / Hiperplasia prostática gigante: hematúria macroscópica com choque hipovolêmico em paciente previamente assintomático

Giant prostatic hyperplasia is a rare condition characterized by very high volume benign prostatic enlargement (>500g). Few cases have been reported so far and most of them are associated with severe lower urinary symptoms. We report the first case of asymptomatic giant prostatic hyperplasia in an elderly man who had a 720g prostate adenoma, sudden gross hematuria and hypovolemic shock. The patient was successfully treated with open transvesical prostatectomy and had an uneventful postoperative recovery.

A hiperplasia prostática gigante é uma condição rara caracterizada por aumento benigno prostático significativo, com volume maior que 500g. Existem poucos casos relatados e, em sua maioria deles está associada a sintomas graves do trato urinário inferior. Relatamos aqui o primeiro caso de hiperplasia prostática benigna assintomática em paciente idoso com próstata de 720g, hematúria macroscópica de início súbito e choque hipovolêmico. O paciente foi submetido com sucesso à prostatectomia suprapúbica, sem intercorrências no intra e pós-operatório.

Quencher group induced high specificity detection of telomerase in clear and bloody urines by AIEgens.

Telomerase is a widely used tumor biomarker for early cancer diagnosis. On the basis of the combined use of aggregation-induced emission (AIE) fluorogens and quencher, a quencher group induced high specificity strategy for detection of telomerase activity from cell extracts and cancer patients' urine specimens was creatively developed. In the absence of telomerase, fluorescence background is extremely low due to the short distance between quencher and AIE dye. In the addition of telomerase, fluorescence enhances significantly. The telomerase activity in the E-J, MCF-7, and HeLa extracts equivalent to 5-10 000 cells can be detected by this method in ∼1 h. Furthermore, the distinguishing of telomerase extracted from 38 cancer and 15 normal urine specimens confirms the reliability and practicality of this protocol. In contrast to our previous results (Anal. Chem. 2015, 87, 6822-6827), these advanced experiments obtain more remarkable specificity.

Giant prostatic hyperplasia: report of a previously asymptomatic man presenting with gross hematuria and hypovolemic shock.

Giant prostatic hyperplasia is a rare condition characterized by very high volume benign prostatic enlargement (>500g). Few cases have been reported so far and most of them are associated with severe lower urinary symptoms. We report the first case of asymptomatic giant prostatic hyperplasia in an elderly man who had a 720g prostate adenoma, sudden gross hematuria and hypovolemic shock. The patient was successfully treated with open transvesical prostatectomy and had an uneventful postoperative recovery.

Identification of two novel mutations C79X and R235Q in the dihydropyrimidine dehydrogenase gene in a patient presenting with hematuria.

A patient with hematuria was shown to have thymine-uraciluria. The dihydropyrimidine dehydrogenase (DPD) activity in peripheral blood mononuclear cells was 0.16 nmol/mg/h; controls: 9.9 +/- 2.8 nmol/mg/h. Analysis of DPYD showed that the patient was compound heterozygous for the novel mutations 237C > A (C79X) in exon 4 and 704G > A (R235Q) in exon 7. The nonsense mutation (C79X) leads to premature termination of translation and thus to a non-functional protein. Analysis of the crystal structure of pig DPD suggested that the R235Q mutation might interfere with the binding of FAD and the electron flow between the NADPH and the pyrimidine substrate site of DPD.

Cytoprotective role of heme oxygenase (HO)-1 in human kidney with various renal diseases.

BACKGROUND: We previously reported that glomerular changes in the renal specimen of a human case with heme oxygenase-1 (HO-1) deficiency were mild, but tubulointerstitial injury advanced progressively. This study examined the patterns of HO-1 production in the kidney in various renal diseases. Furthermore, the critical cytoprotective roles of HO-1 were evaluated in the kidney by comparing HO-1 production and expressions of carboxymethyllysine (CML) and pentosidine, both of which are markers of oxidative stress. METHODS: Renal biopsy or autopsy materials were obtained from a total of 74 patients. Degrees of hematuria and proteinuria and the levels of urinary N-acetyl-beta-D-glucosaminidase (NAG), beta2-microglobulin (beta2m), and creatinine were evaluated. Immunohistochemical studies for HO-1, CML, and pentosidine expressions were performed with their specific antiserum. RESULTS: HO-1 staining was observed within tubular epithelial cells in all of the renal diseases, but was not detected within intrinsic glomerular cells. HO-1 staining tended to be more intense within distal tubuli than in proximal tubuli. Within distal tubuli, there was no significant correlation between intensity of HO-1 staining and degree of hematuria or presence of proteinuria. Within proximal tubuli, HO-1 staining tended to be more intense with greater degrees of hematuria, presence of proteinuria, and moderate tubulointerstitial damage. Intense staining of CML and pentosidine was observed within renal tubular epithelial cells only in HO-1-deficient patients. CONCLUSIONS: HO-1 plays important roles in protecting renal tubuli from oxidative injuries, as these cells are constantly exposed to various oxidative stresses. It is suggested that renal tubular epithelia are more susceptible to oxidative stress due to the lack of this critical enzyme in HO-1 deficiency.

Limitations of urinary telomerase activity measurement in urothelial cancer.

The reported frequency of detectable telomerase activity in spontaneously voided urine samples from patients with urothelial cancer varied from 0 to 85%. We examined stasis in the bladder and specimen storage as interfering conditions in this assay. Telomerase activity in exfoliated cells was measured by a polymerase-chain-reaction-based assay in spontaneously voided urine from urothelial cancer patients. Effects of retention in the bladder and specimen storage from voiding to measurement of telomerase activity were modeled by suspending 10(6) cells from the cancer-derived T24 line in normal urine (pH 6.5) at 37 degrees C and 25 degrees C, respectively. Hematuria was modeled by adding hemoglobin. In T24 cells suspended in urine at 37 degrees C, telomerase activity had decreased to approximately 20% of preincubation activity after 1 h, and had disappeared after 3 h. In urine at 25 degrees C, telomerase activity in T24 cells had decreased to approximately 40% of preincubation activity at 1 h and to <10% at 6 h. When we examined telomerase activity in exfoliated cells in spontaneously voided urine from urothelial cancer patients (excluding first-voided morning specimens), telomerase activity was detected in only 21% of samples (four of 19) despite measurement with 1 h of voiding and steps to avoid hemoglobin interference. Measurement of telomerase activity in spontaneously voided urine is insufficiently sensitive and reliable for the diagnosis of urothelial cancer.

Urinary type IV collagenase: elevated levels are associated with bladder transitional cell carcinoma.

Accumulating experimental evidence has linked the overproduction of extracellular matrix-degrading metalloproteinases with tumor cell invasion. In the present study one member of the metalloproteinase family, type IV collagenase (M(r) 72,000 gelatinase), is shown to be elevated in the urine of patients with transitional cell carcinoma of the bladder. The form of the enzyme in the urine was studied by three independent methods: enzyme-linked immunosorbent assay, Western immunoblotting; and gelatin zymography. Immunoblotting revealed that the enzyme was present as a series of fragments, each retaining the amino terminus of the mature proenzyme. A prominent M(r) 43,000 fragment was associated with the transitional cell carcinoma cases. Zymography demonstrated that multiple enzyme species with gelatinase activity were present in urine and that high-molecular-weight bands of substrate lysis corresponded to complexes between type IV collagenase and tissue inhibitor of metalloproteinases 2. The total amount of type IV collagenase antigen was significantly elevated in the urine of 37 transitional cell carcinoma patients (range, 0-1081 ng/ml; mean, 318.4 +/- 147.3) compared to 19 normal controls (P < or = 0.004) and 17 inflammatory disease controls (P < or = 0.011). Immunohistochemical staining of bladder tumor biopsies verified that the transitional cell carcinoma cells were producing the M(r) 72,000 enzyme. Thus, M(r) 72,000 type IV collagenase, which is present in the urine in many forms including fragments and complexes with inhibitors, may be a useful marker for bladder cancer diagnosis or prognosis.

The enzymatic profile of urine and plasma in bovine urinary bladder cancer (enzootic bovine haematuria).

The enzymatic profile of urine and plasma in field cases of bovine bladder cancer was studied. Urinary lactate dehydrogenase activity was significantly altered along with the isoenzyme pattern. Activity of alkaline phosphatase and beta-glucuronidase was decreased in the affected animals. No significant changes were observed in acid phosphatase, or arylsulphatase A and B activity. In plasma, lactate dehydrogenase activity was elevated without any change in the isoenzyme pattern. No significant changes were observed in the other plasma enzymes studied or in the sialic acid concentration.

Erythrocyte glutathione and its metabolizing enzymes in bovine urinary bladder cancer.

Glutathione and its metabolizing enzymes were studied in erythrocytes of cattle suffering from urinary bladder cancer and associated hematuria. The concentration of glutathione (GSH) and GSH peroxidase activity were subnormal in the affected animals, whereas activities of GSH reductase and GSH S-transferase were not altered. Decreased GSH and GSH peroxidase are likely to make erythrocytes of the affected animals more susceptible to oxygen-induced injury and the radiomimetic effect of bracken fern.

Urinary lactic dehydrogenase as a marker of renal injury in blunt trauma patients with hematuria.

We evaluated the use of urinary lactic dehydrogenase (LDH) in predicting renal injury in a convenience sample of 36 blunt trauma patients with hematuria. The mean +/- SEM urinary LDH for the five patients with renal injuries was 129.4 +/- 35 U/L, which was not significantly different from the mean urinary LDH levels in either the 22 patients without demonstrable genitourinary or retroperitoneal injuries (92.9 +/- 20.7 U/L) or the nine patients with nonrenal genitourinary or retroperitoneal injuries (165 +/- 46 U/L). Urinary LDH at a threshold of 135 U/L was more specific (75% vs 53%, P less than .01) and more accurate (74% vs 57%, P less than .01) than hematuria at a threshold of 50 red blood cells per high-power field in predicting lacerations of the kidney or ureter; urinary LDH was less sensitive than hematuria at these thresholds (67% vs 100%), but not significantly. We conclude that urinary LDH is a nonspecific marker of cellular disruption anywhere along the genitourinary tract in otherwise healthy blunt trauma patients.

A microassay for mammalian renal 25-hydroxyvitamin D3-1-hydroxylase applicable to man.

A micro determination of the renal 25-hydroxyvitamin D3-1-hydroxylase activity was developed that uses as little as 1 mg of rat kidney tissue. The method was applied to the remaining portions of needle kidney biopsy specimens taken for diagnostic purposes from children who had asymptomatic proteinuria and/or hematuria (more than 1-year duration) but were otherwise normal in calcium metabolism and renal function. The 25-hydroxyvitamin D3-1-hydroxylase levels of these children were found to be 66 1,25-dihydroxyvitamin D3 per milligram of tissue per 20 min for an 11-year-old male, 117 pg for a 9-year-old male, and 89 pg for a 10-year-old female.

Urinary acidic hydrolases in renal diseases in children.

Acidic hydrolases were assayed in urines of 19 normal children, 33 children with idiopathic nephrotic syndrome of childhood (INS), 21 children with glomerulonephritides (GN) and 7 children with persistent proteinuria/hematuria, and in plasma of 10 children each with INS or GN. Both plasma and urinary acidic hydrolases were studied in intermittent orthostatic proteinuria. Cbeta-galactosidase and Cbeta-N-hexosaminidase were done in normals and children with active renal disease. Significantly (P less than 0.01) elevated urinary acidic hydrolases excretion in active renal diseases, both in INS and GN, returned to a normal range with regression of the diseases. Increased postural proteinuria was associated with normal urinary acidic hydrolases. Both beta-galactosidase and beta-N-hexosaminidase excretion was higher than similar mol wt proteins in normals and increased further in active renal diseases. The data suggests that increased urinary acidic hydrolases is related to the activity of the renal disease, and not to urinary WBC, hematuria or proteinuria. The likely source of urinary acidic hydrolases thus appears to be the injured renal parenchyma itself.

A distinct human variant of hypoxanthine-guanine phosphoribosyl transferase.

A variant form of hypoxanthine-guanine phosphoribosyl transferase has been found in a neurologically normal pediatric patient who presented with hematuria an episodes of oliguria and azotemia. The level of erythrocyte enzyme activity was 3% of normal. Electrophoretic mobility was more rapid than normal. The Km for hypoxanthine was approximately ten times normal. Immunochemical analysis indicated that the variant enzyme cross reacted with antibody to normal HPRT. A system is described for the systematic characterization of a variant HPRT.

Studies on urinary isozymes of lactic dehydrogenase and beta-glucuronidase in patients with bladder tumors.

Isozymes of urinary lactic dehydrogenase (LDH) were studied in 55 subjects, including 17 patients with bladder tumors. Normal clear urine from healthy persons showed little activity of LDH5, but in 11 out of 17 patients with bladder tumors LDH5 was increased sufficiently to invert the ratio of LDH5/LDH1, although the urine was not contaminated appreciably with leucocytes. Studies on tissue LDH isozymes in 16 tumors specimens strongly suggested that increased LDH5 in the urine of patients with bladder tumors originated from the tumors themselves. beta-Glucuronidase (B-G) isozymes were studied in urine specimens from 10 normal subjects, and 10 patients with bladder tumors and in 5 specimens of normal epithelium and 5 of tumor tissue. Two or three distinct bands of beta-G were separated from specimens of urine and tumor tissue from patients with bladder tumors, but only a single band was found in specimens from normal subjects.