Molecular size distribution of immunoreactive trypsin and renal tubular dysfunction: role in trypsin plasma-urine transfer

In order to investigate the role of circulating free trypsinogen and renal tubular dysfunction in affecting trypsin plasma-urine transfer, serum immunoreactive trypsin (IRT), its urinary output, IRT molecular size distribution, filtrable immunoreactive trypsin, gamma-glutamyltransferase and alpha-glucosidase outputs were studied in 6 control subjects, 9 patients with pancreatic cancer and 15 with chronic pancreatitis. The majority of immunoreactivity was always eluted at a molecular weight of about 24,000 and might therefore be considered as free trypsinogen. Variable amounts of IRT at higher molecular weights, possibly represented by trypsin-inhibitor complexes, were also detected. Increasing IRT levels were generally accounted for by free trypsinogen, regardless of the nature of the disease. Unlike serum free trypsinogen levels, renal tubular damage, evaluated by means of the excretion of two high-molecular weight urinary enzymes, seems to play a prominent role in explaining trypsin plasma-urine transfer.     

Urinary elastase 1 in chronic pancreatic disease

Serum and urine elastase 1, its renal output and clearance and urinary gamma-glutamyltransferase and ribonuclease excretions were measured in 16 patients with pancreatic cancer, 23 with chronic pancreatitis and in 22 healthy controls in order to evaluate elastase 1 plasma-urine transfer in chronic pancreatic disease and to investigate any factors that might influence the clearance of this enzyme. In an additional group of 17 patients with different pancreatic diseases the serum molecular size distribution of elastase 1 after chromatography was ascertained. An increased urinary elastase 1 output was found in 4/16 patients with pancreatic cancer and in 6/23 with chronic pancreatitis. No correlation was found between circulating elastase 1 and its urinary output; a negative correlation was detected between the serum levels of this enzyme and its clearance. The excretion of ribonuclease and gamma-glutamyltransferase was correlated with elastase 1 output and clearance. While the majority of elastase 1 in serum was accounted for by high molecular forms, probably the expression of complexes with serum inhibitors, free circulating enzyme was present in all patients with high serum elastase 1. Our findings suggest that elastase 1 urinary excretion increases in some patients with chronic pancreatic disease regardless of the neoplastic or inflammatory nature of the illness. Although the availability of different amounts of ultrafiltrable enzyme may play a role in influencing elastase 1 plasma-urine transfer, renal tubular damage appears to be the most important factor influencing the increase in the urinary output of elastase 1.     

Circadian Rhythm in Gamma Glutamyltranspeptidase and Leucine Aminopeptidase Urinary Activity in Rats

Urinary gamma glutamyltranspeptidase (GGT) and leucine aminopeptidase (LAP), renal tubular brush border enzymes, have been shown to be sensitive indicators of renal tubular functions. This study documents circadian rhythms in the urinary activity of GGT and LAP, statistically validated and quantified by the cosinor method, in 15 male Wistar rats standardized to a LD 12:12 illumination schedule (light from 0800 hr to 2000 hr) and fed ad libitum. The acrophase of the circadian rhythms in urinary GGT and LAP activity occurred at the end of the rest span of the animals: between 1730 and 1915 for GGT (depending on the mode of expression of the activity) and between 1700 and 1910 for LAP. Of striking resemblance in their timing, both these rhythms were also of large amplitude (about 50% of the mesor for urinary GGT activity and about 45% for LAP one). The circadian acrophases of urinary GGT and LAP activity led in timing the circadian rhythms in urine volume and creatinine excretion by about 13hr. Such findings consistent with the circadian variations found by other investigators in GGT in kidney homogenates or in LAP in human urine thus reflect a periodicity in renal tubular function. The reasons for these circadian variations, still unknown at this time, are discussed. The influence recently demonstrated of the hormonal context on protein and enzyme synthesis at the tubule, and its phase relations to urinary enzyme excretion emphasize how much the circadian rhythm in urinary GGT and LAP activity is well included in the murine time structure. Therefore it should be of interest to consider the circadian rhythm in urinary GGT and LAP release as a marker rhythm of predictive value as to the side effects of nephrotoxic drugs.     

Circadian Rhythm in Gamma Glutamyltranspeptidase and Leucine Aminopeptidase Urinary Activity in Rats

Urinary gamma glutamyltranspeptidase (GGT) and leucine aminopeptidase (LAP), renal tubular brush border enzymes, have been shown to be sensitive indicators of renal tubular functions. This study documents circadian rhythms in the urinary activity of GGT and LAP, statistically validated and quantified by the cosinor method, in 15 male Wistar rats standardized to a LD 12:12 illumination schedule (light from 0800 hr to 2000 hr) and fed ad libitum. The acrophase of the circadian rhythms in urinary GGT and LAP activity occurred at the end of the rest span of the animals: between 1730 and 1915 for GGT (depending on the mode of expression of the activity) and between 1700 and 1910 for LAP. Of striking resemblance in their timing, both these rhythms were also of large amplitude (about 50% of the mesor for urinary GGT activity and about 45% for LAP one). The circadian acrophases of urinary GGT and LAP activity led in timing the circadian rhythms in urine volume and creatinine excretion by about 13hr. Such findings consistent with the circadian variations found by other investigators in GGT in kidney homogenates or in LAP in human urine thus reflect a periodicity in renal tubular function. The reasons for these circadian variations, still unknown at this time, are discussed. The influence recently demonstrated of the hormonal context on protein and enzyme synthesis at the tubule, and its phase relations to urinary enzyme excretion emphasize how much the circadian rhythm in urinary GGT and LAP activity is well included in the murine time structure. Therefore it should be of interest to consider the circadian rhythm in urinary GGT and LAP release as a marker rhythm of predictive value as to the side effects of nephrotoxic drugs.     

Renal clearance and excretion of endogenous substances in the owl monkey

The clearance and excretion of creatinine, calcium, phosphorus, sodium, and potassium by the kidney was evaluated in 62 owl monkeys using timed urine collections and quantitative urinalyses. The endogenous clearance of creatinine was determined for each monkey. Urinary electrolyte excretion and fractional electrolyte excretions (FE) were measured. Linear regression analysis was used to calculate the correlation between urinary excretion and FE for each electrolyte. The coefficient of determination for each analyte was significant (P ? .0001). Determination of FE was found to be an appropriate indicator of the renal handling of electrolytes and, when viewed in conjunction with urinalysis and other serum parameters, an aid in evaluating renal function in the owl monkey. © 1992 Wiley-Liss, Inc.     

Excretion of multiple urinary biomarkers for radical induced damage in rats treated with three different nephrotoxic compounds

In the present study the urinary excretion of seven aldehydes, acetone and coproporphyrin III as non-invasive in vivo biomarkers of free radical damage was measured in rats after treatment with three nephrotoxic compounds: cisplatin, mercuric chloride (HgCl2) and N -acetyl- S -(1,1,2,2-tetrafluoroethyl)-L-cysteine (TFE-Nac). A clear difference between the different nephrotoxic compounds was found in the time interval between dosage and maximal toxicity, as measured by clinical chemical parameters in urine. In rats treated with TFE-Nac and HgCl2 this was fast: 12 h and 24 h after treatment, respectively. In the rats treated with cisplatin, however, nephrotoxicity occurred later: 96 h-108 h after treatment. Urinary creatinine excretion was decreased in all treatments. Therefore, the excretion of the proposed biomarkers was expressed as amount excreted per 12 h urine fraction as well as amount excreted per mol creatinine in each 12 h urine fraction. Urinary excretion of coproporphyrin III was decreased in almost all 12 h urine fractions with all treatments, however, when expressed per mol creatinine, increases were found in urine of rats treated with cisplatin and HgCl2. In cisplatin-treated rats an increase was found in the excretion of formaldehyde per 12 h, but acetaldehyde, propanal and MDA levels were decreased. Expressed per mol creatinine, MDA levels were decreased, but other aldehydes were increased. In HgCl2-treated rats urinary aldehyde excretion expressed per mol creatinine was increased. In TFE-Nac treated animals the urinary levels of acetaldehyde per 12 h were increased and per mol creatinine the levels of some aldehydes were only slightly increased. With none of the treatments did the increase in the biomarkers expressed per mol creatinine exceed the decrease in creatinine excretion. Similar time intervals were found between dosage and maximal excretion of biomarkers as for the time intervals between dosage and maximal toxicity. With all treatments significant increases in the excretion of acetone were found both per 12 h and per mol creatinine, probably related to the increased glucose excretion. It was concluded that no convincing evidence for free radical damage was found in the present study with the employed biomarkers.     

Excretion of multiple urinary biomarkers for radical induced damage in rats treated with three different nephrotoxic compounds

In the present study the urinary excretion of seven aldehydes, acetone and coproporphyrin III as non-invasive in vivo biomarkers of free radical damage was measured in rats after treatment with three nephrotoxic compounds: cisplatin, mercuric chloride (HgCl2) and N -acetyl- S -(1,1,2,2-tetrafluoroethyl)-L-cysteine (TFE-Nac). A clear difference between the different nephrotoxic compounds was found in the time interval between dosage and maximal toxicity, as measured by clinical chemical parameters in urine. In rats treated with TFE-Nac and HgCl2 this was fast: 12 h and 24 h after treatment, respectively. In the rats treated with cisplatin, however, nephrotoxicity occurred later: 96 h-108 h after treatment. Urinary creatinine excretion was decreased in all treatments. Therefore, the excretion of the proposed biomarkers was expressed as amount excreted per 12 h urine fraction as well as amount excreted per mol creatinine in each 12 h urine fraction. Urinary excretion of coproporphyrin III was decreased in almost all 12 h urine fractions with all treatments, however, when expressed per mol creatinine, increases were found in urine of rats treated with cisplatin and HgCl2. In cisplatin-treated rats an increase was found in the excretion of formaldehyde per 12 h, but acetaldehyde, propanal and MDA levels were decreased. Expressed per mol creatinine, MDA levels were decreased, but other aldehydes were increased. In HgCl2-treated rats urinary aldehyde excretion expressed per mol creatinine was increased. In TFE-Nac treated animals the urinary levels of acetaldehyde per 12 h were increased and per mol creatinine the levels of some aldehydes were only slightly increased. With none of the treatments did the increase in the biomarkers expressed per mol creatinine exceed the decrease in creatinine excretion. Similar time intervals were found between dosage and maximal excretion of biomarkers as for the time intervals between dosage and maximal toxicity. With all treatments significant increases in the excretion of acetone were found both per 12 h and per mol creatinine, probably related to the increased glucose excretion. It was concluded that no convincing evidence for free radical damage was found in the present study with the employed biomarkers.     

Polyamine concentrations in red cells and urine of patients with chronic renal failure

Spermidine and spermine concentrations were measured in 6 healthy subjects, 18 patients with chronic renal failure and 6 patients undergoing maintenance hemodialysis. In nondialyzed patients with advanced renal failure (serum creatinine levels greater than 6 mg %), red cell spermidine concentrations were significantly higher than in normal subjects (54.8±14.5 vs. 24.8±63 SD nmoles/ml packed cells). However red cell spermine concentrations were unchanged as compared to normal subjects (18.7±7.3 vs. 12.4±3.4 nmoles/ml packed cells). In patients with serum creatinine levels below 6 mg%, neither red cell spermidine or spermine concentrations were significantly different from normal subjects. There was a significant correlation between red cell spermidine values and both serum urea and serum creatinine levels, but no correlations were observed for red cell spermine. Red cell spermidine values were also significantly higher in patients undergoing maintenance hemodialysis than in normal subjects. In each patient, red cell spermidine concentrations were no different after a hemodialysis treatment than immediately prior to dialysis. In urine, excretion rates of polyamines as well as the precursor diamine, putrescine, were lower in patients with chronic renal failure than in normal subjects. Hence in renal failure, one factor contributing to the accumulation of spermidine in red cells would appear to be a decrease in the urinary excretion of polyamines.     

The source of urinary epidermal growth factor in humans

To clarify the source of human urine EGF, we studied EGF renal clearance in 20 healthy, young adult subjects. Immunoreactive EGF was measured hourly in EDTA plasma, heparin plasma, serum and urine of 12 males and 8 females during a 3 h study period. Plasma and urine creatinine and creatinine clearance were measured and calculated hourly. Mean (and SEM) creatinine clearance was similar in males and females (118 +/- 12 vs 105 +/- 6 ml/min). EGF was not detectable in plasma, whereas relatively high levels were measured in serum (2.5 +/- 0.25 vs 1.5 +/- 0.18 ng/ml in males and females respectively p less than 0.05). Urine EGF excretion averaged 1641 +/- 233 ng/h in males and 1507 +/- 191 ng/h in females (p greater than 0.05). A significant correlation was observed between urine creatinine and urine EGF concentrations in both male (r = 0.98, p less than 0.01) and female (r = 0.94, p less than 0.01) subjects. EGF immunoreactivity in urine and serum eluted from G-75 sephadex columns similarly to recombinant 6000 Mr hEGF. Urine excretion of EGF approximated 1.5 micrograms/h or 25 ng/mg creatine. The high concentrations of EGF found in urine in the face of non-detectable levels of EGF in plasma favor the hypothesis that EGF in urine is derived from kidney synthesis and secretion. The significant positive correlation between urine creatinine and urine EGF suggests a functional correlation between glomerular filtration and the process of tubular EGF excretion.     

吲哚美辛联合生长抑素对ERCP术后胰腺炎的预防作用

目的:研究吲哚美辛联合生长抑素对内镜逆行胰胆管造影(ERCP)术后胰腺炎的预防作用及对血清淀粉酶的影响。方法:选取2015年7月至2016年6月在我院行ERCP术的患者共72例,根据随机数字法分为观察和对照组,每组36例。对照组在术前使用生长抑素完成治疗,观察组在此基础上联合吲哚美辛栓剂完成治疗。分析和比较两组患者ERCP术后5、10、24、48h的血清淀粉酶水平,ERCP术后48h胰腺炎的发生率、肝功能变化情况和临床症状改善情况。结果:术前,两组患者血清淀粉酶水平比较无显著差异(P0.05),术后5h,两组患者的血清淀粉酶水平较高,和术后5h相比,两组术后10、24、48h的血清淀粉酶水平明显降低(P0.05),但观察组各时点血清淀粉酶水平均低于对照组(P0.05)。术前,两组患者GGT、ALP、AST水平比较无显著差异(P0.05),术后48h,两组患者GGT、ALP、AST水平较术前无明显变化(P0.05)。术后48 h,观察组的胰腺炎发生率显著低于对照组[8.33%(3/36) vs. 36.11%(13/36)](P0.05)。观察组的皮肤瘙痒、腹泻、恶心、厌食、感染的减轻率均高于对照组(P0.05)。结论:吲哚美辛联合生长抑素能有效降低ERCP术后胰腺炎的发生率,降低血清淀粉酶水平。     

Elevated Amylase and Lipase Levels in Patients Using Glucagonlike Peptide-1 Receptor Agonists or Dipeptidyl-Peptidase-4 Inhibitors In the Outpatient Setting

ObjectiveTo investigate the effects of glucagonlike peptidase-1 (GLP-1) receptor agonists and dipeptidyl-peptidase-4 (DPP-4) inhibitors on serum amylase and serum lipase levels in patients with type 2 diabetes.MethodsIn 90 patients with type 2 diabetes, treatment was initiated with a GLP-1 agonist or a DPP-4 inhibitor. A comparison group consisted of 33 patients with type2 diabetes and similar characteristics who were not prescribed these agents. Baseline serum amylase and lipase levels were measured in all patients and repeated periodically. We determined the percentage of patients with elevated levels of serum amylase or lipase (or both) in both groups.ResultsAmong all 90 patients who received a GLP-1 receptor agonist or a DPP-4 inhibitor, 32 (36%) had an increase in serum amylase or lipase (or both) in comparison with 6 of 33 patients (18%) with such increases in the comparison group. Interestingly, the serum lipase levels increased more than the serum amylase values in all groups. To ascertain that this was not a chance laboratory error, serum samples were submitted to a second independent laboratory, and the same results were obtained. Usually, use of the medication was discontinued when serum lipase or amylase values were found to be elevated at any level.ConclusionBoth GLP-1 receptor agonists and DPP-4 inhibitors are associated with increased levels of serum lipase more than serum amylase in many patients with type2 diabetes, possibly suggesting the presence of pancreatic inflammation. Whether this finding may potentially lead to acute pancreatitis or chronic pancreatitis, as reported in rat models, is currently unknown. Careful observation of patients taking these medications may be prudent. (Endocr Pract. 2012;18:472-477)     

Serum, urinary, and salivary nitric oxide in rheumatoid arthritis: complexities of interpreting nitric oxide measures

Nitric oxide (NO) may play important roles in rheumatoid arthritis (RA). RA is an inflammatory disease involving joints and other systems including salivary glands. To assess NO production in RA patients, we compared levels of serum, urine, and salivary nitrite and nitrate (NOx) in patients with RA and normal subjects, and we examined the relationships of these measures to disease activity. Serum, urine, and NOx levels as well as renal creatinine, NOx clearance and fractional excretion rates were compared in 25 RA patients and 20 age- and gender-matched healthy controls. Subjects were hospitalized for 3 days and placed on a NOxrestricted diet. NOx was assayed using nitrate reductase and the Griess reagent. RA activity was assessed using standard clinical and laboratory measures. While consuming a restricted diet for 3 days to eliminate the effects of oral intake of NOx, 24 hour urinary NOx excretion decreased in both RA patients and healthy controls. Urine NOx levels at all time points were not significantly different between RA patients and normal subjects. Serum NOx levels also decreased during the 3 days of NOx restriction, but RA patients had higher serum NOx levels at all time points compared with the control group. Likewise, serum NOx/creatinine ratios were higher in RA patients than in controls. Although basal salivary flow rate and tear flow were lower in RA patients, salivary NOx levels did not differ between normal and RA subjects. While renal creatinine clearance was not different between the two groups, we found that RA patients had lower renal NOx clearance and lower renal NOx fractional excretion. After correction of p values for multiple comparisons, there were no significant relationships for the RA group between measures of disease activity and the urinary NOx, serum NOx, or urinary NOx clearance. Despite interest in the use of NO as a marker of disease activity, alterations in renal NOx clearance and fractional excretion in RA make it difficult to assess in vivo NO production even with strict dietary restriction of NOx intake.     

Ftorafur therapy in acute pancreatitis

The authors tested Ftorafur (N1-2'-furanidyl-5-fluorouracyl) in patients with acute pancreatitis on the basis of experimental and clinical data. The daily dosage was 200 mg (3-4 mg/kg body weight). In the course of treatment the serum and urine levels of amylase and the changes in WBC were studied. The results were compared to that obtained in patients with acute pancreatitis but were not given Ftorafur. Urine amylase levels decreased significantly in response to Ftorafur treatment over three days. The decrease of serum amylase levels and WBC was not significant in either group. The advantages of Ftorafur treatment are as follows: levels of amylase in serum and urine are normalized earlier, the duration of treatment, hence costs are decreased, Ftorafur produced a cytoprotective effect due to the inhibition of protein synthesis in the pancreas.     

Platelet activating factor (PAF) inhibitor (TCV-309) reduces caerulein- and PAF-induced pancreatitis. A morphologic and functional study in the rat.

Caerulein-induced acute pancreatitis was studied in rats. Consistent with this type of acute pancreatitis morphological (edema, leukocytic infiltration and acinar cell vaculization) and biochemical (increase in pancreatic protein content. PAF release and serum amylase) changes developed 5 hours after caerulein administration. In addition increase in pancreatic weight and decrease in pancreatic blood flow were noticed. PAF administration caused pancreatic damage similar in some parameters to caerulein-induced pancreatitis, along with reduction of pancreatic blood flow, increase in pancreatic protein content, and serum amylase. TCV-309, a selective PAF antagonist, administered prior to caerulein and/or PAF, reduced caerulein-induced pancreatitis and prevented PAF-induced pancreatitis. Results of our present studies indicate the crucial role of PAF in pathogenesis of experimental acute pancreatitis.     

Circadian variation in renal function of the obese rat.

The influence of food and water intake on renal function was assessed by comparisons between the hyperphagic Zucker obese rat and its lean littermate, which demonstrates nocturnal dominance in activity. Serum creatinine and cortisol levels, creatine kinase activities, creatinine and urine clearances, and sodium and potassium excretion rates were measured over a 24-hour period in both lean and obese rats (n = 24 each). Six rats in each group were studied every 8 h to permit characterization over a 12-hour light/dark cycle at 2-hour intervals. Urine and creatinine clearances were increased in lean rats during the dark phase coincident with onset of eating. Similarly, renal sodium and potassium excretion rates were markedly increased during the dark cycle, despite relatively constant serum potassium and sodium levels over the 24-hour period. In contrast, no circadian patterns in urine and creatinine clearances were found in the obese rat, which exhibits continuous feeding habits throughout the 24-hour period. Moreover, renal electrolyte excretion in the obese rat was modestly increased during the dark cycle, unlike the significant differences over time observed in lean rats. Serum creatinine levels were increased during the dark cycle in both rat groups. Creatine kinase activity, a measure of ambulatory activity, was constant in lean rats during the study period. Although creatine kinase activity was increased in obese rats during the dark cycle, no correlations with renal functional parameters were found. These results indicate that differences in food and water intake are significant determinants in diurnal cyclic changes in renal function.     

乌司他丁治疗急性胰腺炎的临床疗效及机制研究

目的:探讨乌司他丁对急性胰腺炎患者的临床疗效及可能机制。方法:收集我院收治的重症急性胰腺炎患者66例,随机分为实验组和对照组。所有患者均给予禁食水、充分补液、纠正电解质紊乱等常规支持对症治疗。对照组予奥曲肽,实验组予乌司他丁,共治疗7天。测定两组患者治疗前、后各血清白介素-6(IL-6)、白介素-8(IL-8)及肿瘤坏死因子-α(TNF-α)水平;治疗前、治疗第1、3天及治疗后进行血常规检测,观察白细胞计数(WBC),并进行血淀粉酶(AMS)、尿淀粉酶(UAMY)测定;分别记录两组患者临床症状及体征恢复时间,判定临床疗效。结果:1治疗后,两组患者血清IL-6、IL-8及TNF-α水平均较治疗前显著下降,且实验组较对照组下降更明显(P0.05);2治疗后,两组患者白细胞计数及血、尿淀粉酶水平均较治疗前明显下降,且实验组较对照组下降更明显(P0.05);3治疗后,实验组各项临床症状及体征消失时间均明显短于对照组(P0.05)。结论:乌司他丁可有效改善急性胰腺胰腺炎患者的各项临床症状,这可能与其显著降低其血清IL-6、IL-8、TNF-α、淀粉酶水平、白细胞计数及尿淀粉酶水平有关。     

Human ribonucleases. Quantitation of pancreatic-like enzymes in serum, urine, and organ preparations

Antibodies against pure human pancreatic ribonuclease (RNase) were used to study ribonuclease levels in human tissues and body fluids. The antibodies completely inhibit the activity of purified RNase as well as ribonuclease activity in crude pancreatic extracts. RNase activity is inhibited by 70-80% in serum and urine, indicating that a significant proportion of the RNases in these preparations are structurally like the pancreatic enzyme. In contrast, inhibition of RNase activities from spleen (8%) and liver (30%) was inefficient suggesting that most of the RNases in these tissues are structurally unlike the pancreatic enzyme. A competitive binding radioimmunoassay (RIA), sensitive in the range of 1-100 ng of RNase, was developed to quantitate the pancreatic like enzymes. The RIA of crude tissue preparations and samples fractionated by gel filtration was compatible with inhibition results. Enzymes structurally like pancreatic RNase could be quantitated despite the presence of other RNase activities. Immunological quantitation of pancreatic like RNases was also found to be much more simple and precise than enzymatic assays comparing RNA and polycytidylate substrates. We suggest the immunological assays will be useful in the quantitation and definition of tissue of origin of RNases in serum of patients with pancreatic carcinoma.     

Renal function after long-term treatment with lithium.

Daily urine volumes, plasma creatinine concentrations, and creatinine clearance were measured in 106 patients with unipolar and bipolar affective disorders attending a "lithium" clinic. Urine volumes exceeded 3.51 in only six patients, plasma creatinine concentrations exceeded 150 mumol/1 (1.7 mg/100 ml) in only five, and creatinine clearance was below 50 ml/min in 16. Renal function was assessed by measuring creatinine clearance and renal tubular function, including response to 20 hours of water deprivation, in a representative sample of 30 patients from the lithium clinic and 30 psychiatric patients matched for age and sex who were taking other psychotropic drugs. Creatinine clearance and tubular function, including urine osmolality after water deprivation, were not significantly different between the two groups. Urinary excretion of arginine vasopressin (AVP), however, was much greater in the lithium-treated patients, who therefore had a diminished tubular responsiveness to AVP. The findings do not support suggestions that long-term lithium treatment results in seriously impaired renal function, renal damage, and polyuria. Compared with other series, however, the patients were being maintained with low serum lithium concentrations, which apparently area as effective prophylactically as higher concentrations.     

Aqueous extract of black tea (Camellia sinensis) prevents ethanol+cholecystokinin-induced pancreatitis in a rat model

Black Tea Extract (BTE), a phytocompound has been attributed with a plethora of health-promoting actions. We have previously demonstrated that BTE inhibits chronic hepatitis in a rat model induced with high-fat and ethanol (EtOH). This study reports that BTE prevents altered pancreatic acinar cell functions, oxidative stress, inflammatory changes and DNA damage in the EtOH+cholecystokinin (CCK)-induced model of pancreatitis. The EtOH+CCK model rats were administered with BTE, and were examined the activity of pancreatic digestive enzymes (amylase and lipase), proinflammatory cytokines (IL-6 and TNF-alpha), oxidative and antioxidative enzymes (nitric oxide, NO; malondialdehyde, MDA; superoxide dismutase, SOD; catalase, CAT), antioxidant level (glutathione, GSH), histopathological changes and the integrity of genomic DNA. Results show that because of chronic EtOH treatment, serum level of amylase and lipase (two biomarkers for pancreatitis) and pancreatic levels of MDA and NO (two biomarkers of oxidative stress) increased significantly, which could be effectively blunted by BTE. BTE could normalize EtOH+CCK-induced suppressed activities of SOD and CAT, and GSH content of pancreatic tissue. Also, histopathological and inflammatory changes during EtOH+CCK-induced pancreatitis could be blunted by BTE. Furthermore, BTE could effectively reduce EtOH+CCK-induced increase in DNA fragmentation and damage. These findings suggest that BTE prevents pancreatitis caused by chronic EtOH+CCK toxicity presumably by enhancing antioxidant, anti-inflammatory and antiapoptotic activity in rats.     

Studies on urinary gamma-glutamyl transpeptidase in nephrotic syndrome patients

(1) Variations in the levels of GGT were measured in urine specimens taken in the early morning in control and in 20 consecutive adult patients with uncomplicated nephrotic syndrome. (2) The urinary GGT activity was increased in all cases of nephrotic syndrome patients investigated with different etiology. (3) A significant correlation was found between urinary GGT activity and serum albumin (r = 0.727) but not with serum cholesterol (r = 0.129). (4) These findings suggest that enhanced excretion of urinary GGT may be stimulated by decreased albumin concentration or oncotic pressure but does not appear to be due to leakage from plasma. (5) A systematic study on urinary GGT showed that GGT activity was decreased to the upper limit of normal control values in nephrotic syndrome patients after remission.