Impact of Helicobacter pylori infection on serum gastrin in haemodialysis patients.

BACKGROUND: Helicobacter pylori infection is associated with increased gastrin release in patients with normal renal function. Hypergastrinaemia is a common finding in haemodialysis patients and, in many cases, may be linked to H. pylori infection. The aim of this study was to examine the effect of H. pylori infection, and its eradication, on elevated gastrin levels in haemodialysis patients. METHODS: Eighty-nine dyspeptic patients were included in the study. While 44 patients had normal renal function, the remaining 45 were end-stage renal failure patients. Patients were assigned to one of four groups according to their H. pylori and renal function status. Infected patients were re-evaluated after 2 months following eradication treatment. Serum gastrin levels were measured in these groups both before and after eradication treatment. RESULTS: Haemodialysis patients with H. pylori infection had higher serum gastrin levels than did H. pylori negative haemodialysis patients (321+/-131 pg/ml vs 154+/-25 pg/ml) (P<0.05). Mean serum gastrin concentration was 152+/-21 pg/ml in the non-uraemic H. pylori-positive group. This value was 58+/-17 pg/ml in the non-uraemic H. pylori-negative group (P<0.05). There were significant decreases in serum gastrin levels from pre- to post-eradication of H. pylori in the infected haemodialysis and non-uraemic patient groups (312+/-131 pg/ml to 179+/-85 pg/ml and 152+/-21 pg/ml to 72+/-2.4 pg/ml respectively, P<0.05). Four patients in group Ib and 5 patients in group IIb who had persistent infection did not have a decrease in serum gastrin level. All patients with successful eradication had a decrease in serum gastrin concentration. CONCLUSION: Our findings suggest that H. pylori infection contributes to hypergastrinaemia in haemodialysis patients. More research is needed regarding the clinical consequences of hypergastrinaemia in these individuals.     

Gastrin and partial gastrectomy in duodenal ulcer patients 25 years postoperatively

Serum gastrin concentrations were measured in 26 patients (Group A) who underwent partial gastrectomy for duodenal ulcer disease at least 25 years previously. The basal serum gastrin level was 31.6 +/- 1.5 pg/ml, increasing significantly after food stimulation to 36.8 +/- 2.4 pg/ml (p less than 0.05). In 16 of these patients (Group B), endoscopic biopsy specimens were taken from the minor and major curvatures of the stomach, from the jejunal part of the gastrojejunostomy, and from the duodenum. Mucosal gastrin concentrations measured were 0, 20.4 +/- 3 ng/g, and 30 +/- 7.1 ng/g, respectively. Ten of these patients (Group C) had a repeated gastroscopy with food stimulation of the duodenal pouch, using a balloon catheter in the lower duodenum. Serum gastrin concentrations after pouch stimulation did not differ significantly compared with basal values. No changes in the mucosal gastrin concentrations during pouch stimulation were seen. In conclusion, since no gastrin could be detected in the gastric mucosa and the mucosal gastrin concentration in the duodenum was 50 times lower than reported in other studies, the gastrin release measured after food stimulation could have been of extragastric or extraduodenal origin.     

Evaluation of serum S100ao protein in patients with renal cell carcinoma

In order to evaluate the clinical significance of S100ao protein, we measured serum S100ao protein in 36 patients with renal cell carcinoma by EIA developed by Kimura et al. In addition, the distribution of S100ao protein was studied by the immunohistochemical method. Previous study demonstrated that mean level of serum S100ao protein in healthy volunteers was 203 +/- 107 pg/ml, therefore the cut off level was set to 524 pg/ml. The results obtained in this study were as follows: 1) The mean level of serum S100ao protein was 1162 +/- 2056 pg/ml, and its positive rate was 44% in 36 patients with renal cell carcinoma. When the patients were divided into 2 groups according to tumor stage, the mean level of serum S100ao protein in the high stage group was significantly higher than that in the low stage group (p less than 0.01). 2) In the sequential study of serum S100ao protein, patients with progressive disease showed a gradual increase in the level of serum S100ao protein while patients with no evidence of tumor showed a normal level of serum S100ao protein. 3) There was no correlation between the level of serum S100ao protein and the histological grade of renal cell carcinoma. 4) Immunohistochemical analysis (10 cases) showed that S100ao protein was observed in all of 10 renal cell carcinomas. Thus, the present study suggests that serum S100ao protein might be a useful clinical marker especially in monitoring patients with renal cell carcinoma.     

Prostaglandins E and F in endocrine diarrheagenic syndromes.

The role of prostaglandins in endocrine diarrheagenic syndromes was evaluated by measuring peripheral concentration of immunoreactive PGE and PGF in patients with non-endocrine diarrhea as well as those with the Zollinger-Ellison (Z-E) syndrome, MCT, carcinoid tumors and the WDHA syndrome. In 21 normals, PGE and PGF levels averaged 272 +/- 18 and 119 +/- 14 pg/ml, respectively. Twenty eight patients with diarrhea of non-endocrine origin (mainly inflammatory bowel disease) had levels indistinguishable from normal, i.e. 353 +/- 25 and 77 +/- 37 pg/ml, respectively. Among 29 patients with the Zollinger-Ellison syndrome (mean gastrin 6127 +/- 3267 pg/ml) only 2 had significantly elevated PGE levels; mean PGE levels, 382 +/- 32 pg/ml, were not significantly different from normal and did not correlate with either diarrhea or the serum gastrin concentration. In contrast, 18 of 22 patients with carcinoid tumors (mean blood serotonin concentration 1655 +/- 604 ng/ml; mean urinary excretion of 5 HIAA 66.8 +/- 16.7 mg/day) had elevated peripheral concentrations of PGE. The mean PGE level (1367 +/- 245 pg/ml) was significantly elevated (P less than 0.001). Nonetheless PGE levels did not correlate with diarrhea, blood concentrations of serotonin, or urinary indole excretion. MCT (mean serum calcitonin 24.5 +/- 6.3 ng/ml) was similarly associated with consistent (18/19) elevation in peripheral concentrations of PGE (mean 1922 +/- 541 pg/ml; P less than 0.001). Inthis syndrome, PGE levels were higher in patients with diarrhea and in those with markedly elevated serum thyrocalcitonin levels. Finally, 8 of 21 patients with the WDHA syndrome had increased levels of PGE. Although 13 of 17 patients had high levels of VIP (mean 8133 pg/ml), 2 patients had hyperprostaglandinemia in the face of normal peripheral concentrations of VIP. In one patient the serum PGE level was elevated prior to resection of the primary pancreatic neoplasm (9939 pg/ml) as well as the subsequent extirpation of a solitary hepatic metastasis (1063 pg/ml); following each procedure the diarrhea abated and the PGE level returned to normal. In none of these syndromes were mean PGF levels elevated. The study has documented hyperprostaglandinemia in some endocrine diarrheagenic syndromes and validated the usefullness of measurements of PGE in patients with unexplained diarrhea.     

大肠癌患者血清及癌细胞胃泌素表达与其临床生物学行为的关系

目的　观测大肠癌患者血清、癌组织中胃泌素的表达 ,观察大肠癌细胞内胃泌素分泌颗粒的超微结构 ,旨在探讨血清胃泌素、胃泌素型癌细胞与大肠癌临床生物学行为的关系。方法　用放射免疫法和免疫组化法检测 5 3例大肠癌患者血清胃泌素、癌组织中胃泌素的表达。用免疫电镜技术观察 10例大肠癌细胞内胃泌素分泌颗粒的超微结构。结果　与对照组比较 ,大肠癌组术前血清胃泌素水平明显增高 ,分化良好者增高尤为明显 (P <0 .0 5 ,P <0 .0 1)。大肠癌组织胃泌素免疫组化阳性率为 5 6.6% ( 3 0 /5 3 ) ,高分化腺癌阳性率明显高于中、低分化腺癌。胃泌素阳性胶体金颗粒见于癌细胞内不同电子密度的分泌颗粒中和微绒毛膜表面。结论　大肠癌患者血清胃泌素水平增高 ,癌组织胃泌素表达阳性 ;大肠癌细胞形成胃泌素分泌颗粒释放胃泌素 ;血清胃泌素、胃泌素型癌细胞与大肠癌临床生物学行为有密切关系。     

Plasma and tumor gastrin in patients with primary hyperparathyroidism

It is well known that primary hyperparathyroidism is often associated with peptic ulcer. The purpose of this study is to confirm the relationship between the gastrin-levels before and after parathyroidectomy in fourteen patients with primary hyperparathyroidism, and to determine the localization of gastrin in the surgically resected parathyroid tumor. The results obtained were as follows: 1) Three patients had peptic ulcer (gastric ulcer and duodenal ulcer), the incidence being 21%. 2) The basal serum gastrin levels were 123.0% +/- 68.1 pg/ml before operation and decreased to 90.2 +/- 44.5 pg/ml after operation. In the 3 patients with slightly elevated gastrin levels, the mean level before operation was 209.1 +/- 61.2 pg/ml. The gastrin level decreased to 116.4 +/- 62.0 pg/ml after operation. 3) Gastrin immunoreactivity was detected in 10 out of 14 tumors and its localization was at the periphery of tumor cells. From these results, we conclude that extragastric gastrin secretion from parathyroid tumors may be one of the cause of peptic ulcer in patients with primary hyperparathyroidism.     

Gastric secretion and serum gastrin in human small bowel bypass.

Jejunolieal bypass (JIB) patients provide a unique opportunity to study the relationship between small bowel loss and gastric secretory function. Preoperatively, and approximately one year postoperatively, measurements of gastric secretion were taken in 37 patients who underwent JIB for massive obesity. Basal acid output increased by 0.52 plus or minus 0.35 mEq/hr (P greater than.2), and peak stimulated acid output increased by 1.99 plus or minus 0.96 mEq/30 min (P smaller than .05). A separate group of 26 postoperative and 17 preoperative (control) JIB patients had fasting serum gastrin levels measured by radioimmunoassay. Postoperative patients had levels of 37 plus or minus 5 pg/ml, and control patients had levels of 36 plus or minus 4 pg/ml (P greater than .5). We conclude that following JIB for obesity, there is no significant change in basal acid secretion or in serum gastrin. There is a small, but statistically significant, increase in peak stimulated acid output. We currently find no clinical correlation with this change.     

Effect of secretin on gastrin release from gastrinoma cells in vitro

Secretin appears to have a direct effect on gastrinoma cells, which results in a paradoxic increase in the serum gastrin level in patients with the Zollinger-Ellison syndrome. To evaluate this effect, gastrinoma cells were challenged with secretin in acute cell dispersion or after 2 weeks in culture. Acutely dispersed cells were incubated for 15 minutes or 3 hours with and without secretin 10(-6) mol/L. (sec). There was no significant difference in gastrin release between control and sec groups in the two acute incubation periods. At 15 minutes the control value was 47 +/- 1 and the sec value was 54 +/- 1 ng/ml, while at 3 hours the control value was 59 +/- 1 and the sec value was 61 +/- 1 ng/ml. In the cell culture preparation, secretin stimulated gastrin release at all doses (control 463 +/- 85, SEC 10(-10) mol/L 603 +/- 37, sec 10(-8) mol/L 706 +/- 37, sec 10(-6) mol/L 798 +/- 48 pg/ml ([p less than 0.05, Student t test]). These results indicate that secretin stimulates gastrin release directly from cultured gastrinoma cells in a dose-dependent manner but does not stimulate gastrin release from acute cell dispersion. This might be attributed partly to the recovery of secretin receptors in the cultured cells.     

Basal and meat extract plasma gastrin before and after parietal cell vagotomy and selective gastric vagotomy with drainage in patients with duodenal ulcer.

Basal and meat extract stimulated plasma gastrin (PG) levels and basal and stimulated gastric acid secretion were evaluated pre and postoperatively in duodenal ulcer patients who underwent parietal cell vagotomy without antral drainage (normal duodena) (PC, n=32) or selective vagotomy with drainage (pyloric stenosis) (SV +P, n=11). Before operation, both groups had comparable basal PG values of 52+/-13 pg/ml (PCVP) AND 51+/-18 PG/ML (SV+P), while the peak gastrin level to meat extract stimulation was 173+/-40 pg/ml for the total group of patients. After both operations basal PG levels increased (107+/-18 pg/ml (PCV) and 152+/-45 pg/ml (SV+P) and the gastrin response to meat extract stimulation was augmented after PCV, while the response after SV+P was the same as before operation. Patients with PCV often demonstrated an acid response following meat extract stimulation (3.6+/-0.9 mEq HC1/hr), and pentapeptide stimulation (18.8+/-2.0 mEq/hr) while patients with SV/P showed a minimal response (1.3+/-1.2 mEq HC1/hr meat extract), and 10.7+/-1.8 mEq/hr pentapeptide stimulation. The comparatively intact acid response in the PCV patients may augur a high ultimate recurrence rate.     

The effect of subarachnoid hemorrhage on blood and CSF atrial natriuretic factor

Atrial natriuretic factor (ANF) is a diuretic natriuretic peptide hormone produced by both the heart and brain which has been postulated to play a role in the hemodynamic and sodium instability that frequently follows subarachnoid hemorrhage (SAH). Levels of ANF were measured in 12 patients with nontraumatic SAH and nine control patients with unruptured cerebral aneurysms. At surgery, the mean plasma ANF level (+/- standard deviation) of the SAH group was significantly higher than that of the control group (158.1 +/- 83.8 vs. 57.8 +/- 45.3 pg/ml, respectively; p = 0.01). There was no significant difference in serum sodium concentration, blood pressure, or central venous pressure between these groups. Nine patients with SAH due to aneurysm rupture had plasma ANF levels similar to those in three patients with SAH due to other causes. Four patients with moderate to severe SAH had significantly higher mean cerebrospinal fluid (CSF) ANF values (17.7 +/- 12.8 pg/ml) than five patients with minimal SAH (0.6 +/- 0.9 pg/ml) or the control group of nine patients (3.7 +/- 1.3 pg/ml) (p less than 0.05). Five patients with moderate to severe SAH had significantly higher plasma ANF values (202.6 +/- 72.2 pg/ml) than five with minimal SAH (86.8 +/- 29.2 pg/ml) or the control group (57.8 +/- 45.3 pg/ml) (p less than 0.05). Plasma ANF values were substantially higher than CSF ANF content in the SAH group (p less than 0.01) and in the control group (p = 0.05). From these data it is concluded that: 1) plasma ANF is elevated significantly after SAH; 2) this rise appears unrelated to the cause of hemorrhage, serum sodium concentration, blood pressure, or central venous pressure, but is related to the extent of the hemorrhage; 3) ANF concentrations in the CSF are significantly lower than in plasma, and are elevated after moderate to severe SAH; and 4) the source of CSF ANF is probably the plasma, and the source of plasma ANF is likely the heart.     

Parathyroid carcinoma versus parathyroid adenoma in patients with profound hypercalcemia

The metabolic manifestations and operative findings in 10 patients with a diagnosis of parathyroid carcinoma were analyzed to determine whether they differ from those in patients with parathyroid adenomas and similar degrees of hypercalcemia. Two groups of patients with parathyroid adenomas were used for comparison. Group A consisted of eight patients with "atypical" benign adenomas (mean preoperative level of serum calcium: 13.4 mg/dl); group B consisted of 13 patients with benign typical adenomas--all with preoperative serum calcium levels greater than or equal to 13.0 mg/dl (mean: 14.2 mg/dl). The patients with carcinoma (mean preoperative level of serum calcium: 15.3 mg/dl) had a frequency of osteoporosis and osteitis fibrosa cystica (50%) comparable with that of group A (33%) and group B (62%). Seventy percent of the patients with carcinoma had renal disease (nephrolithiasis, nephrocalcinosis, or impaired renal function), whereas only 38% of group A and 15% of group B had similar disorders. The patients with carcinomas had the highest frequency of combined bone and renal disease (50% versus 14% in group A and 15% in group B). Anemia, peptic ulcer disease, and hypertension occurred with similar frequencies in the three groups. Three patients with recurrent parathyroid carcinoma died of profound hypercalcemia, renal failure, or cardiac arrhythmia. In general, although patients with parathyroid carcinomas have more profound metabolic abnormalities than do patients with primary hyperparathyroidism, the metabolic manifestations in patients with parathyroid carcinoma are comparable with those in patients with parathyroid adenomas and profound hypercalcemia. Furthermore atypical adenomas share many anatomic and histopathologic features with parathyroid carcinomas, and distinguishing between the two is sometimes possible only in cases of tumor recurrence.     

腹腔镜和开腹结直肠手术的炎性反应比较

目的对比分析腹腔镜和开腹结直肠手术患者全身和腹腔炎性反应的差异,为腹腔镜手术对结直肠肿瘤中的应用提供理论依据。方法对51例2004年4-8月间收治的乙状结肠和直肠恶性肿瘤患者,采用腹腔镜辅助手术25例(LAP组),开腹手术26例(OPEN组)。术毕骶前留置引流管。观察并比较两组患者的一般情况和炎性反应及与手术相关的各项指标。结果两组患者在年龄、性别、ASA分级、术前血红蛋白及白蛋白水平、肿瘤Dukes分期和手术方式差异均无统计学意义(P＞0．05)。在切口长度、手术时间、肠道功能恢复时间、住院时间的比较中,LAP组占有明显优势(P＜0．05)。腹腔引流量在术后第1天,两组间差异无统计学意义(P＞0．05)；而术后2-4 d,LAP组明显低于OPEN组(P＜0．05)。LAP组术后第1天,周围血中性粒细胞[(7．30±2．62)×10~9/L]、白介素(IL)-10[(19．46±3．31)pg/ml]和C反应蛋白(CRP)[(2．76±2．17)mg/dl]水平均显著低于OPEN组(P＜0．05)。术后第4天两组间差异无统计学意义(P＞0．05)。术后第1天,两组腹腔引流液的IL-10、肿瘤坏死因子(TNF)及CRP水平差异无统计学意义(P＞0．05),术后第4天LAP组IL-10 [(22．53±15．47)pg/ml]明显低于OPEN组(P＜0．05)。结论术后早期,腹腔镜结直肠手术的腹腔炎性反应与开腹手术相当,而全身炎性反应较开腹手术轻。腹腔镜结直肠手术临床上体现出恢复快、并发症少、住院天数少的优势。     

Acute effect of experimental truncal vagotomy on serum gastrin concentrations.

We studied the acute effect of transthoracic truncal vagotomy or sham vagotomy (control) on fasting serum gastrin concentrations in 22 gastric fistula dogs. A significant (p less than 0.05) decrease in serum gastrin concentration was detectable within 2.5 minutes after truncal vagotomy, and by 120 minutes serum gastrin has decreased to 15 +/- 1 pg/mL in the vagotomy group compared to 28 +/- 3 pg/mL in the control group (p less than 0.001). However by 24 hours after vagotomy, when maximal acid output was reduced by approximately 50%, fasting serum gastrin had increased nearly twofold above control levels in the vagotomy group (p = 0.06) and this increase persisted at day 7 (p less than 0.05). Thus truncal vagotomy had a biphasic effect on serum gastrin concentrations in dogs (acute inhibition followed by stimulation). While the mechanism for the acute fall in gastrin is probably an acute denervation of postganglionic neurons that innervate gastrin cells, the mechanism for the subsequent rise in serum gastrin remains uncertain.     

Radioimmunoassay of gastrin in human saliva

We have developed a personal procedure for the radioimmunoassay of gastrin (lower detection limit 3 pg/ml). Using 5-fold concentrated lyophilized salivary samples, we are able to detect the basal content of gastrin immunoreactivity in saliva of normal fasting people (mean +/- SD: 1.38 +/- 0.61 pg/ml) compared to plasma gastrin (mean +/- SD: 28.88 +/- 11.00 pg/ml). We found that after meal stimulus, the value of salivary as well as plasma gastrin concentration increased (the correlation coefficient r among salivary and plasma gastrin being 0.899; p less than 0.001). We believe that gastrin appears in a very low concentration in saliva and that it is not produced by the gland, but derives probably from the serum clearance.     

回肠袢式造口术和结肠造口术对老年左侧结直肠癌患者的临床疗效比较

目的观察回肠袢式造口术以及结肠造口术对老年左侧结肠癌患者的临床疗效对比。方法临床纳入老年结肠癌患者90例,根据随机数字表法分为回肠袢式造口术组与结肠造口术组,回肠袢式造口术组进行回肠袢式造口术,结肠造口术组进行结肠造口术。采用SPSS 16.0统计学软件进行数据处理,两组手术情况比较、血清胃泌素、肝细胞生长因子(HGF)水平采用t检验;两组患者术后并发症情况比较用(%)表示,χ~2检验,以P0.05为差异说明存在统计学意义。结果回肠袢式造口术组住院时间、首次排气时间、手术时间明显短于结肠造口术组(P0.05);血清胃泌素(59.3±24.2)pg/ml、HGF水平(853.6±94.9)pg/ml,均明显低于结肠造口术组(69.9±25.9)pg/ml、(1 009.6±100.3)pg/ml(t=2.01、7.59,P0.05);回肠袢式造口术组并发症感染率仅为2.2%(1/45),明显低于结肠造口术组的26.7%(12/45),(χ~2=10.88,P0.05);差异均有统计学意义。结论老年结肠癌患者采用回肠袢式造口术,患者术后恢复迅速,术后并发症低,临床效果确诊,值得临床推广。     

Effect of colectomy on cholecystokinin and gastrin release.

Studies were conducted to determine the effect of resection of the colon on the release of cholecystokinin (CCK) and gastrin. A standard food stimulation test was performed in five dogs. Peripheral blood samples were collected for future measurement of CCK and gastrin by specific radioimmunoassay. Each dog underwent subtotal colectomy with side-to-end ileoproctostomy. The food stimulation test was repeated at approximately weekly intervals for eight weeks after colectomy. Basal plasma CCK levels of 139 +/- 21 pg/ml before colectomy did not change after colectomy. Total amount CCK released after food was increased significantly at both four (5.94 +/- 0.78 ng min/ml) and eight (13.00 +/- 2.72 ng min/ml) weeks after colectomy in comparison with that observed prior to colectomy (2.94 +/- 0.54 ng min/ml). Basal serum gastrin levels of 28 +/- 9 pg/ml did not change significantly after colectomy. Total amount of gastrin released after food was increased significantly at both two (8651 +/- 2294 pg min/ml) and three (6940 +/- 1426 pg min/ml) weeks after operation, but at none of the later weeks. The precolectomy output, used for comparison, was 5608 +/- 1346 pg min/ml. It was concluded that resection of the colon leads to an increase in release of CCK and gastrin after food stimulation. This finding provides further evidence that the colon contains a factor that inhibits the release of CCK and gastrin, and that the colon functions as an endocrine organ.     

Beta-adrenergic regulation of gastrin release from gastrinoma cells

The effect of epinephrine on the plasma gastrin level was investigated in three patients with Zollinger-Ellison syndrome (ZES) and in 14 normal subjects. Two ZES patients had undergone total gastrectomy, and the third had undergone subtotal gastrectomy before our study. A significant increase in plasma gastrin, from 23 +/- 5 pg/ml to 53 +/- 20 pg/ml, in response to intravenous epinephrine (40 ng/kg.min), was observed in the normal subjects. This response was completely abolished by beta-blockade. In the ZES patients, epinephrine (40 ng/kg.min) also resulted in an increase in the plasma concentration of gastrin. The basal and maximum concentrations of gastrin were 580 and 1680 pg/ml in patient 1, 145000 and 320000 pg/ml in patient 2, and 200 and 1800 pg/ml in patient 3, respectively. beta-Adrenergic blockade suppressed the epinephrine-stimulated gastrin release in these patients as well. Graded intravenous doses of epinephrine given to the ZES patients resulted in elevation of the plasma gastrin in a dose-dependent manner. Insulin hypoglycemia caused an increase in both plasma epinephrine and plasma gastrin in ZES patients and normal subjects. A significant correlation between plasma gastrin and epinephrine during insulin hypoglycemia was observed in both groups. Exercise, with use of a bicycle ergometer, resulted in an increase in plasma epinephrine. An increase in plasma gastrin with exercise was observed in the ZES patients, and this was also suppressed by beta-blockade. The results suggest that gastrinoma cells, like normal G cells, are equipped with beta-adrenergic receptors that regulate gastrin release.     

Serum levels of basic fibroblast growth factor reflect disseminated disease in patients with testicular germ cell tumors

The potential role of angiogenesis stimulators in the pathogenesis of different tumor entities has been confirmed in several studies. We measured the serum levels of basic fibroblast growth factor (bFGF), vascular endothelial growth factor (VEGF) and platelet derived growth factor (PDGF) in 51 patients with testicular germ cell tumors and in 39 healthy volunteers. Serum concentrations of bFGF, VEGF and PDGF-AB were determined by enzyme-linked immunosorbent assay. The median serum bFGF level for tumor patients was 3.46 pg/ml (range 0-61.6) compared to 0.7 pg/ml (0-11) in the control group (P<0.01). In patients with metastatic disease, the median serum bFGF level was 10.3 pg/ml (0-61.6) in contrast to 2.8 pg/ml (0-50) in patients with localized disease (P<0.01). The median serum VEGF and PDGF levels were 270 pg/ml (0-1,903) and 37,837 pg/ml (9,075-108,800), respectively, for tumor patients and 200 pg/ml (44-585) and 23,000 pg/ml (4,250-70,650) in the control group ( P<0.05). Our data suggest that angiogenesis, as reflected by serum concentrations of bFGF, VEGF and PDGF, plays a functional role in the growth and progression of testicular germ cell tumors.     

Sex hormone-binding globulin in breast cancer

Serum level of sex hormone-binding globulin (SHBG) was measured by immunoradiometric assay in fifty two breast cancer patients and twenty nine healthy female volunteers. The results are as follows: 1) Although the serum SHBG concentration showed no significant difference between the breast cancer group and the healthy control group, the serum SHBG concentration in postmenopause was significantly higher in the breast cancer group (63.8 +/- 31.2nmol/ml/ml; mean +/- S.D.) than in the healthy control group (40.1 +/- 15.4nmol/ml). 2) Subsequently in the postmenopausal breast cancer group, the serum SHBG concentration was significantly higher in the estrogen receptor (ER)-negative cancer group (97.8 +/- 12.7nmol/ml) than in the ER-positive cancer group (55.8 +/- 32.1nol/ml). 3) No significant relationships were showed between the serum SHBG concentration and obesity or serum estradiol concentration in postmenopausal patients. 4) The serum SHBG concentration showed significant decrease 3 months after radical operation for breast cancer in postmenopausal patients. These results suggest the possibility of the SHBG synthesis in breast cancer tissue.