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PubMed1997

Changes in rat sleep after single and repeated injections of the long-acting somatostatin analog octreotide.

Somnogenic activity is attributed to both growth hormone (GH) and GH-releasing hormone (GHRH). The aim of our experiments was to study sleep after suppression of the somatotropic axis by means of administration of a long-lasting somatostatin analog, octreotide. Rats received subcutaneous injections of physiological saline (baseline), octreotide (1, 10, and 200 microg/kg), or a control solution just before light onset, and sleep-wake activity and cortical brain temperature were recorded for 23 h. Each dose of octreotide slightly promoted rapid eye movement sleep (REMS) during the 12-h light period. Non-REM sleep (NREMS) was strongly suppressed for 1 h in response to 10 and 200 microg/kg octreotide. This was followed by slight increases in NREMS time and significant enhancements in electroencephalogram slow-wave activity during NREMS after 200 microg/kg octreotide. The octreotide-induced inhibition of the somatotropic axis, as determined by plasma GH levels, vanished by the time sleep increased. Another group of rats received 10 microg/kg octreotide twice a day for 5 days. This treatment elicited persistent decreases in both NREMS time and NREMS intensity. The results support the previously reported REMS-promoting activity of somatostatin in rats. The decreases in sleep after repeated injections of octreotide are attributed to a withdrawal of the normal sleep-promoting activity of GH. The role of GHRH-GH in octreotide-induced acute suppression of NREMS is currently not clear. Other mechanisms, such as mimicking central transmitter functions of somatostatin by octreotide, should also be considered.

Animals↗
PubMed1997

Octreotide in hyperinsulinism.

In a limited number of case reports in infants, octreotide raised the blood glucose concentrations and decreased glucose requirements sufficiently to avoid pancreatectomy. This response occurs in the presence of frequent feedings and diazoxide therapy, and lasts from 1 month to greater than 5 years. As expected, octreotide reduces growth indices such as growth factors and growth rate in short-term assessment. However, an insufficient sample size, a lack of follow-up, and poor study design provide inconclusive data. Among the few case reports in adults with benign or malignant insulinoma, octreotide can significantly raise blood glucose concentrations. In long-term follow-up, octreotide has alleviated or reduced the frequency of hypoglycemic episodes for periods of 5 months to 2.5 years. Octreotide was administered subcutaneously in regimens of 100-1500 micrograms in three to four divided doses or as a continuous infusion. Continuous subcutaneous infusion may be attempted in patients intolerant to intermittent administration. Octreotide may worsen existing hypoglycemia as result of suppressing glucagon and growth hormone in the presence of unresponsive pancreatic hyperinsulinism. While the long-term effects of growth remain undetermined, current findings suggest octreotide may provide a reasonable addition or alternative to diazoxide in controlling symptoms of congenital hyperinsulinism. Octreotide may be useful in management of hypoglycemic symptoms in adult patients requiring medical treatment for insulinoma who are refractory or intolerant of diazoxide. Additional long-term studies are needed to address the cost effectiveness of octreotide therapy, identify patients most likely to respond, and determine the impact of octreotide on height.

Adult↗
PubMed2003

Preparation and stability of poly(ethylene glycol) (PEG)ylated octreotide for application to microsphere delivery.

The purpose of this study was to prepare poly(ethylene glycol) (PEG)ylated octreotide and investigate the stability against acylation by polyester polymers such as poly(lactic acid) and poly(lactic-co-glycolic acid). Octreotide was modified by reaction with monomethoxy PEG-propionaldehyde (molecular weight 5,000) in the presence of sodium cyanoborohydride. The mono-PEGylated fraction was isolated by reversed-phase high-performance liquid chromatography (HPLC) and characterized by matrix-assisted laser desorption/ionization time-of-flight mass spectrometry (MALDI-TOF MS). Circular dichroism demonstrated no significant secondary structural differences between mono-PEGylated octreotide (mono-PEG-octreotide) and intact octreotide. As a test system for the stability study against acylation reaction, lactic acid (LA) solutions with various concentrations and pH values were prepared with water dilution and subsequent accelerated equilibration at 90 degrees C for 24 hours. Native octreotide was found to be acylated in all the diluted LA solutions with different concentrations (42.5%, 21.3%, and 8.5%, wt/wt) and pH values (2.25, 1.47, and 1.85, respectively). The remaining amounts of intact octreotide continuously decreased to 50% through 30 days of incubation at 37 degrees C. MALDI-TOF MS identified the octreotide to be acylated by LA units. However, acylation reaction of mono-PEG-octreotide in LA solutions was negligible, and the remaining amounts of intact one through 30 days of incubation in LA solutions were also comparable to the initial concentration. These data suggest that mono-PEG-octreotide may prevent the acylation reaction in degrading PLA microspheres and possibly serve as a new source for somatostatin microsphere formulation.

Antineoplastic Agents, Hormonal↗
PubMed1989

The growth hormone responses to octreotide in acromegaly correlate with adenoma somatostatin receptor status.

We studied the correlation between the presence of somatostatin (SRIH) receptors in GH secreting tumors and the in vivo GH responsiveness to the SRIH analog octreotide in 11 acromegalic patients. To test in vivo octreotide (SMS 201-995) responsiveness, the patients were given a single dose (100 micrograms, sc) and their plasma GH levels were measured for several hours. Somatostatin receptor content was measured by receptor autoradiography on frozen tumor tissue sections using either a somatostatin-28 analog or a SRIH octapeptide analog (Tyr3-octreotide) as iodinated radioligands. In eight acromegalic patients, who had complete and long lasting GH inhibition after octreotide administration, SRIH receptors with high affinity for octreotide were distributed homogeneously in the tumor tissue. Two patients had moderate, short duration, and incomplete inhibition of GH secretion after octreotide administration, and their tumors had very low capacity and/or affinity SRIH receptors. A further patient who had a moderate response to octreotide had SRIH receptors that were nonhomogeneously distributed throughout the tumor. These data suggest that the therapeutic efficacy of octreotide may be related to tumor SRIH receptor levels; the best in vivo responses to octreotide occurred in patients whose tumors contained a high density of homogeneously distributed receptors which had a high affinity for octreotide.

Acromegaly↗
PubMed1992

Clinically nonfunctioning pituitary adenoma and octreotide response to long term high dose treatment, and studies in vitro.

We have studied seven patients with a clinically nonfunctioning or alpha-subunit-secreting pituitary macroadenoma, four of whom received long term, high dose octreotide treatment. We have attempted to correlate the presence of somatostatin receptors (SS-R) in the adenomas and the outcome of octreotide treatment, as measured by tumor size, improvements in visual field defects, and hormonal response. The presence of SS-R in the pituitary adenomas was demonstrated in vivo using [111indium]octreotide scintigraphy and in vitro by autoradiography of tissue fragments obtained after transsphenoidal surgery. Adenomas from six of the seven subjects were SS-R positive. High dose (1200 micrograms, sc, daily) octreotide treatment was given to four subjects, three of whom were SS-R positive. Improvement of the visual field defects was observed in three of four patients (including the SS-R-negative subject), although no computed tomographic scan-assessed tumor size reduction was found. Two of four patients showed small but significant reductions in serum FSH concentrations (to 83% and 93% of initial values) with treatment. These in vivo responses to high dose octreotide treatment could not be predicted by pretreatment responses to 200 micrograms TRH or 100 micrograms octreotide. Tissue fragments for cell culture were obtained from six patients, and in vitro release of gonadotropins and/or alpha-subunit could be demonstrated in five cultures. In vitro, octreotide (10 nmol/L) significantly decreased gonadotropiin or subunit release in three of five cultures, whereas bromocriptine (10 nmol/L) significantly reduced the release in four of five cultures and to a significantly greater extent than octreotide. In conclusion, in six of seven patients with a clinically nonfunctioning or alpha-subunit-secreting pituitary adenoma, SS-R were demonstrated in the tumor. In vitro incubation of adenoma cells with octreotide resulted in mild inhibition of gonadotropin or alpha-subunit release. Although in vivo long term treatment with high doses of octreotide did not result in substantial tumor size reduction, improvement of visual field defects was observed in three of four subjects.

Adenoma↗
PubMed1996

Somatostatin analog octreotide inhibits the growth of differentiated thyroid cancer cells in vitro, but not in vivo.

Somatostatin and its analogs are antiproliferative in a wide range of normal and neoplastic tissues. In this study we investigated the effect of octreotide (SMS 201-995) on the invasion and growth of three follicular thyroid cancer (FTC) cell lines from one patient in vitro and in vivo. FTC133 was established from the primary tumor, FTC236 from a cervical lymph node metastasis, and FTC238 from a lung metastasis. Invasion was the ability of tumor cells to penetrate 8-microns pore polycarbonate membranes coated with Matrigel. Invasion and proliferation were analyzed using the MTT assay. For in vivo experiments, athymic nude mice were sc inoculated with 500,000 calls of FTC133. The animals were treated twice daily with octreotide sc (100-300 micrograms/kg). RIA studies yielded dose-dependent high plasma levels of octreotide (3.43-6.5 ng/mL). Octreotide had a biphasic effect, enhancing growth at low concentrations (1-10 nmol/mL) and inhibiting it at high concentrations (100 nmol to 1 mumol/mL). Octreotide had also a dose-dependent biphasic effect on the invasion of FTC, inhibiting the invasion of all follicular thyroid cancer lines at high concentrations. However, it affected invasion less than growth. Octreotide (10 nmol/mL) stimulated the invasion of FTC133 by 13%, whereas stimulation was lower in both FTC metastases (FTC236, 6%; FTC238, 7%; P < 0.01). At higher concentrations (100 nmol to 1 mumol/mL), octreotide inhibited invasion of FTC133 by 17% (FTC236, 15%; FTC238, 17%; P < 0.01). During a 3-week treatment period, octreotide had no antiproliferative effect on the growth of FTC133 cells in nude mice. In conclusion, octreotide at low concentrations stimulates and at high concentrations inhibits the growth and invasion of follicular thyroid cancer cells in culture. However, it has no effect on the growth of FTC cells in animal experiments. Thus, the value of octreotide as an antitumoral agent in follicular thyroid cancer must be critically questioned.

Animals↗
PubMed2003

Octreotide as a therapeutic option for management of chylothorax.

OBJECTIVE: To report a case of post-cardiac surgery-induced chylothorax treated with octreotide and review the literature on octreotide efficacy. CASE SUMMARY: A 5-month-old boy with Down syndrome was admitted for atrioventricular canal repair. On admission, he was taking captopril and furosemide. On postoperative day 4, he exhibited signs of chest wheezing and crackles, but was without cough or fever. Chest X-ray revealed a moderate right-sided pleural effusion. Accordingly, a pleural catheter was inserted and drained an average of 7.14 mL/h of chylous fluid that day. Laboratory analysis of the pleural fluid revealed a triglyceride level of 89 mg/dL, without bacterial growth. Based on those findings, the diagnosis was chylothorax. Because of the continuous extensive tube drainage, octreotide 3.5 micro g/kg/h was begun. The average daily chyle drainage was reduced from 7.14 one day before octreotide initiation to 0.83 mL/h on day 4 of octreotide therapy. After 4 days of therapy (postoperative day 8), octreotide was discontinued because of the satisfactory response and the pleural catheter was removed. DISCUSSION: In our case and the other few cases reported, octreotide showed acceptable efficacy in the management of chylothorax. The mechanism by which octreotide decreases chyle production includes reducing the intestinal absorption of fats, mainly triglycerides, and increasing fecal fat excretion. CONCLUSIONS: Octreotide may have reduced chyle production in our patient. Further reports and studies assessing octreotide efficacy in the management of chylothorax are warranted.

Cardiac Surgical Procedures↗
PubMed2005

Octreotide in insulinoma patients: efficacy on hypoglycemia, relationships with Octreoscan scintigraphy and immunostaining with anti-sst2A and anti-sst5 antibodies.

OBJECTIVE: We studied the efficacy of octreotide treatment on hypoglycaemia in patients with insulinoma and its relationships with Octreoscan scintigraphy and the presence of tumoral somatostatin receptors sst2A and sst5. DESIGN AND METHODS: 17 patients with insulinoma were evaluated using (i) evaluation of blood glucose, insulin and C-peptide during a short 100 mug octreotide test in fasting patients and/or treatment over 8 days-8 months with octreotide, (ii) Octreoscan scintigraphy and (iii) immunostaining of the tumor with anti-sst2A and anti-sst5. RESULTS: Octreotide was effective on hypoglycaemia in 10/17 patients. Octreoscan scintigraphy detected 4/17 insulinomas. sst2A receptor was detected in 7/17 insulinomas and sst5 in 15/17 insulinomas. Octreotide was effective on hypoglycaemia in those seven patients with sst2A receptor-expressing insulinoma, and in three patients with undetectable sst2A receptor and detectable sst5; it was ineffective in six patients whose tumor expressed the sst5 receptor with undetectable sst2A and in one patient with undetectable sst2A and sst5 receptor. CONCLUSIONS: Octreotide is an effective treatment of hypoglycaemia in more than 50% of patients with insulinoma. Detection of responsive patients was better based on a positive short test with subcutaneous octreotide than on the results of Octreoscan scintigraphy. Positive anti-sst2 receptor immunostaining is associated with efficacy of octreotide treatment, but does not account for all cases of responsiveness to octreotide. Expression of sst5 receptor does not appear to explain per se the efficacy of octreotide on sst2A-negative insulinomas.

Adolescent↗
PubMed1995

Stimulation of hepatic insulin-like growth factor-binding protein-1 and -3 gene expression by octreotide in rats.

It has recently been demonstrated in various clinical experiments that native somatostatin and its long-acting analogues increase circulating levels of insulin-like growth factor-binding protein-1 (IGFBP-1) within 1-2 h, independent of effects on circulating insulin or glucose levels. Using human hepatoma cells in vitro the somatostatin analogue, octreotide, has been shown to increase IGFBP-1 mRNA within 24 h indicative of a direct stimulatory effect of octreotide on IGFBP-1 synthesis. In order to ascertain whether octreotide acutely stimulates IGFBP-1 mRNA in vivo, placebo or two doses of octreotide were injected subcutaneously into three groups of rats. One hour after saline or octreotide administration, liver, kidney and serum were obtained for the measurement of IGFBPs-1 to -6 mRNA in tissue and IGFBPs and IGF-I in serum. Octreotide increased liver IGFBP-1 (562%) and IGFBP-3 (23%) mRNA expression with a concomitant rise in the circulating 30 kDa (106%) and 38-42 kDa (23%) IGFBPs. No detectable changes were seen in other liver IGFBP transcripts, other circulating IGFBPs or in any of the kidney IGFBP transcripts. Serum IGF-I increased by 37% in the animals receiving the high octreotide dose. No concomitant changes were observed in glucose or insulin levels. These data show that octreotide acutely stimulates hepatic IGFBP-1 and -3 mRNA in vivo in rats. The stimulating effect on IGFBP-3 presents a possible hitherto unknown form of regulation of IGFBP-3 whilst the effect on IGFBP-1 indicates that the stimulatory effect of octreotide on circulating IGFBP-1 described in clinical trials may be due to increased hepatic production. The present findings may be of importance in the clinical use of octreotide.

Animals↗
PubMed2004

Effect of octreotide on human pancreatic cancer cells after transfected with somatostatin receptor type 2 gene.

AIM: To observe the effect of octreotide on apoptosis rate of human pancreatic cancer cells PC-3 after transfected with somatostatin receptor type 2 (SST2) gene. METHODS: SST2 plasmid was transfected into PC-3 cells by liposome. Result of transfection was detected by immunocytochemical staining and Western blotting. Apoptosis rates of PC-3 cells under different dosages of octreotide were measured by MTT assay and flow cytometry (FCM). RESULTS: Apoptosis rate caused by octreotide of transfected PC-3 cells was 7.56+/-1.06% at the dosage of 0.20 microg/mL, 9.25+/-1.73% at the dosage of 0.40 microg/mL and 14.18+/-2.71% at the dosage of 0.80 microg/mL. Apoptosis rate caused by octreotide of non-transfected PC-3 cells was 5.76+/-0.75% at the dosage of 0.20 microg/mL, 6.69+/-0.80% at the dosage of 0.40 microg/mL and 7.26+/-1.28% at the dosage of 0.80 microg/mL. Transfected PC-3 cells growth inhibition rate caused by octreotide was 9.36+/-1.34% at the dosage of 0.20 microg/mL, 12.03+/-1.44% at the dosage of 0.40 microg/mL and 20.23+/-4.21% at the dosage of 0.80 microg/mL. Non-transfected PC-3 cells growth inhibition rate caused by octreotide was 6.44+/-0.66% at the dosage of 0.20 microg/mL, 7.65+/-0.88% at the dosage of 0.40 microg/mL and 9.29+/-1.32% at the dosage of 0.80 microg/mL. We found that octreotide caused higher apoptosis rate and inhibition rate in transfected groups than in non-transfected groups (P<0.05) at the tested dosages (0.20, 0.40 and 0.80 microg/mL). CONCLUSION: Deficiency of SST2 was probably the major reason why octreotide had little effect on PC-3 cells. Transfecting SST2 gene could strengthen the ability of octreotide of killing PC-3 cells. It provided an experimental evidence for using both octreotide and transfection with SST2 gene on clinical treatment of pancreatic cancer.

Apoptosis↗
PubMed2004

Antineoplastic effects of octreotide on human gallbladder cancer cells in vitro.

AIM: To investigate whether octreotide can inhibit the growth of human gallbladder cancer cells in vitro and to elucidate the antineoplastic mechanism of octreotide in gallbladder cancer. METHODS: A human gallbladder cancer cell line, GBC-SD, was cultured in vitro. The antiproliferative effects of octreotide were examined by means of an MTT assay and a colony forming ability assay. Morphological variation was investigated under scanning electron microscopy and transmission electron microscopy. Cell cycle analysis and apoptosis rate was evaluated by flow cytometry (FCM) after staining by propidium iodide. DNA fragmentation was assayed by agarose gel electrophoresis. Immunohistochemical staining was performed to evaluate the expressions of mutant-type p53 and bcl-2. RESULTS: The growth curve and colony forming ability assay showed significant inhibition of octreotide to the proliferation of GBC-SD cells in culture in a time- and dose-dependent manner. After exposure to octreotide, GBC-SD cells showed typically apoptotic characteristics, including morphological changes of chromatin condensation, vacuolar degeneration, nucleus fragmentation and apoptotic body formation. In FCM profile apoptotic cells showed increased sub-G(1) peaks in the octreotide group, significantly higher than the control group (P=0.013). There was also an augmentation in the cell proportion of G(0)/G(1) phase (P=0.015), while the proportion of S phase and G(2)/M phase remained unchanged (P=0.057 and P=0.280, respectively). DNA agarose gel electrophoresis displayed a ladder after exposure to 1 000 nmol/L octreotide. After being treated with octreotide, the expressions of both mutant-type p53 and bcl-2 decreased considering the percentage of positive cells (P<0.05). CONCLUSION: Octreotide has a negative action to the proliferation of GBC-SD cells, and the mechanism may be related to cytostatic and cytotoxic effects. The reduction of mutant-type p53 and bcl-2 expressions may be associated with the apoptosis induced by octreotide.

Antineoplastic Agents↗
PubMed2003

Inhibitory effect of octreotide on gastric cancer growth via MAPK pathway.

AIM: Somatostatin and its analogues may suppress the growth of various tumor cells. However, the effect of octreotide on growth of gastric adenocarcinoma is still largely unknown. This study was to explore if octreotide could inhibit the growth of gastric adenocarcinoma and its probable mechanisms. METHODS: Proliferation of gastric cancer cell line affected by octreotide was determined by (3)H-thymidine incorporation. After xenografts of human gastric cancer were implanted orthotopically in stomach, nude mice were administrated octreotide for 8 weeks. The mRNA of somatostatin receptor in the SGC-7901 cells was detected by reverse transcription polymerase chain reaction technique. Extracellular signal-regulated protein kinase and c-Fos in gastric cancer tissues were measured by immunohistochemistry and Western blot. Activator protein-1 binding activity was examined by electrophoretic mobility sift assay. RESULTS: (3)H-thymidine incorporation into SGC-7901 cells was significantly decreased by octreotide in a concentration dependent manner. Either size or weight of tumors treated with octreotide was significantly reduced in vivo. The inhibition rate for tumor was 62.3 % in octreotide group. The genes of somatostatin receptors 2 and 3 were expressed in SGC-7901 gastric cancer cell lines. Extracellular signal-regulated protein kinase and c-Fos protein level were decreased in gastric adenocarcinoma treated with octreotide. Moreover, fetal calf serum stimulated activator protein-1 binding activity could be suppressed by octreotide potentially. CONCLUSION: Inhibition of sequential molecular events in MAPK pathway may interpret the mechanisms underlying the effect of octreotide on the growth of gastric adenocarcinoma.

Adenocarcinoma↗
PubMed1999

Octreotide stimulates Ca++ secretion by the gallbladder: a risk factor for gallstones.

BACKGROUND: Gallstone formation during octreotide therapy has been linked to elevated levels of gallbladder bile Ca++, a well-known prolithogenic factor. Although the subcutaneous administration of octreotide raises gallbladder bile Ca++ in prairie dogs, the mechanism for this effect is unknown. Octreotide has been shown to increase gallbladder Na+ and water absorption in Ussing chamber studies. Given the known effects of octreotide on gallbladder ion transport, we hypothesized that octreotide may also promote gallstone formation by stimulating gallbladder Ca++ secretion, thereby raising the lumenal concentration of biliary Ca++. METHODS: After cholecystectomy, prairie dog gallbladders were mounted in Ussing chambers, and standard electrophysiologic parameters were recorded. Unidirectional fluxes of Ca++ and Na+ were measured before and after serosal exposure to 50 nmol/L octreotide. RESULTS: Under basal conditions normal prairie dog gallbladder absorbed mucosal Ca++. Serosal octreotide converted the gallbladder from a state of basal Ca++ absorption to one of net Ca++ secretion by stimulating serosa to mucosa Ca++ flux. As anticipated, octreotide increased net Na+ absorption by stimulating mucosa to serosa Na+ flux and decreased tissue conductance and short-circuit current significantly compared with baseline values. CONCLUSION: Fifty nanomoles per liter octreotide stimulated Ca++ secretion by gallbladder epithelium, a possible mechanism for increased biliary Ca++ in prairie dogs receiving subcutaneous injections. Ca++ secretion linked to octreotide therapy may induce gallstones by raising biliary levels of Ca++, a known prolithogenic factor.

Animals↗
PubMed1999

Differential regulation of somatostatin receptor type 2 (sst 2) expression in AR4-2J tumor cells implanted into mice during octreotide treatment.

Octreotide is a somatostatin analogue that is widely used for cancer therapy and tumor imaging. Its efficacy in tumors depends mainly on the expression of the somatostatin receptor type 2 (sst 2). Desensitization and down-regulation of sst 2 after agonist exposure can have important consequences for patients under ongoing octreotide therapy because it may induce temporary tumor unresponsiveness and impair sst 2-based tumor scintigraphy. Therefore, we have investigated the effect of octreotide on sst 2 expression in vitro, as well as in a tumor mouse model. In vitro, short exposure to octreotide induced rapid dose-dependent down-regulation of sst 2 in the rat pancreatic AR4-2J cell line. Within 0.5 h, 80% of sst 2 had disappeared from the cell surface. A total recovery required 24 h and was shown to depend on protein synthesis, but not on new sst 2 mRNA transcription, indicating that sst 2 was probably degraded during the down-regulation process. Similar results were obtained in vivo. On the other hand, long-term continuous release of octreotide for 7 days, as achieved with octreotide-containing osmotic minipumps, caused sst 2 up-regulation in vivo, but not in vitro. Furthermore, this up-regulation of sst 2 in tumor-bearing scid mice was shown to depend on constant exposure of the animals to octreotide, as it was not observed when octreotide was given discontinuously in two s.c. daily injections. These results demonstrate that the continuous release of a small amount of octreotide, which in cancer therapy may be achieved with long-acting release formulations of the peptide, can induce sst 2 up-regulation on cancer cells. This may improve the efficacy of both tumor imaging and long-term octreotide therapy.

Animals↗
PubMed2001

[Effect of octreotide on intragastric pH in patients with duodenal ulcer bleeding].

OBJECTIVE: To evaluate the effect of octreotide on the intragastric pH of patients with duodenal ulcer bleeding during the period of 24 hours and to observe if it can advance the effect of hemostasis by endoscopic injection of epinephrine. METHODS: Twenty-four patients with duodenal ulcer bleeding were randomly divided into three groups, eight in each. Patients in group 1 received an intravenous injection of 0.1 mg of octreotide followed by continuous intravenous drip of octreotide at a constant speed of 25 microg/h for 24 hours. The patients in group 2 received an intravenous injection of 0.1 mg of octreotide followed by continuous intravenous drip of octreotide at a constant speed of 42 microg/h for 24 hours. The patients in group 3 received an intravenous injection of 40 mg of omeprazole followed by continuous intravenous drip of omeprazole at a constant speed of 8 mg/h for 24 hours. Intragastric pH was continuously recorded with a pH meter. The patients with active ulcer bleeding was treated with injection of epinephrine via endoscope and then received intravenous drip of octreotide (with the same dosage as in group 1, n = 42) or omeprazole (with the same dosage as in group 3, n = 54) for 72 hours and were given omeprazole (20 mg Bid). RESULTS: The mean and median intragastric pH values among the patients in group 2 treated by a larger dosage of octreotide (6.7 +/- 0.5 and 6.9 +/- 0.4) were similar to those in the group 3 treated by omeprazole (6.8 +/- 0.4 and 7.0 +/- 0.4). There was no statistically significant difference between these two groups in percentage of intragastric pH above 4, 6, and 7 The mean and median of intragastric pH among the patients in group 1 treated by a smaller dosage of octreotide were statistically significantly smaller (5.2 +/- 0.5 and 5.4 +/- 0.4) than those in the omeprazole group. There was no statistically significant difference between octreotide treatment and omeprazole treatment in terms of volume of blood transfusion (0.7 +/- 0.5 vs. 0.6 +/- 0.4 L), rebleeding rate (11.6% vs. 12.9%), emergency operation rate (7.1% vs. 3.7%), and mortality (2.3% vs. 3.7%). CONCLUSION: Octreotide effectively inhibits the secretion of gastric acid. However, the dosage in common use clinically fails to increase the intragastric pH to the best situation needed for effective hemostasis. Only a large dosage (1.10 mg/d) works.

Adult↗
PubMedDate not supplied

Effect of octreotide administration on serum interleukin-6 (IL-6) levels of patients with acute edematous pancreatitis.

BACKGROUND/AIMS: Based on former studies in experimental animals on the effect of octreotide on serum and ascitic levels of tumor necrosis factor-alpha and interleukin-6 in the field of necrotizing pancreatitis, the present study was designed to investigate the effect of octreotide on serum interleukin-6 of patients with acute edematous pancreatitis. METHODOLOGY: A total of 36 patients with acute edematous pancreatitis and initiation of symptoms 12 hours before their admission were enrolled in the study; 20 were treated with octreotide 200 microg tid and 16 with octreotide 500 microg tid for five days. Blood was sampled at regular time intervals. Interleukin-6 was determined by an enzyme-immunoassay and C-reactive protein by nephelometry. RESULTS: Mean concentrations of interleukin-6 of patients treated with octreotide 200 microg tid were 59.52 pg/mL before and 94.08, 46.25, 49.94, 58.16 and 26.08 pg/mL at 3, 6, 24, 48 and 72 hours after the start of therapy respectively. Respective values of patients treated with octreotide 500 microg tid were 57.19, 53.07, 57.83, 36.06, 54.29 and 65.49 pg/mL. Mean C-reactive protein of patients treated with octreotide 200 microg tid were 67.37 mg/L before and 48.51, 106.08 and 95.58 mg/L at 24, 48 and 72 hours after the start of therapy respectively. Respective values of patients treated with octreotide 500 microg tid were 65.51, 60.56, 90.68 and 64.22 mg/L. CONCLUSIONS: A transient, but not statistically significant, decrease of serum interleukin-6 levels was documented after administration of octreotide in the field of acute edematous pancreatitis. That decrease was earlier after the application of the 500 microg tid dose than the 200 microg tid dose. Studies with a greater number of patients are mandatory to fully clarify the effect of octreotide, if any, on acute pancreatitis.

Acute Disease↗
PubMed1990

[Long-term treatment of acromegaly with the somatostatin analog octreotide (Sandostatin). On the predictive significance of acute tests].

Twelve acromegalic patients were treated (mean +/- SD) 26 +/- 15 months with daily doses of 440 +/- 330 micrograms of the somatostatin analogue octreotide acetate (SMS 201-995, Sandostatin). The levels of somatomedin-C (Sm-C) decreased by 63% from 8.1 +/- 7.7 U/ml to 3.0 +/- 1.3 U/ml. Before starting therapy a long oral glucose tolerance test (oGTT) and a TRH test were performed both without and after s.c. injection of 100 micrograms octreotide. Under long-term treatment with octreotide four of twelve patients reached normal Sm-C-values. The GH levels of all of these patients were continuously suppressed to less than 2 ng/dl in an oGTT after a test dose of 100 micrograms octreotide s.c. till the end of the test (5 1/2 hours after octreotide injection). The other eight patients had a relief of acromegalic symptoms and five had a decrease of their Sm-C-levels, but none of them reached normal Sm-C-values. None of these patients had a continuous suppression of GH after a test dose of octreotide in an oGTT. Hyperprolactinemia (n = 4) was observed only in those patients with an insufficient response to octreotide. The GH-response to TRH showed neither without nor after injection of octreotide a correlation with the results of long-term treatment. Thus it is concluded that GH-suppression in a long oGTT after administration of a test dose of 100 micrograms octreotide acetate s.c. allows to identify those acromegalic patients who will benefit from long-term treatment with the somatostatin analogue octreotide acetate.

Acromegaly↗
PubMed1994

Controlled trial of different dosages of octreotide in the prevention of hyperamylasemia induced by endoscopic papillosphincterotomy.

Pancreatic reaction after endoscopic papillosphincterotomy (EPT) is a common event occurring in about 70% of cases. Acute pancreatitis may also develop in 1%-6% of cases. Previous attempts to prevent this reaction with an inhibitor of exocrine pancreatic secretion such as somatostatin provided conflicting results. The somatostatin long-acting analogue octreotide has recently proposed for the prevention of ERCP/EPT-induced pancreatic reaction. Therefore we tested the prophylactic effect of a subcutaneous administration of octreotide in two different dosages in 60 consecutive patients undergoing EPT for common bile duct stones and benign papillary stenosis. They were given either octreotide 0.2 mg (20 cases), or octreotide 0.1 mg (20 cases), or placebo (20 cases) before the procedure. Serum amylase levels were determined at baseline and 2, 4, 8 and 24 hours thereafter. The differences were statistically significant at 2 hours between subjects pretreated with octreotide 0.2 mg and control subjects (p = 0.01); at 4 and 8 hours after the procedure between both octreotide-treated groups and control subjects (octreotide 0.1 mg: p < 0.05, at 4 and 8 hrs; octreotide 0.2 mg: p = 0.01, at 4 hrs, and p < 0.01, at 8 hrs). In patients with previous episodes of relapsing pancreatitis, the increase in serum amylase was significantly reduced in the octreotide 0.2 mg group vs control group, at 4 hrs (p < 0.05) and 8 hrs (p < 0.05). Our data suggest that octreotide 0.2 mg has a greater prophylactic efficacy than 0.1 mg in reducing pancreatic reaction after EPT.

Adult↗