3D navigation in surgery of Eagle syndrome.

NTRODUCTION: Eagle's syndrome is a rare condition caused by the elongation of the styloid process (> 4 cm) or calcification of the stylohyoid ligament. Patients with Eagle's syndrome typically present various clinical symptoms, such as headache, facial pain, neck pain, pulsating pain, sore throat, foreign body sensation, dysphagia, dysphonia, cough, voice changes, otalgia or vertigo. 3D printing refers to processes in which successive layers of material are formed from 3D computer tomography data to synthesize a three-dimensional object. This new diagnostic technique of rapid prototyping technology led to innovative new applications in biomedicine. OBJECTIVE: The primary goal for this case study was to find out, whether the nowadays so popular 3D technology aids in the treatment of the Eagle syndrome or other similar craniofacial abnormalities during the surgical procedure. CASE PRESENTATION: We report a case of a patient who initially presented a combination of symptoms like headache, sore throat, neck pain, which exacerbated with the movement of the head. This case report provides a brief review of the diagnosis and surgical management of the Eagle's syndrome with the help of 3D model navigation. CONCLUSION: Eagle's syndrome is difficult to diagnose due to its wide variability in symptoms. The inherent accuracy and other properties of 3D printing have allowed it to have exciting applications in anatomy education and surgery, with great benefit to the maxillofacial surgery. With the assistance of 3D technology, it is much easier for the surgeon to plan the surgical approach and the surgery, and significantly reduce the operation time (Fig. 3, Ref. 22).

Is the prevalence of the medication-related osteonecrosis of the jaws underestimated, evaluation in oncological and non-oncological disease.

OBJECTIVES: The purpose of this study was to evaluate the prevalence of medication-related osteonecrosis of the jaw in Slovak population and compare the literature findings, whether the prevalence of MRONJ is underestimated. BACKGROUND: Antiresorptive drugs significantly increase quality of life, although during therapy, or in post-treatment period, osteonecrosis of the jaws might occur as a severe adverse effect. Medication-related osteonecrosis of the jaws (MRONJ) is a severe problem that has been observed in the past few years. METHODS: This multi-centric study evaluates the prevalence in Slovak population, assesses the values from 4 largest centres of maxillofacial surgery in Slovakia (1166 patients with MRONJ) and provides the comparison of literature review. RESULTS: Between 2010-2015, there was increasing number of newly diagnosed patients with MRONJ (1166 overall MRONJ patients) annually, except 2012 (mean growth of 123.88 %). This finding was supported by a statistical analysis of the rising tendency of prevalence in literature, where there was a significant difference in prevalence of non-oncologic patients before and after 2010 t(15) = 2.725, p = 0.016. The 6-year prevalence was 1.34 % in population with antiresorptive drugs intake, for osteoporosis 0.47 %, for breast cancer 4.10 %, prostate cancer 3.99 % and multiple myeloma 21.26 %. CONCLUSION: This study considers that there is a significant rising tendency of MRONJ in non-oncological patients, what could be caused by underestimation of the risk for development MRONJ in these patients. There should be a better cooperation and information among dentists and doctors indicating the antiresorptive treatment and strong emphasis on primary prevention before the initial treatment even in non-oncological patients (Tab. 5, Fig. 7, Ref. 69).

Plasmocytoma, multiple myeloma and plasma cell neoplasms in orofacial region.

A neoplastic proliferation of B cell lymphocyte is called plasma cell neoplasms, results from malignant plasma cells transformation in bone marrow. The authors present a clinical study and overview of this pathology in maxillofacial region for six years (Tab. 2, Ref. 14).

Randomised clinical trial: a 1-week, double-blind, placebo-controlled study of pancreatin 25 000 Ph. Eur. minimicrospheres (Creon 25000 MMS) for pancreatic exocrine insufficiency after pancreatic surgery, with a 1-year open-label extension.

BACKGROUND: Pancreatic exocrine insufficiency (PEI) often occurs following pancreatic surgery. AIM: To demonstrate the superior efficacy of pancreatin 25 000 minimicrospheres (Creon 25000 MMS; 9-15 capsules/day) over placebo in treating PEI after pancreatic resection. METHODS: A 1-week, double-blind, randomised, placebo-controlled, parallel-group, multicentre study with a 1-year, open-label extension (OLE). Subjects ≥18 years old with PEI after pancreatic resection, defined as baseline coefficient of fat absorption (CFA) <80%, were randomised to oral pancreatin or placebo (9-15 capsules/day: 3 with main meals, 2 with snacks). In the OLE, all subjects received pancreatin. The primary efficacy measure was least squares mean CFA change from baseline to end of double-blind treatment (ancova). RESULTS: All 58 subjects randomised (32 pancreatin, 26 placebo) completed double-blind treatment and entered the OLE; 51 completed the OLE. The least squares mean CFA change in the double-blind phase was significantly greater with pancreatin vs. placebo: 21.4% (95% CI: 13.7, 29.2) vs. -4.2% (-12.8, 4.5); difference 25.6% (13.9, 37.3), P < 0.001. The mean ± s.d. CFA increased from 53.6 ± 20.6% at baseline to 78.4 ± 20.7% at OLE end (P < 0.001). Treatment-emergent adverse events occurred in 37.5% subjects on pancreatin and 26.9% on placebo during double-blind treatment, with flatulence being the most common (pancreatin 12.5%, placebo 7.7%). Only two subjects discontinued due to treatment-emergent adverse events, both during the OLE. CONCLUSIONS: This study demonstrates superior efficacy of pancreatin 25 000 over placebo in patients with PEI after pancreatic surgery, measured by change in CFA. Pancreatin was generally well tolerated at the high dose administered (EudraCT registration number: 2005-004854-29).

Squamous cell carcinoma of the oral cavity.

OBJECTIVES: A number of treatment modalities are available in the management of oral cavity cancer. These are surgery (operation OP), irradiation (radiotherapy RT), chemotherapy (CHT), or complex therapy performed as a combination of the later three methods with various survival rates. A multidisciplinary team approach in every individual case is required. BACKGROUND AND METHODS: Authors analysed retrospectively a group of 622 patients (553 men, 69 women), mean age 58.6 years (range 23-88 years) hospitalised in the Department of Oral and Maxillofacial Surgery, Faculty Hospital and Faculty of Medicine Comenius University in Bratislava within the years 1992-2001 with primary untreated histologically confirmed squamous cell carcinoma of oral cavity (beside cancer of the lip and salivary glands). Gender, age, location and TNM staging of the disease, clinical and histopathological evaluations of the neck lymph nodes and relationship to the treatment modalities were recorded. The authors compared some parameters of the results obtained during their previous study within the years 1977-1986 (453 patients). RESULTS: The number of cases with squamous cell carcinoma of oral cavity increased by 37.31% in total as well as that of cases with advanced disease, especially stage IV (318 patients = 56.6%) increased by 7.6%. In the studied group there occurred cases that were clinically falsely negative by NO (11.04%) as well as falsely positive by N1 (39.1%) when examined by palpation of lymph nodes. The overall 5-year survival rate remained at the same level (55.4 %), the early and late stages did not change the survival rate at the 5th year (I = 75.1%, II = 69.9%, III = 47.5%, IV = 25.1%). Regarding the complexity of treatment, the best 5-year survival rates showed the complex three-modal therapy (CHT + OP + RT = 23.5%), comparing to the dual (OP + RT or CHT + RT = 19.4%) and mono-modal therapy (OP or RT alone = 17.2%). In the complex therapy, the mean disease-free interval improved (30.2 vs 39.4 months) due to a change in the sequence of therapy modalities. CONCLUSION: The increase in the number of cases with advanced disease has a warning trend. The reasons of this trend remain unclear. In spite of the fact that the overal 5-year survival was found not to improve, the quality of life regarding the mean disease-free interval in the group of patients under the complex treatment is considered to be a positive result (Tab. 3, Fig. 4, Ref. 27). Full Text (Free, PDF) www.bmj.sk.

The role of the glucocorticoid-dependent mechanism in the progression of sodium taurocholate-induced acute pancreatitis in the rat.

The effects of glucocorticoids on acute pancreatitis (AP) have remained contradictory. The aim of this study was to investigate the time courses of the effects of the exogenous glucocorticoid agonists dexamethasone (DEX) and hydrocortisone (HYD) and a glucocorticoid antagonist (RU-38486) and to characterize the local and systemic responses in AP in rats. The glucocorticoid antagonist and agonists were administered just before AP induction. Serum amylase activity determinations, IL-6 bioassays, pancreatic weight/body weight ratio measurements, and survival analysis were performed. Liver and lung injuries were assessed via neutrophil leukocyte infiltration in myeloperoxidase (MPO) assays, tissue adenosine triphosphate (ATP) level determinations, and histology. In the glucocorticoid agonist groups, the survival rate increased, while the serum amylase level, the IL-6 activity, and the pancreatic weight/body weight ratio decreased significantly as compared with the control and RU-treated groups. AP resulted in significant decreases in tissue ATP levels in both the liver and the lung. In the DEX- or HYD-treated groups, the liver ATP levels were significantly elevated, while both the liver and the lung MPO levels were attenuated as compared with the AP and RU-treated groups. These results suggest that glucocorticoids may play important roles in mitigating the progression of the inflammatory reaction during the early phases of AP.

Cholecystokinin fails to promote pancreatic regeneration in diabetic rats following the induction of experimental pancreatitis.

The aim of the present study was to investigate the spontaneous and cholecystokinin-octapeptide (CCK-8)-promoted laboratory changes and morphological alterations in rats with arginine (Arg)-induced pancreatitis in which diabetes had been induced with streptozotocin (STZ). Male Wistar rats were used in our experiments. Pancreatitis was induced by arginine, diabetes by STZ and regeneration was promoted by CCK-8. The serum amylase, glucose and insulin levels, the pancreatic contents of protein, DNA, amylase, trypsinogen and lipase, the pancreatic weight/body- weight ratio (pw/bw) and the plasma glucagon level were examined 1, 3, 7, 14 and 28 days after pancreatitis induction. Pancreatic tissue samples were examined by light microscopy and immunostaining on paraffin-embedded sections. The insulin and glucagon-containing cells were visualized by using monoclonal antibodies. The administration of low doses of CCK-8 accelerated the processes of regeneration following Arg-induced pancreatitis, but in rats that were also diabetic, pancreatic regeneration was not observed. The administration of low doses of CCK-8 seems to reduce the pancreatic beta -cell number and function in diabetic rats. The pancreatic endocrine function was further deteriorated by simultaneous Arg-induced pancreatitis. The diabetic state appeared to shift the normal pancreatic enzyme content (decreased amylase and increased trypsinogen) in this study.

Evaluation of pancreatic exocrine function by secretin-enhanced magnetic resonance cholangiopancreatography.

AIM: To assess the feasibility and usefulness of secretin-enhanced magnetic resonance cholangiopancreatography (S-MRCP) for evaluation of pancreatic exocrine function. METHODOLOGY: S-MRCP was performed in 20 patients with mild (n = 8) or severe (n = 12) chronic pancreatitis (according to the grade of exocrine pancreatic insufficiency indicated by the Lundh test) and in 10 volunteers without pancreatic disease. MRCP images were evaluated before and 10 minutes after the intravenous administration of 0.5 IU/kg secretin. The changes in pancreatic tissue T2 signal intensity and duodenal filling after the injection of secretin were determined by means of S-MRCP. The S-MRCP findings were then compared with those of the Lundh test. RESULTS: The pancreatic T2 signal intensity showed a significant elevation after secretin administration in the volunteers and in the patients with mild or severe chronic pancreatitis. This elevation was significantly lower in patients with mild and severe chronic pancreatitis than in the volunteers (66.85+/-15.77 and 24.45+/-5.85 vs. 200.0+/-45.07, respectively). After administration of secretin. the diameter of the duodenum was significantly increased in all three groups. This duodenal filling was significantly reduced in patients with mild or severe exocrine pancreatic insufficiency as compared with the volunteers (4.12+/-1.33 and 1.70+/-0.77 vs. 15.38+/-1.73, respectively). There was no significant difference in pancreatic T2 signal intensity changes or in duodenal filling in patients with mild or severe exocrine pancreatic insufficiency. There were significant correlations between the pancreatic T2 signal intensity changes and the duodenal filling and the results of the Lundh test (r = -0.616 and -0.78). CONCLUSION: These results demonstrate that the administration of secretin increases the T2 signal intensity of the pancreatic tissue and the diameter of the duodenum to different extents in normal subjects and in patients with chronic pancreatitis. This suggests that S-MRCP can provide information of value in the assessment of an exocrine pancreatic insufficiency.

Continuous enteral feeding has an attenuating effect on the exocrine pancreas in rats.

INTRODUCTION: Recent clinical observations suggest that continuous enteral feeding (CEF) may exert a beneficial effect in the management of inflammatory pancreatic diseases. Its effects on the exocrine pancreas, however, remain only partially investigated. AIM: To examine the effects of CEF on the exocrine pancreas in rats. METHODOLOGY: Eight male Wistar rats were intrajejunally cannulated, and CEF was started on postoperative day 6. In 10 control animals, laparotomy was followed by intragastric feeding (GF) with the same nutriment (Osmolite, Abbott) from postoperative day 6. The daily discharge was 24 kcal in both groups. After 5 days of feeding, the pancreas was removed; its weight and its protein, DNA, trypsin, and lipase contents were determined; and the exocrine pancreas was also examined for structural changes. RESULTS: The results revealed no significant difference in body weight loss between the two groups of animals, whereas the pancreas weight/body weight ratio was lower (p < 0.01) in the CEF group. The pancreatic protein, DNA, and enzyme contents were decreased (p < 0.01) after CEF as compared with the values for the GF group. Histologic examinations demonstrated clear decreases in acinar size and in the zymogen content of the pancreas in the CEF animals. CONCLUSION: This study clearly indicates that CEF reduces the enzyme production of the pancreas.

[Effect of continuous enteral feeding on pancreas exocrin function in rats]. / Folyamatos enteralis táplálás hatása a hasnyálmirigy exocrin múködésére patkányban.

The aim of this study was to examine the effects of continuous enteral feeding (CEF) on the exocrine pancreas in rats. Eight male Wistar rats were intrajejunally cannulated and CEF was started on postoperative day 6. In 10 control animals, laparotomy was followed by intragastric feeding (GF) with the same nutriment (Osmolite, Abbott, 254 mosm/l) from postoperative day 6. The daily discharge was 24 kcal in both groups. After five days of feeding, the pancreas was removed, its weight and its protein, DNA, trypsin and lipase contents were determined. The results revealed no significant difference in body weight loss between the two groups of animals, whereas the pancreas weight/body weight ratio was lower (p < 0.01) in the CEF group. The pancreatic protein, DNA, trypsin and lipase contents were decreased (p < 0.01) after CEF as compared with the values for the GF group.

Oxidative stress in distant organs and the effects of allopurinol during experimental acute pancreatitis.

BACKGROUND: The present study was aimed at an assessment of the role of oxygen-derived free radicals in the development of local and systemic manifestations of L-arginine (Arg)-induced acute pancreatitis and at an evaluation of the protective effect of the xanthine oxidase inhibitor allopurinol. METHODS: Acute pancreatitis was induced in male Wistar rats by injecting 2 x 250 mg/100 g body weight of Arg intraperitoneally at an interval of 1 h, as a 20% solution in 0.15 M NaCl. Control rats received the same quantity of glycine. In a third group, 200 mg/kg of allopurinol was administered subcutaneously 30 min before the first Arg injection. Rats were killed at 6, 12, 24, or 48 h following Arg administration. Acute pancreatitis was confirmed by a serum amylase level elevation and typical inflammatory features were observed microscopically. Tissue concentrations of malonyl dialdehyde (MDA), superoxide dismutase (Mn- and Cu,Zn-SOD), glutathione peroxidase (GPx), and catalase were measured in the pancreas, liver, and kidney. RESULTS: The tissue concentration of MDA was significantly elevated in each organ. The activities of Mn-SOD, Cu,Zn-SOD, GPx, and catalase were quickly depleted in the pancreas and kidney, whereas only the Mn-SOD and GPx activities were reduced in the liver after the onset of pancreatitis. Histologic examination revealed acinar cell necrosis in the pancreas, but only mild alterations in the liver and kidney. Allopurinol pretreatment prevented the generation of reactive oxygen metabolites in the pancreas and reduced their formation in the kidney. CONCLUSION: Oxygen-derived free radicals are generated in the pancreas, liver, and kidney at an early stage of Arg-induced acute pancreatitis. The liver and the kidney, but not the pancreas, are able to defend against oxidative stress. The prophylactic application of allopurinol significantly restrains the generation of free radicals in pancreas and kidney.

Effects of galanin(1-16) on pancreatic secretion in anesthetized and conscious rats.

Galanin, a 29-amino acid peptide, has been demonstrated in pancreatic nerve endings and found to inhibit insulin release in the rat. However, the data available concerning its effects on exocrine pancreatic secretion are contradictory. The aim of the present study was to evaluate the effects of a synthetic porcine galanin sequence, Gal(1-16), on stimulated pancreatic secretion in hyperglycemic anesthetized and conscious rats. Male Wistar rats were anesthetized and surgically prepared with pancreatic and femoral vein catheters. In anesthetized animals, the pancreatic secretion was continuously stimulated with 150 ng cholecystokinin octapeptide (CCK-8)/kg body weight per 30 min, dissolved in saline or 10% glucose. Synthetic Gal(1-16) (0.3 or 1 nmol/kg per h) was infused over a 60-min period. In conscious rats, 1, 3, or 10 nmol Gal(1-16)/kg per h was administered in a continuous saline or 10% glucose infusion over a 30-min period. The pancreatic secretory volume and protein output were determined in 30-min samples in both models. In anesthetized rats, 0.3 nmol Gal(1-16)/kg per h did not modify pancreatic secretion during CCK-8 stimulation. However, both the pancreatic secretory volume and the protein output were significantly inhibited compared with the basal levels by 1 nmol Gal(1-16)/kg per h. The inhibitory effect of Gal(1-16) on pancreatic secretion was more marked with CCK-8/glucose (53.9%) than with CCK-8/saline stimulation (20.1%). In conscious rats, significant inhibitory effects of 1 nmol Gal(1-16)/kg per h in saline were observed (18%). During glucose infusion, a dose-dependent inhibition of 1, 3, and 10 nmol Gal(1-16)/kg per h on pancreatic secretory volume and protein output (35% inhibition at 1 nmol/kg per h) was observed. In conclusion, the inhibitory effect of Gal(1-16) on exogenous and endogenous CCK-stimulated pancreatic secretion was found to be more potent in the presence of glucose both in anesthetized and in conscious rats. These results may suggest an indirect (insulin-mediated) inhibitory effect of porcine Gal(1-16) on pancreatic secretion in the rat.

Assessment of pancreatic enzyme secretory capacity by a modified Lundh test.

BACKGROUND: The Lundh test is a usual means of estimating the enzyme secretory capacity of the gland. During this procedure, however, a major proportion of the test meal is removed from the duodenum together with the gastric, duodenal, and pancreatic secretions and the bile. This study was undertaken to compare the pancreatic enzyme secretion induced by the Lundh procedure with that resulting from stimulation of the normal digestive process, by reinfusion of the aspirated duodenal juice. METHODS: Nine men (mean age: 46.7, range 42-55 yr) free from pancreatic disease were studied. Pancreatic secretion was measured via a multiple lumen tube by aspiration of the duodenal juice. After a basal period the Lundh test meal was placed in the stomach and the duodenal juice was completely aspirated. On a separate day, the procedure was repeated, but the aspirated duodenal juice was reinfused into the upper jejunum. RESULTS: In the first 30 min of the test period, the enzyme outputs were the same on both test days. In the 30-60-min period, the lipase output, and in the 75-90-min period, the amylase output was significantly lower during the Lundh test compared with the jejunal reinfusion test. The CCK levels were significantly above the basal level at 20 and 40 min, but the increase was significantly lower during the traditional Lundh test. No significant difference in gastrin release was observed during either the Lundh or the reinfusion test. CONCLUSIONS: In the traditional Lundh test, the trypsin secretory capacities of the gland are measured appropriately, but the lipase and amylase secretory capacity and the CCK release are not fully represented compared with the reinfusion test. An association between the lower CCK release and lipase amylase secretion is suggested.

The pathogenesis of L-arginine-induced acute necrotizing pancreatitis: inflammatory mediators and endogenous cholecystokinin.

This study was aimed at an assessment of the role of oxygen-derived free radicals, cytokines and endogenous cholecystokinin (CCK) in the pathogenesis of L-arginine (Arg)-induced acute pancreatitis in rat. We measured the levels of malonyl dialdehyde (MDA), glutathione peroxidase (GPx), catalase and superoxide dismutase (Mn- and Cu, Zn-SOD) in pancreatic tissue, the serum levels of tumor necrosis factor-alpha (TNF-alpha), interleukin-6 (IL-6) and CCK, and evaluated the protective effect of the xanthine oxidase inhibitor allopurinol and a novel CCK receptor antagonist KSG-504. Acute pancreatitis was induced in male Wistar rats by injecting 2x 250 mg/100 g body weight of Arg intraperitoneally in an 1-h interval, as a 20% solution in 0.15 M NaCl. Control rats received the same quantity of glycine. 200 mg x kg(-1) allopurinol 30 min before the first Arg treatment or 50 mg x kg(-1) KSG-504 30 min before and 6, 18 and 36 h after the first Arg injection was administered subcutaneously. Rats were killed at 6, 12, 24 and 48 h following Arg administration, and acute pancreatitis was confirmed by a serum amylase level elevation and typical inflammatory features observed microscopically. The serum level of amylase reached the peak level at 24 h after the Arg injection (30,800 +/- 3,813 versus 6,382 +/- 184 U x L(-1) in the control) and normalized at 48 h. The tissue concentration of MDA was significantly elevated at 24 h, and reached the peak value at 48 h (5.00 +/- 1.75 versus 0.28 +/- 0.05 nM x mg(-1) protein in the control). The catalase and Mn-SOD activities were significantly decreased throughout the study, while the GPx activity was significantly reduced at 6 and 12 h, and the Cu, Zn-SOD activity was significantly lower at 12 h after the Arg injection as compared with the controls. Both the TNF-alpha and the IL-6 levels were already elevated significantly at 12 h and peak at 24 h versus the controls (19.1 +/- 7.9 U x mL(-1) and 57.6 +/- 11.2 pg x mL(-1) versus 3.1 +/- 0.8 U x mL(-1) and 15.2 +/- 3.1 pg x mL(-1), respectively). No significant changes in plasma CCK levels were observed. Allopurinol treatment markedly reduced the serum amylase elevation (12.631 +/- 2.257 U x L(-1) at 24 h), prevented the increase in tissue MDA concentration (0.55 +/- 0.09 nM x mg(-1) protein at 48 h) and significantly ameliorated the pancreatic edema, necrosis and inflammation at 48 h after Arg administration. KSG-504 administration did not exert any beneficial effect on the development of histopathological changes neither modified the serum amylase or cytokine levels. Oxygen-derived free radicals and cytokines are involved, while endogenous CCK does not seem to play a role in the pathogenesis of Arg-induced acute pancreatitis.

Recovery of exocrine pancreas six months following pancreatitis induction with L-arginine in streptozotocin-diabetic rats.

The aim of the present work was to investigate the laboratory and morphologic alterations in the pancreas 6 months after pancreatitis induction with L-arginine (Arg) in normal and streptozotocin (STZ)-diabetic rats. The amylase content of the pancreas was significantly decreased in the Arg-treated groups vs. the control group. No significant changes were observed in the DNA, soluble protein and lipase contents of the pancreas. In the STZ-treated groups, the serum glucose level was significantly elevated, whereas the serum immunoreactive insulin (IRI) level was significantly decreased vs. the control group. In these treated groups, the amylase content of the pancreas was also significantly decreased, but that of trypsinogen was significantly elevated vs. the control group. Histologic sections revealed periductal fibroses, adipose tissue and tubular complexes in the Arg-treated rats, but centroacinar hyperplasia was not observed in these groups. No alterations were observed on histological examination in the diabetic rats vs. normal rats 6 months following pancreatitis induction. In conclusion, a major restitution of the pancreatic enzyme content, but moderate histologic alterations were detected 6 months following pancreatitis induction with Arg. The diabetic state appeared to shift the normal pancreatic enzyme content (decreased amylase and increased trypsinogen) in this long-term study, but not to modify the recovery of the exocrine pancreas 6 months following Arg-induced pancreatitis.

[Diagnostic value of fecal elastase test in pancreatic exocrine deficiency]. / A széklet elasztáz-teszt diagnosztikus értéke exokrin pancreas-elégtelenségben.

The diagnostic value of the estimation of faecal elastase-1, the new noninvasive direct pancreatic function test was evaluated in a total of 35 patients. Twenty one patients were diagnosed with chronic pancreatitis and categorized according to grades of exocrine pancreatic insufficiency based on the Lundh test, 14 patients in the control group had gastrointestinal disorders. Faecal elastase 1 was measured by ELISA method. The sensitivity, specificity, positive and negative predictive value and diagnostic accuracy of elastase determination was 71.4%, 92.8%, 88.2%, 81.2% and 83.7%, respectively in chronic pancreatitis. In the severe exocrine pancreas insufficiency group (n = 14), the sensitivity was 85.7%, while in the group with mild insufficiency (n = 7) the sensitivity was only 42.8%. The determination of faecal elastase is useful in the diagnosis of severe exocrine pancreas insufficiency, but it is not sensitive enough in the mild form of the disease.

Pancreatic secretory responses in L-arginine-induced pancreatitis: comparison of diabetic and nondiabetic rats.

The aim of this work was to study cholecystokinin-octapeptide (CCK-8)-stimulated pancreatic secretion after the induction of pancreatitis with L-arginine (ARG) in rats with or without streptozotocin (STZ) diabetes. One, 3, 7, and 14 days after pancreatitis induction, rats were surgically prepared with pancreatic duct and femoral vein cannulae under urethane anesthesia. Graded doses of CCK-8 ranging from 9 to 2,400 ng/kg/30 min were administered intravenously. In the control group, the step-wise increasing doses of CCK-8 resulted in a characteristic dose-response curve for the pancreatic volume, protein and amylase secretion (maximal volume, protein and amylase output at 600 ng/kg/30 min of CCK-8: 157 +/- 20.2 microl/30 min, 28.3 +/- 1.18 mg/30 min, and 3,750 +/- 92 IU/30 min, respectively). In rats with pancreatitis, the pancreatic volume (both basal and maximal) and amylase secretion were significantly elevated on day 1 versus the control group; then on days 3,7, and 14, the pancreatic secretory volume and amylase were progressively and significantly decreased versus the control group. However, the protein output was continuously decreased versus the control group on days 1, 3, 7, and 14. In diabetic rats, the maximal volume and protein and amylase output were all significantly decreased versus the control group throughout the experiment. In the diabetes + pancreatitis group, the maximal volume and protein and amylase output were all significantly increased versus the diabetes group on days 1, 3, 7, and 14. These results indicate that in the early phase of ARG-induced pancreatitis, the pancreatic secretion is characterized by increases in secretory volume and amylase, with a simultaneous decrease in protein output. Simultaneous diabetes seems to moderate the CCK-8-stimulated secretory changes in both the early and late phases after ARG-induced pancreatitis.

Effect of a liquid meal given as a bolus into the jejunum on human pancreatic secretion.

Major features of pancreatic secretion stimulated by a meal depend on intestinal phase mechanisms. However, an intrajejunal (i.j.) meal infusion is widely used for the treatment of inflammatory pancreatic diseases when the resting of the gland is desired. This study was undertaken to compare the effects of an intragastric (i.g.) and an i.j. complete fluid (Lundh) test meal on pancreatic enzyme secretion. Eight men (mean age, 43 years; range, 31-48) free from pancreatic disease were studied. Pancreatic secretion was measured via a multiple-lumen tube by aspiration of the duodenal juice. After a fasting period, the Lundh test meal was placed in the stomach or the upper jejunum. After the i.g. administration of the test meal, the aspirated duodenal juice was reinfused into the jejunum. The effect of atropine infusion (0.5 microg/kg/h) on the pancreatic enzyme secretion was studied. The pancreatic amylase, trypsin, and lipase outputs were determined. The plasma levels of cholecystokinin (CCK) and of gastrin were measured by bioassay and radioimmunoassay, respectively. The trypsin, amylase, and lipase secretions increased significantly after either an i.g. or an i.j. test meal intake. The trypsin, amylase, and lipase outputs were significantly decreased during the i.j. perfusion as compared with i.g. administration. The gastrin levels increased significantly after i.g., but remained unchanged after i.j. administration. The CCK release attained its maximum 40 and 60 min after the i.g. and i.j. test meal, respectively. However, the CCK release was significantly lower during the i.j. administration as compared with i.g. perfusion. An atropine infusion significantly reduced the i.g. and i.j. test meal-stimulated enzyme outputs. An i.j.-administered meal stimulates the pancreatic enzyme secretion, but this effect is significantly lower than that which occurs on i.g. administration. The i.j. meal-stimulated secretion of pancreatic enzymes is subject to both cholinergic and peptidergic regulation. The deficiency of gastrin and the delayed and decreased CCK release are believed to account for the reduced enzyme output.

[Endoscopic therapy of pancreas divisum]. / A pancreas divisum endoscopos kezelésének lehetóségei.

Pancreas divisum is the most frequent congenital ductal anomaly of the pancreas: it occurs in 5-10% of the population. In the majority of patients, this congenital anomaly is of no clinical importance. In a certain subset of patients, however, pancreas divisum is clinically important as a cause of abdominal pain, acute recurrent pancreatitis or chronic obstructive pancreatitis. The authors, experience on endoscopic drainage of the minor papilla is reported. In the history of patient 1., three episodes of recurrent pancreatitis and permanent upper abdominal pain were explored. ERP revealed a pancreas divisum and a mild irregularity and dilation of the dorsal pancreatic duct. A 7 F stent (length: 6 cm) was implanted in the dorsal pancreatic duct following a papillotomy on the stenotic minor papilla. A repeated Lundh test revealed a 58% improvement in the exocrine pancreatic function. No recurrence of pancreatitis has been observed in spite of the moderate continuous abdominal pain. In patient 2., ERP demonstrated a pancreas divisum and a severely dilated dorsal pancreatic duct as causes of the previous permanent abdominal pain. An 8 F stent (length: 5 cm) was inserted through the minor papilla without endoscopic sphincterotomy. A significant improvement in exocrine pancreatic function (70%) ensued. No abdominal pain has since been observed. In conclusion, dorsal pancreatic duct stenting (mainly in cases involving a dilated pancreatic duct) seems to have a beneficial effect in patients with both recurrent acute pancreatitis or chronic obstructive pancreatitis evoked by pancreas divisum.