László Pávics

The possible role of F-18 FDG positron emission tomography in the differential diagnosis of focal pancreatic lesions

Purpose To compare the diagnostic values of different methods for the differentiation of malignant from benign pancreatic lesions. Methods In 22 patients with focal pancreatic lesions, the carbohydrate antigen (CA) 19-9 level was measured; abdominal ultrasound (US), computed tomography (CT), endoscopic retrograde cholangiopancreatography (ERCP), and F-18 fluorodeoxyglucose (FDG) positron emission tomography (PET) were performed; and the value of these methods were analyzed for their use in cancer diagnosis. Results Malignant lesions were identified in six patients and verified by surgery or clinical follow-up. The CA 19-9 level was elevated in four of the five patients examined (sensitivity, 80%). In all six cases, US and CT revealed hypoechogenic and hypodense areas (sensitivity, 100%). In one patient, ERCP was unsuccessful but yielded true-positive results in three others (sensitivity, 60%). The sensitivity of FDG PET was 100%. Sixteen focal cases of pancreatic disease proved to be benign. The CA 19-9 level was elevated in four of them (specificity, 73%). Hypoechogenic and hypodense areas were evident on US and CT in eight patients. The specificity of CT was 50% (8 of 16 cases). The specificity of US was 47% (7 of 15 cases). The specificity of successful ERCP was 92%. Fourteen negative FDG-PET results were truly negative. In two patients, however, the PET findings proved to be falsely positive (specificity, 88%). Conclusions FDG-PET is an effective tool to differentiate malignant from benign focal pancreatic lesions. In persons with focal pancreatic hypoechogenic or hypodense lesions detected by CT or US and an elevated CA 19-9 level, FDG PET should be the next step in the diagnostic strategy.

Leaky Gut in Patients with Diarrhea-Predominant Irritable Bowel Syndrome and Inactive Ulcerative Colitis

Background/Aims: Defective epithelial barrier has been implicated in the pathogenesis of irritable bowel syndrome (IBS) and inflammatory bowel diseases. The aim of this study was to investigate gut permeability in patients with inactive ulcerative colitis (UC) and in patients with IBS. Methods: IBS patients of the diarrhea-predominant (IBS-D) and of the constipation-predominant subgroup (IBS-C), patients with inactive UC and healthy subjects were enrolled. Gut permeability was evaluated by measuring 24-hour urine excretion of orally administered 51Cr-EDTA. Clinical symptoms were evaluated in IBS-D patients and correlated to colonic permeability. Results: There was a significant decrease in the proximal small intestinal permeability in IBS-C patients compared to controls (0.26 ± 0.05 vs. 0.63 ± 0.1%; p < 0.05). Distal small intestinal permeability showed no significant difference in the studied group of patients compared to controls. Colonic permeability of IBS-D and inactive UC patients was significantly increased compared to controls (2.68 ± 0.35 and 3.74 ± 0.49 vs. 1.04 ± 0.18%; p < 0.05, p < 0.001). Colonic permeability of IBS-D patients correlated with stool frequency. Conclusions: Elevated gut permeability is localized to the colon both in IBS-D and in inactive UC patients.

Clinical value of technetium-99m-HMPAO-labeled leukocyte scintigraphy and spiral computed tomography in active Crohn's disease

Clinical value of technetium-99m-HMPAO-labeled leukocyte scintigraphy and spiral computed tomography in active crohns disease

Feasibility of 11C-Acetate PET/CT for Imaging of Fatty Acid Synthesis in the Atherosclerotic Vessel Wall

Fatty acids are a common constituent of atherosclerotic plaque and may be synthesized in the plaque itself. Fatty acid synthesis requires acetyl-coenzyme-A (CoA) as a main substrate, which is produced from acetate. Currently, 11C-acetate PET/CT is used for the evaluation of malignancies. There are no data concerning its potential for the characterization of atherosclerotic plaque. Therefore, the purpose of the present study was to examine the prevalence, distribution, and topographic relationship of arterial 11C-acetate uptake and vascular calcification in major arteries. Methods: Thirty-six patients were examined by whole-body 11C-acetate PET/CT. Tracer uptake in various arterial segments was analyzed both qualitatively and semiquantitatively by measuring the blood-pool–corrected standardized uptake value (target-to-background ratio). CT images were used to measure calcified plaque burden. Results: 11C-acetate uptake was observed at 220 sites in 32 (88.8%) of the 36 study patients, and mean target-to-background ratio was 2.5 ± 1.0. Calcified atherosclerotic lesions were observed at 483 sites in 30 (83.3%) patients. Sixty-four (29.1%) of the 220 lesions with marked 11C-acetate uptake were colocalized with arterial calcification. However, only 13.3% of all arterial calcification sites demonstrated increased radiotracer accumulation. Conclusion: Our data indicate the feasibility of using 11C-acetate PET/CT for imaging of fatty acid synthesis in the atherosclerotic vessel wall. This study provides a rationale to incorporating 11C-acetate PET into further preclinical and clinical studies to obtain new insights into fatty acid synthesis in atherosclerotic lesions and to evaluate whether it may be used to monitor pharmacologic intervention with fatty acid synthase inhibitors.

The effects of somatostatin and octreotide on the human sphincter of Oddi

OBJECTIVE Somatostatin acts at different sites in the human gastrointestinal tract and generally inhibits the release and effects of many gastrointestinal hormones and neuropeptides. Together with its long-acting analogue octreotide, somatostatin is widely used in the treatment of hormone-producing tumours, variceal bleeding, etc., but multi-centre trials have failed to prove a beneficial effect in the treatment of acute pancreatitis or in the prevention of post-ERCP pancreatitis (pancreatitis following endoscopic retrograde cholangiopancreatography). The aim of the present work was to study the effects of somatostatin and octreotide on the human sphincter of Oddi by means of quantitative hepatobiliary scintigraphy (QHBS). METHOD Fifteen cholecystectomized patients were enrolled in the study, six in the somatostatin group and nine in the octreotide group. QHBS was performed initially with a standard protocol (baseline data), then repeated after 0.1 mg octreotide or a 250 microg bolus + 250 microg/h somatostatin administration. In the 60th min of QHBS, 0.5 mg glyceryl trinitrate (GTN) was administered sublingually. RESULTS QHBS demonstrated that both somatostatin and octreotide caused a marked impairment in the bile flow: the half-time of excretion (T1/2) over the common bile duct was significantly prolonged compared with baseline data (somatostatin group: common bile duct T1/2 180 min versus 59.7+/-31 min; octreotide group: common bile duct T1/2 140.9+/-60.5 min versus 30.7+/-11.7 min). Glyceryl trinitrate administration accelerated the transpapillary bile flow, with significant decreases in the elevated T1/2 in both groups. CONCLUSION Increased transpapillary flow induced by glyceryl trinitrate may be beneficial in the treatment of acute or post-ERCP pancreatitis.

Diagnosis of gallbladder dyskinesia by quantitative hepatobiliary scintigraphy

Aim: The aim of the present study was to develop a new pharmacologic method during hepatobiliary scintigraphy by which patients with functional and organic forms of gallbladder (GB) dysfunction can be differentiated. Methods: Quantitative hepatobiliary scintigraphy (QHBS) was performed on 31 patients with impaired GB motility selected by cerulein-augmented ultrasonography. Nineteen patients had acalculous biliary pain (ABP) and suspected GB dyskinesia, 6 patients had celiac disease, and 6 patients had type II diabetes mellitus. Sixty minutes after the isotope administration, 1 ng/bwkg/min cerulein (CCK10) was infused for 10 minutes, and then from the 90th minute, an equivalent dose of CCK10 was infused in the presence of 0.5 mg sublingual glyceryl trinitrate (GTN) in 12 or placebo in 7 consecutive patients. The GB ejection fraction (GBEF) was calculated repeatedly in time periods from 60 to 90 and from 90 to 120 minutes. Results: In the majority of patients with ABP and suspected GB dyskinesia, CCK10 and GTN coadministration normalized the previously impaired GB-emptying. When the cumulative results of all 12 patients were calculated, we demonstrated significant differences (P = 0.003) in the GBEF between the first (CCK10) versus the second (CCK10 plus GTN) stimuli: 19 ± 11% versus 40 ± 17%, respectively. In contrast, in 12 patients with celiac sprue and diabetes mellitus, no differences in the GBEF were detected when the first (CCK10 alone) versus the second (CCK10 plus GTN) stimuli was compared: 21 ± 10% versus 22 ± 13%, respectively. Finally, placebo and CCK10 coadministration in 7 consecutive patients with ABP and suspected GB dyskinesia did not influence the GBEF as compared with CCK10 alone: 13 ± 9% versus 15 ± 10%, respectively. Conclusion: GTN and CCK10 coadministration induces a significant improvement of the GBEF in patients with GB dyskinesia. The application of this new pharmacologic test during QHBS permitted the noninvasive separation of those patients with secondary impaired GB-emptying as a result of GB dyskinesia from those with primary forms of GB hypokinesia.

Regional cortical blood flow changes following sodium lactate infusion in Alzheimer's disease

Bilateral temporoparietal hypoperfusion is a characteristic single photon emission computed tomography (SPECT) finding in Alzheimers disease (AD). Lactate is a metabolic vasodilator and is known to provoke increased cerebral blood flow (CBF) in healthy adults. This work investigated whether lactate, which is present in high concentrations in AD cerebrospinal fluid, affects AD‐specific perfusion abnormalities. Twenty mild‐to‐moderately demented AD probands participated in the self‐controlled study. The regional CBF was examined utilizing 99mTc‐HMPAO SPECT after sodium lactate infusion (0.5 m, 5 mL/kg body weight) and 0.9% NaCl infusion, one on each of two separate days. Despite the vasodilatator effects of sodium lactate, AD rCBF patterns did not show increase in temporo‐parietal regions after its infusion. AD‐specific bi‐temporo‐parietal reduction in CBF was accompanied by further hypoperfusion in the parieto‐occipital areas after the sodium lactate infusion in seven patients, while no CBF changes were observed in the case of the remaining 13 probands. The pattern of the CBF abnormalities was not correlated with the apolipoprotein E genotype. The decreased vascular responsiveness to sodium lactate reflects disturbed vasoregulatory processes in AD and it is unlikely that lactate would have any relevance in the treatment of AD‐related cerebral hypoperfusion, but could be used to improve the value of perfusion SPECT in the diagnosis of AD.

Gallbladder hypomotility in diabetic polyneuropathy

This study was performed to evaluate the gallbladder motility in long-standing diabetes mellitus. The gallbladder function of diabetic patients was measured by means of quantitative hepatobiliary scintigraphy, and the severity of the associated autonomic and sensory polyneuropathy was determined. The presence of a marked gallbladder hypomotility was established, and a positive correlation was observed between the severity of the autonomic disturbance and the contractile disorder. This study underlines the important role of the neuropathy in the development of gallbladder hypomotility accompanying long-term diabetes mellitus.A study was made of the pathogenic role of gallbladder hypomotility, which is presumably responsible for the high incidence of gallstone disease in long-standing diabetes mellitus. The gallbladder motility of diabetic patients (n = 10) was measured by means of quantitative hepatobiliary scintigraphy, and the severity of concomitant autonomic and sensory polyneuropathy was determined. The presence of marked gallbladder hypomotility was proven, and a positive correlation was observed between the severity of autonomic neuropathy and the contractile disorder. In this group of diabetic patients, a hypaesthetic sensory polyneuropathy too was recognized, the degree of which exhibited a positive correlation with the autonomic neuropathy score. This study underlines the important role of the autonomic neural dysfunction in the development of gallbladder hypomotility accompanying long-term diabetes mellitus.

Validation of CT doses of SPECT/CT and PET/CT hybrid devices: Lessons learned

The aim of the study was to check the validity of computed tomographic (CT) doses exhibited by SPECT/CT and PET/CT hybrid devices. Dose measurements were taken from four SPECT/CT and four PET/CT cameras commercially available from different manufacturers. A calibrated ionization chamber was placed in whole-body or head phantoms for the acquisition of CT images with clinically used parameters. Computed tomography dose index (CTDIvol) values were calculated according to the IEC 60601-2-44:1999 formula. The measured CTDIvol doses were compared with those preprogrammed by the manufacturer. In the case of the whole-body phantom, the differences between the measured and displayed values varied between −31 and +24% [European document RP162 (2012) sets up the limit for acceptance criterion as ±20%]. The head phantom data showed either an agreement between −10 and +24%, or an underestimation by two-fold. The latter seemed to be because, while preprogramming the doses, the manufacturer had used the whole-body phantom instead of a proper head phantom. The results of the work demonstrate the need for individual dosimetric calibration of every single X-ray tube. Dosimetric checks should be included in the regular quality control programmes of the SPECT/CT and PET/CT devices. Special attention should be paid to head-and-neck and paediatric protocols, in which the use of a head phantom is recommended for dose calibration.

Erdheim-Chester's disease of the heart: a diagnostic conundrum and collision with the same mass in the orbit.

Erdheim-Chesters disease is a rare multisystem xanthogranulomatosis, afflicting the skeletal system with the occasional involvement of soft tissues. We delineate an unusual case of a cardiac variant of Erdheim-Chesters disease presenting with pericardial effusion and as a collision with a synchronous orbital manifestation. We describe our diagnostic pathway and propose a novel treatment option involving nonsteroidal anti-inflammatory drugs. The role of cyclo-oxygenase in the disease process and inhibition thereof by NSAIDs is hypothesized and discussed.