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Two groups of patients, with laparoscopic cholecystectomy (LC) were prospectively studied. All patients had serial plain abdominal X-ray examinations at various intervals after operation, to record the position of clips placed during LC. Seventy-one patients had less cystic duct (CD) dissection and > or =4 clips placed during the procedure. One hundred and fifteen patients had a larger CD dissection and only 4 clips placed (2 on the cystic artery and 2 on the CD, without additional clips on smaller vessels). In the former group, 7 patients had clip migration within 1 month and 11 within 1 year vs 1 either at 1 month or 1 year in the latter group (p = 0.01 and <0.001, respectively). During the follow-up, a 72-year-old man belonging to the former group had a recurrent common duct brown pigment stone containing a metallic clip 26 months after operation. He was treated successfully by endoscopic sphincterotomy. Factors predisposing to clip migration were short cystic stump, inadvertent clip dislodgment or incorrect placement, cystic duct ischemic necrosis, and local suppurative complications. Data from 29 patients with GS formed around suture material or phytobezoars observed during a prospective study and from the physicochemical and structural analysis of a cumulative series of 64 GS containing foreign bodies are also presented and discussed. It is suggested that metallic clips can migrate from their initial sites at various intervals within the peritoneal cavity or into the common duct and serve as a nidus for GS formation. Metallic clip migration in most cases is due to technical factors and can usually be prevented. However, it is not possible to prevent either clip migration or GS formation in every case, since even well-placed clips can migrate due to suppurative complications or local ischemic damage, and, once that penetration within the bile tract has occurred, GS are usually going to form, irrespective of the nature and the shape of the foreign body.

Isolated atrial inversion in situs inversus is a rare congenital cardiac malformation. Its physiology resembles transposition of great vessels, and the best option for its surgical treatment is the atrial switch operation. In this article, we present a case of isolated atrial inversion in concordance with visceral situs inversus diagnosed at birth by echocardiography and cardiac catheterization, which was successfully treated at 8 months of age by a Senning procedure.

Secretory IgA (SIgA) is the main agent protecting the mucosal districts against both infectious microorganisms and inert foreign macromolecules. A lack of secretory immunity has previously been described in patients with allergic rhinitis, but it is a controversial finding. The discrepant results of SIgA levels found in allergy may partially be due to methodological problems. Sixty patients with previously demonstrated allergic rhinitis, treated or not with specific desensitization therapy and free from clinical manifestation of rhinitis were studied. Normal volunteers and patients with selective 11S IgA deficit, without allergic pathology, were investigated as controls. The titration of SIgA in nasal secretions, performed by an original immunoisoelectro-focusing method, showed significantly decreased values in allergic patients. An evaluation of the IgE level in nasal secretion was performed by ELISA. Low rates of IgE were also found in the intercritic period.

High-resolution US yields important information for the study of Crohn's disease. A more accurate follow-up is possible by the integration of US with radiological and clinical findings. Sixty-two patients with suspected or known Crohn's disease were examined with double-contrast small bowel enema and high-resolution US. The latter allowed the demonstration of such pathologic findings as mesenteric thickness greater than 15 mm, submucosal thickness (third hyperechoic layer greater than 50% of total bowel wall thickness), lymphadenopathies, and fluid collections. The authors suggest that US grading be performed, and radiological correlations made. The combined use of the two techniques yields better results and allows a better assessment of the patients, which is very useful for both prognosis and therapy.

The casual observation of high serum levels in (TATI) of tumor associated trypsin inhibitor in patients with osteosarcoma inspired us to evaluate the use of this peptide in the diagnosis of various bone diseases. We determined the serum concentrations of TATI in 35 patients with various bone diseases, i.e. degenerative diseases, bone metastasis and osteosarcomas. The cut off, determined as the 99th percentile of TATI serum levels in healthy volunteers was 32 micrograms/l. TATI has a better sensitivity in osteosarcomas (83%) than in metastatic bone diseases (33%). Its specificity in non-malignant bone diseases was not exceptional (82%). This is probably because TATI may also behave as on acute phase protein, the levels of which can rise in non-malignant diseases and also as a result of a tissue reaction in primary bone tumors.

Conventional radiology is the main diagnostic tool for the visualization of osteoarticular lesions in rheumatoid arthritis. Articular effusions and popliteal cysts were examined with US. This paper is aimed at proving US capabilities in yielding important information about articular and peri-articular soft tissues in the early phases of rheumatoid arthritis. Over the last 30 months, the shoulder, wrist, hand, knee, and hip of 73 rheumatoid patients were studied by means of US and conventional and microfocal radiography. The patients were divided into 2 groups according to the time of onset of the disease. In group A, US demonstrated early synovial exudative inflammation, whereas conventional and microfocal radiography mainly demonstrated soft tissue swelling. In group B (where the first onset dated back to over 1 year), US demonstrated exudative and proliferative changes, together with recurrences. The authors believe US to be able to recognize the early changes of rheumatoid arthritis: as a matter of fact, US shows articular and periarticular soft tissues abnormalities and allows a differential diagnosis to be made between exudative and proliferative forms.

The diagnostic capability of ultrasound in symptomatic gastric cancer is stressed, on the basis of a prospective study of 64 neoplastic and 19 non-neoplastic patients. Aspecific signs are described which suggest the presence of five layers within the gastric wall as an index of absence of disease. The prospective importance of ultrasound investigation in 5 neoplastic patients with aspecific symptoms is emphasized.

A case of cardiac echinococcosis in a 22 year-old woman is reported. Clinical findings and cardiac catheterization data offered only presumptive evidence of an intraventricular mass but failed to make a positive diagnosis of cardiac involvement by hydatid disease. Using Two-Dimensional Echocardiography (2-DE) we were able to identify a rounded structure with multiple loculation into the right ventricle, highly suggestive of a hydatid cyst. Surgery confirmed our findings. We confirm the ability of 2-DE to detect and characterise intracardiac masses and we suggest that 2-DE could be considered the procedure of choice in the diagnosis of cardiac hydatid disease.

Exercise two-dimensional echocardiography (2D-ECHO) can be used to detect coronary artery disease in patients (pts) by the development of stress-induced transient asynergy in areas without wall motion abnormalities when at rest. The aim of the study is to verify the accuracy of exercise 2D-ECHO in the identification of high risk pts with multivessel disease after the first acute myocardial infarction (AMI). Technically adequate 2D-ECHO examinations were obtained in 21 of 28 (75%) consecutive patients after acute myocardial infarction. 30-50 days after acute myocardial infarction, these 21 pts (19 males and 2 females, mean age +/- SD = 54.3 +/- 8.7) underwent 2D-ECHO during bicycle exercise in supine position. The marker of multivessel disease was the development, during the stress test, of new areas of asynergy not adjacent to the infarcted area (i.e. transient remote asynergy). Two months after acute myocardial infarction all pts underwent coronary angiography to verify the severity of coronary obstruction (reduction of luminal diameter greater than or equal to 75% in the non infarct related vessel).(ABSTRACT TRUNCATED AT 250 WORDS)

The effects of erythromycin estolate, a well known hepatotoxic macrolide antibiotic, on isolated rat hepatocyte viability and on subcellular Ca2+ transport have been investigated. Erythromycin estolate (0.5 mM), but not erythromycin base and erythromycin ethylsuccinate, induced 100% cell death after 60 min incubation, and caused maximal inhibition of mitochondrial and microsomal Ca2+ sequestration activities at 0.1 mM concentration. Sodium lauryl sulphate, which is the surfactant moiety of the erythromycin estolate molecule, caused effects similar to those exhibited by erythromycin estolate. Disorders of the intracellular calcium homeostasis seem to play a role in the lauryl sulphate-mediated hepatotoxic action of erythromycin estolate.

For the Cr(VI) selective separation from biological materials we have developed a highly rapid extraction-separation method with liquid anion exchanger as Amberlite LA-1 or LA-2. The analytical determination of Cr(VI) in organic phase was carried out using electrothermal atomic absorption spectroscopy (ETA-AAS). After i.v. administration of 0.5 and 2.5 mg/kg b.w. of K2Cr2O7 in male Wistar rats the biological samples, collected at different times, were immediately analyzed. Cr(VI) was not detected in whole blood one minute after administration of the lower dose. In blood of rats receiving higher dose an incomplete reduction of Cr(VI) was observed. Such data demonstrate a highly rapid but limited metabolic capacity of hematic compartment to reduce Cr(VI) to trivalent status. "In vitro" incubation of K2Cr2O7 (4 microM) with rat erythrocytes or plasma at 37 degrees C showed a rapid reduction of Cr(VI) in red cells while plasma samples demonstrated a limited reductive power. These results obtained with a new and specific analytical method, confirmed a trigger role of red cells in Cr(VI) metabolism.

Incubation of a rat hepatocyte plasma membrane fraction with micromolar concentrations of either glutathione disulfide or various glutathione S-conjugates resulted in a several-fold increase in the rate of ATP hydrolysis. This stimulation was further enhanced when the plasma membrane fraction had been pretreated with agents that arylate or oxidize sulfhydryl groups, suggesting that this ATPase activity is modulated by the protein thiol status of the plasma membrane. It is proposed that this newly discovered ATPase may function in the cellular extrusion of both glutathione disulfide and glutathione S-conjugates.

Infusion of cystamine into the isolated, perfused rat liver resulted in tissue damage preceded by the formation of cystamine-protein mixed disulfides which were mainly detected in the plasma membrane fraction. Hepatotoxicity was prevented when dithiothreitol was infused after cystamine or when the calcium antagonist, verapamil, was co-infused with the disulfide. In isolated hepatocytes, the formation of cystamine-protein mixed disulfides was associated with an inhibition of plasma membrane Ca2+-ATPase activity and a decreased rate of Ca2+ efflux from the cells. This resulted in intracellular Ca2+ accumulation which was followed by a stimulation of both phospholipid hydrolysis and proteolysis, as indicated by enhanced rates of release of radioactivity from hepatocytes prelabeled with [14C]arachidonate and [14C]valine, respectively. Preincubation of hepatocytes with the calmodulin inhibitor, calmidazolium, or with the phospholipase inhibitors, chlorpromazine and dibucaine, inhibited the stimulation of [14C]arachidonate release by cystamine. However, none of these agents prevented the onset of cystamine toxicity in hepatocytes. In contrast, pretreatment of the cells with antipain or leupeptin, two inhibitors of Ca2+-activated proteases, abolished the stimulation of proteolysis by cystamine and also protected the cells from cystamine toxicity. Our results suggest that the perturbation of intracellular Ca2+ homeostasis by cystamine is caused by the inhibition of Ca2+ efflux associated with the formation of cystamine-protein mixed disulfides in the plasma membrane and that subsequent cytotoxicity results from Ca2+-activation of a nonlysosomal proteolytic system.

Authors have studied AFP serum levels in 289 lung cancer. Only 2 cases (0.7%) showed little increase of this glycoprotein and liver pathologies were present in both patients, authors believe immunohistochemical study is necessary in lung cancers that show AFP increase.

Previous studies have indicated that the presence of cytotoxic levels of menadione (2-methyl-1,4-naphthoquinone) causes rapid changes in intracellular thiol and Ca2+ homeostasis in isolated rat hepatocytes. The present investigation was undertaken to examine these effects in the intact liver. Rat livers were therefore perfused with Krebs-Henseleit buffer containing 1.3 mM Ca2+ using a single-pass mode, and the perfusate Ca2+ level was monitored with an on-line Ca2+-selective electrode. Infusion of menadione elicited an increased O2 uptake by the liver, followed by a dose-dependent decrease in the perfusate level of Ca2+. Hepatic accumulation of Ca2+ was accompanied by stimulation of cytosolic phosphorylase a activity. Cessation of menadione infusion resulted in gradual recovery of perfusate Ca2+ to base levels. Ca2+ uptake was not accompanied by decreases in reduced pyridine nucleotide or ATP levels in the liver as evidenced by measurements either during maximal Ca2+ uptake or after recovery. However, Ca2+ uptake was correlated with decreased glutathione and increased glutathione disulfide levels in the liver, both of which reversed during recovery from Ca2+ uptake. Moreover, depletion of hepatic glutathione by pretreatment with diethylmaleate resulted in increased Ca2+ uptake during menadione infusion. The amount of protein-bound mixed disulfides showed a particularly striking relationship to Ca2+ uptake, reaching a maximal level during Ca2+ uptake and reversing toward normal value during recovery from Ca2+ accumulation. The present findings suggest that menadione-induced Ca2+ uptake is due to plasma membrane dysfunction as a result of loss of protein thiol groups critical for maintaining the plasma membrane Ca2+ extrusion mechanism. Our model offers a particularly useful opportunity to study mechanisms underlying toxic disturbances in Ca2+ homeostasis in the intact liver, since Ca2+ fluxes can be monitored under conditions in which cellular control mechanisms are not obliterated by excessive toxicity.

Chromium concentrations in the air were measured in seven different workroom environments, where exposure to water soluble hexavalent or trivalent compounds was expected. Urinary excretion of chromium was measured before and after the same arbitrarily chosen working day. End-of-shift urinary chromium and its increase above pre-exposure levels were closely related to the concentration of water soluble chromium (VI) in the air. The values corresponding to 50 micrograms m-3 in the air, which is the current threshold limit value in most countries, were 29.8 and 12.2 micrograms g-1 of creatinine, respectively. Urinary chromium in workers exposed to water insoluble chromates or to water soluble chromic (III) sulphate was definitely higher than that observed in subjects not occupationally exposed to chromium compounds, but it cannot be recommended as short-term exposure test for evaluation of the job-related hazard.

Using a sensitive ETA ASS method, urinary thallium (Tl-U) has been measured in a group of non-exposed individuals and in two groups of workers with suspected industrial exposure. In non-exposed subjects (72 healthy males aged 41 +/- 11 years) the Tl-U mean value was 0.22 mu/l (range 0.05-0.61). Significantly higher values were found in two groups of workers (30 and 21 subjects) employed in two cement factories and two cast iron foundries (mean Tl-U value: 0.38 and 0.33 mu/l, respectively; range 0.06-1.2). Thallium has been determined in coal, raw materials and, in one factory, also in environmental samples, but no detectable levels were found. The analytical problems connected to urinary thallium determination and the preliminary results of biological monitoring in non-exposed individuals and in workers are discussed.

Total and hexavalent chromium were measured in bile samples obtained from cannulated bile ducts of male rats iv administered with potassium dichromate at various doses corresponding to 0.1, 0.5, and 1 mg of chromium. The evaluation of the hexavalent form was performed by separation with a liquid anion exchanger and electrothermal atomization-atomic absorption spectrophotometric determination. Within 2 hr 1.35-2.23% of the chromium injected was recovered in bile as total chromium, the hexavalent form accounting for less than 1% of the total chromium collected, which seems almost entirely excreted as trivalent chromium. Since Cr(VI) administered iv was quickly reduced to Cr(III) in blood, the possibility exists for chromium in trivalent form to penetrate into the liver cells and to be excreted in the bile, possibly by binding to a carrier such as the low-molecular-weight substance described by Yamamoto et al. (A. Yamamoto, O. Wada, and T. Ono, Toxicol. Appl. Pharmacol. 59, 515, 1981).

Addition of silver nitrate or silver lactate to freshly isolated hepatocytes caused dose-dependent loss of cell viability, measured by trypan blue exclusion, at concentrations within 30-70 microM. Silver cytotoxicity was accompanied by a decrease in hepatic thiol concentration and an increase in lipid peroxidation. Treatment of hepatocytes with the reduced glutathione (GSH)-depleting agent diethylmaleate markedly increased their vulnerability to silver toxicity whereas protective effects were produced by the thiol-reducing agent, dithiothreitol. Both alpha-tocopherol, which protected from the onset of silver-associated lipid peroxidation, and the iron chelator agent, deferoxamine failed to prevent loss of cell viability. These data suggest that perturbation of intracellular thiol homeostasis may play a critical role in the mechanism underlying silver-induced lethal damage to isolated rat hepatocytes.

Neurone-specific enolase, a serum marker of neuroendocrine tumours has been determined in small-cell anaplastic bronchial carcinomas, in typical and atypical carcinoid. The marker presents good sensitivity in small-cell tumours and in atypical carcinoids, while blood levels are within normal limits in cases of typical carcinoid. The low serum levels of neurone-specific enolase found in typical carcinoid suggest a failure of the enzyme to express itself in the circulation owing to the poor or lack of cellular necrosis.

The concentration of total urinary chromium (Cr-U) in two different groups of healthy occupationally non-exposed subjects living in the Italian regions of Lombardia and Veneto has been determined using an ETA-AAS direct method. The age, sex, residence and smoking habits were correlated with CrU excretion. The mean CrU value found in subjects living in Lombardia (n = 310, males 170 and females 140) was 0.59 + 0.26 microgram/l (range 0.08 - 2.10); in Veneto subjects (n = 238, males 187 and females 51) the mean value was 0.52 +/- 0.31 microgram/l (range 0.05 - 1.90). A significative difference between male and female values and a decrease of CrU levels with age increasing have been evidenced in both groups. Smoking habits seem to influence metal urinary levels while, on the other hand, no influence of living sites was observed. Some analytical problems of ETA-AAS Cr determination systems are discussed and "normal" CrU values measured in this study are compared with data reported in the literature.