[Post-transplant lymphoproliferative disease in liver transplant recipients--Merkur University Hospital single center experience]. / Post-transplantacijska limfoproliferativna bolest u bolesnika s transplantacijom jetre - iskustvo KB Merkur.

Post-transplant lymphoproliferative disorder (PTLD) is an increasingly recognized condition as the number of solid organ and bone marrow transplant recipients increases. It can be a life threatening fulminant disorder and affects approximately 8% of solid organ transplant recipients. Epstein-Barr virus (EBV) is closely involved in the pathogenesis of PTLD and the majority of PTLD cases arise in response to primary infection with EBV or to re-activation of previously acquired EBV. The principal risk factors underlying the development of PTLD are the degree of overall immunosuppression and EBV serostatus of the recipient. The most commonly used pathologic classification of PTLD is the World Health Organization classification, which divides PTLD into three categories: early lesions, polymorphic PTLD, and monomorphic PTLD. Early lesions are characterized by reactive plasmacytic hyperplasia. Polymorphic PTLD may be either polyclonal or monoclonal and is characterized by destruction of the underlying lymphoid architecture, necrosis, and nuclear atypia. In monomorphic PTLD, the majority of cases (>80%) arise from B cells, similar to non-Hodgkin's lymphoma in immunocompetent hosts. The most common subtype is diffuse large B-cell lymphoma, but Burkitt's/Burkitt's-like lymphoma and plasma cell myeloma are also seen. Rarely T-cell variants occur, which include peripheral T-cell lymphomas and, rarely, other uncommon types, including gamma/delta T-cell lymphoma and T-natural killer (NK) cell varieties. Hodgkin's disease-like lymphoma is very unusual. An accurate diagnosis of PTLD requires a high index of suspicion, since the disorder may present subtly and/or extranodally. Radiologic evidence of a mass or the presence of elevated serum markers (such as increased LDH levels) are suggestive of PTLD, with positive finding on ultrasonography, computed tomography, magnetic resonance and/or positron emission tomography scanning (possibly indicating metabolically active areas) also favoring the diagnosis. The management of PTLD poses a major therapeutic challenge and although there is reasonable agreement about the overall principles of treatment, there is still considerable controversy about the optimal treatment of individual patients. EBV-related PTLDs are a significant cause of mortality in patients undergoing orthotopic liver transplantation with the observed mortality rate of up to 50%. This paper presents the experience acquired at Merkur University Hospital in the diagnosis and treatment of patients with liver transplantation and PTLD.

[Acute plastic bronchitis--case report]. / Akutni odljevni bronhitis--prikaz bolesnika.

Plastic bronchitis is a rare disorder characterized by formation and sometimes dramatic expectoration of bronchial casts. It may occur at any age, but most published cases refer to pediatric population. We report a case of an 81-year-old man hospitalized at intensive care unit, who presented with the appearance of plastic bronchitis type I. He had profuse expectoration of several pieces, a few cm long and up to 1 cm wide, of wormlike reddish-brownish "tissue". Histologically, it was a slimy purulent secretion with abundant fibrin and blood and with cytopathic effect of herpes virus. The pathogenesis of plastic bronchitis is not clear.

[Hepatocellular carcinoma initially diagnosed by fine needle aspiration cytology of the pelvic bone metastasis]. / Hepatocelularni karcinom primarno dijagnosticiran citoloskom punkcijom metastatskog procesa u zdjelicnoj kosti.

Hepatocellular carcinoma mostly develops in patients with liver cirrhosis due to chronic hepatitis C virus (HCV) infection. A case is presented of a patient with hepatorenal syndrome as a sequel of liver cirrhosis due to HCV infection. Primary tumor of the liver was not diagnosed by routine procedures, but by fine needle aspiration cytology of the extensive osteolytic lesion of the pelvic bone, performed as part of the pre-transplantation workup. Transplantation procedure was abandoned because of inappropriate donor liver (hepatic artery thrombosis), and palliative pain-relieving irradiation was recommended. However, hepatic coma developed very rapidly and the patient died within a month of the diagnosis of metastatic hepatocellular carcinoma. Although hepatocellular carcinoma metastases are not rare, massive bone infiltration from a primary tumor undetectable by routine methods is not frequently encountered.

[Erythroblasts in the peripheral blood of adult patient as an adverse prognostic sign--a case report]. / Eritroblasti u perifernoj krvi odraslog bolesnika kao nepovoljan prognosticki predznak--prikaz bolesnika.

Red blood cells (RBC) normally lose their nuclei before appearing in peripheral blood. After having undergone differentiation in bone marrow, blood cells must cross the blood-marrow barrier to enter the bloodstream. Erythroblasts, or nucleated red blood cells (NRBC), do not distort easily, so they cannot escape this barrier. Therefore, with the exception of the neonatal period, the presence of NRBCs in peripheral blood is always a pathologic finding. NRBCs may be found in the course of severe diseases and are associated with poor prognosis and higher mortality. The underlying pathophysiology of NRBCs in peripheral blood is not fully understood. It is hypothesized that their appearance could be provoked by either increased erythropoiesis or bone marrow micro-architectural damage mostly caused by inflammation and/or decreased tissue oxygenation. In addition, it is known that the mortality is higher in NRBC-positive patients as compared with NRBC-negative patients. Hereby we present a patient admitted to the hospital with the symptoms of cardiac failure and decompensated liver cirrhosis. The patient was already known to have liver cirrhosis of ethylic etiology, cardiac decompensation caused by hypertensive heart disease with permanent atrial fibrillation, chronic obstructive pulmonary disease, diabetes mellitus type 2, and cholelithiasis. During hospital stay, the patient developed acute pancreatitis and, soon after that, a stroke with left hemiparesis followed by cardiopulmonary arrest. Then he was transferred to the intensive care unit. Despite appropriate therapy, intensive care treatment and cardiopulmonary support, the patient's general state worsened, he developed multiple organ failure and died on day 10 of intensive care unit stay. Three days earlier, NRBCs were detected in peripheral blood and their concentration increased during the next two days before death. NRBCs are known to appear 1-3 weeks before death, but their appearance does not seem to be related to one particular cause of death. Still, detection of NRBCs is an independent risk of poor outcome, where the mortality increases with the increasing NRBC concentration. Detection of NRBCs in blood is a relatively early phenomenon prior to death, so screening for NRBCs may aid in the early identification of patients at high risk, and in making duly decision for NRBC-positive patients to obtain ongoing intensive care treatment.

[Treatment of acute pancreatitis]. / Lijecenje akutnog pankreatitisa.

BACKGROUND: Acute pancreatitis is an autodigestive disease in which the pancreatic tissue is damaged by the digestive enzimes produces by the acinar cells and is associated with severe upper abdominal pain. The severity of acute pancreatitis ranges from edema to necrosis of the gland. The edematous form of the disease occurs in about 80-85% of patients and is self-limited, with recovery in few days. In the 15-20% of patients with the most severe form of pancreatitis, hospitalization is prolonged and commonly associated with infection and other complications including multiple organ failure. The main causes of acute pancreatitis in adults are gallstones, other gallbladder (biliary) diseases and alcohol abuse. Treatment of acute pancreatitis-depends on the severity oft he condition. Generaly, the patients need, hospitalisation with administration of intravenous fluid to help restore blood volume, pain control, supplemental oxygen as required and correction of electrolite and metabolic abnormalities. Antibiotic prophylaxis has not been shown as an effective preventive treatment. Early enteral feeding is based on a high level of evidence, resulting in a reduction of local and sistemic infection. Begin oral feeding once abdominal pain has resolved and the patients regains appetite. The diet should be low in fat and protein. Patients suffering from infected necrosis causing clinical sepsis, pancreatic abscess or surgical acute abdomen are candidates for early intervention. CONCLUSION: During recent years the management of acute pancreatitis has changed. This has been due particulary in response to the general availability of computed tomography, improved intensive care facilities, knowledge about the central role of pancreatic infection and refinements in surgical and other interventional techniques.

[Clinical aspects and therapy of toxic hepatitis]. / Klinicka slika i terapija toksicnih hepatitisa.

The different types of hepatotoxicity can be induced by drugs. Approximately 2%-5% of patients require hospitalization for jaundice. Drug-induced hepatic lesions are responsible for 10% of hepatitis cases in adults. Most hepatotoxic drug reactions are idiosyncratic and classified either as immunologic (hipersensitivity) or metabolic. In contrast to intrinsic hepatotoxins, these reactions are not dose-dependent nor predictable. The enzyme system responsible for drug biotransformation in liver is cytochrome P450, a large multigene family of enzymes with 300 members. Clinical presentation in patients who develop drug hepatotoxicity can be asymptomatic with mild biochemical abnormalities, resembling acute hepatitis or chronic autoimmune hepatitis, veno-occlusive disease and cirrhosis. Withdrawal of the drug usually leads to reversal of the lesion. A spectrum of drug induced hepatotoxicity, diagnosis and treatment is reviewed.

[The urea breath test]. / Izdisajni test ureje.

Helicobacter pylori is infective cause of peptic ulcer and a risk factor for gastric carcinoma. The discovery of the bacterial ed to importance of finding a new reliable and inexpensive diagnostic method for detection of infection before and after eradication therapy. Urea breath test is isotope based test. It has become the most specific and sensitive method in detection of Helicobacter pylori infection, therefore many other isotope based tests become popular in diagnostic of gastrointestinal diseases. Because of its simplicity and no need in using endoscopy in the procedure it is very popular in primary diagnosis and in controlling eradication. It is successfully used in diagnostics of Helicobacter pylori and bacteria eradication success testing, where it is one of most reliable diagnostic methods.

[The rapid urease test]. / Brzi ureazni test.

Today there are many methods in diagnostics of Helicobacter pylori infection. They are divided in two major groups based on using of endoscopy (invasive and non-invasive methods). Helicobacter pylori bacteria are specific because of having very big amounts of urease enzyme that divides urea on NH3 and CO2 which enables environment suitable for survival. Rapid ureas test is based on detecting of the enzyme activity. Because of its simplicity and high sensitivity and specificity it belongs to methods that are used in every day practice in endoscopic laboratories.

[Gastric ulcer and Helicobacter pylori infection]. / Zelucani ulkus i infekcija Helicobacterom pylori.

Helicobacter pylori infection and the use of non-steroidal anti-inflammatory drugs (NSAID) are considered to be the two major risk factors implicated in the development of gastric ulcer. Helicobacter pylori infection related chronic gastritis is known to be the underlying condition which may lead to gastric ulcer. Development of gastric ulcer as the consequence of underlying chronic gastritis is caused by many factors. Treating Helicobacter pylori infection entails the healing of gastric ulcer, it concomitantly prevents recurrences and complications of gastric ulcer, primarily bleeding, and changes the natural course of gastric ulcer disease. Continuation of antisecretory maintenance treatment beyond ulcus healing and eradication of Helicobacter pylori infection is only indicated in risk groups. Patients with gastric ulcer caused by NSAID use are managed with antisecretory therapy.

[Gastroesophageal reflux disease and Helicobacter pylori infection]. / Gastroezofagealna refluksna bolest i infekcija Helicobacterom pylori.

Gastroesophageal reflux disease (GERD) is one of the common diseases of the upper gastrointestinal system. It is present in the whole world population, especially frequent in the developed countries. It evolves from pathological reflux which exposes the esophagus to the gastric contents which must overcome esophageal defense system. Many factors have been found to be involved in the pathogenesis of GERD; the most important one is the relaxation of the lower esophageal sphincter. Intensity of the disease is proportional to the amount of gastric contents refluxing from the stomach and the duration of esophageal exposure to this contents. GERD is currently in the spotlight because of its special significance in the development of very specific disease in the lower part of the esophagus--Barrett's esophagus, as well as esophageal adenocarcinoma which has lately been increasing in prevalence. Today, unrecognized and inadequately cured GERD is known to be a high risk factor for adenocarcinoma of the esophagus. In recent years the relation between GERD and Helicobacter pylori infection has been the topic of investigation by many prominent researchers. Therapy of GERD is based on inhibition of acid secretion. There are many different therapeutic agents available, however, proton pump inhibitors (PPI) are considered to be the most effective in the treatment of this disease.

[Helicobacter pylori and malignant diseases of the stomach]. / Helicobacter pylori i maligne bolesti zeluca.

The association between Helicobacter pylori infection and gastric malignancies, cancer and MALT lymphoma, has been suggested through several lines of evidence during the last decade. Although unresolved issues still cast doubts on the real weight of these association, in the sequence of events that leads to gastric cancer or lymphoma, Helicobacter pylori appears to play a prominent role in the very initial steps as causative agent of chronic gastritis. The subsequent events in the sequence--atrophy, intestinal metaplasia, dysplasia and cancer are multifactorial involving environmental agents, host response and characteristics of the bacterial strain itself. Recognition of the causal role of Helicobacter pylori infection in the cancer induction theoretically presents tools for its prevention. The ongoing studies will show in the future whether eradication or prevention of infection are followed by a reduction in risk of cancer. Lymphomas arising from gastric mucosa-associated lymphoid tissue (MALT) may be a clonal evolution starting from the infection. In low-grade gastric MALT lymphoma cure of the infection induces complete remission in the majority of patients. Longer follow-up investigations are necessary to determine if remissions indicate a cure of the disease.