We are presenting a case of acute stridor in a 78-year-old patient with a history of chronic obstructive pulmonary disease (COPD). In the left lateral pulmonary graph, a shadow with levels was noticed. An expiratory and inspiratory plateau was recorded on the flow-volume curve. Bronchological examination ruled out the presence of bronchial and tracheal obstruction. Extramural tracheal compression was confirmed. Proximal endoscopy and barium meal examination were performed. As a result, the patient was diagnosed with hiatal hernia which had caused the acute stridor. The patient was referred to a surgeon.
Ulcerative colitis is a chronic, inflammatory bowel disease which can clinically be manifested either only with bowel symptomatology or with extraintestinal symptomes. A prospective study analysed 107 patients with ulcerative colitis (57 male and 50 female, mean age 41.25, range 21-70). The presence of the most common extraintestinal manifestations (EM) (myoskeletal, skin, ocular and hepatobiliary) has been analyzed. Out of the whole number of the examined, these manifestations were verified in 23 (21.49%) patients (10 male and 13 female, mean age 43.25, range 27-70). Patients with EM suffered longer from UC on the average, that is 6.06 years, while the others suffered for 4.44 years. Peripheral arthritis was the most common EM, verified in 13 (56.52%) patients. In 9 (39.14%) patients two or more EM were verified. In 77.27% patients, EM were clinically detectable after the intestinal symptomatology. No statistically significant difference was established in the duration of disease between patients with one EM and those with several EM. Patients with EM had more extensive and more active UC on average, in relation to others. No statistically significant difference was established, in extension and activity of disease, between patients with and without EM. The fact that EM can affect the clinical course of UC, therapy response and the quality of patient's life, oblige the doctors to be very cautious during the evaluation of patients with UC in order to recognize EM on time. In case of the above-mentioned illnesses without clinically manifested or undeveloped UC, large bowel screening should be performed to diagnose possible UC in the subclinical stage.
Summary. A prospective study included 30 patients with chronic renal insufficiency undergoing chronic chemodialysis, with or without digestive problems, who underwent proximal endoscopy for pretransplantation balance in the period 1998-2000. The study included patients admitted to the Institute of Nephrology and Chemodialysis of the Clinical Centre in Nis and Nephrology Clinic of the Clinical Centre of Serbia, Belgrade. The control group was composed of 21 patients with no chronic renal insufficiency treated and examined at Gastroenterology and Hepatology Clinic of the Clinical Centre in Nis who underwent proximal endoscopy. The patients were randomly selected. By proximal endoscopy performed in patients undergoing chronic dialysis, the following pathological changes were confirmed: erosions in 9 (30%), angiodysplasias in 2 (6.67%), ventricular ulcers in 1 (3.33%), duodenal ulcers in 1 (3.33%), ventricular polyps in 1 (3.33%), and a regular finding was established in 16 (53.34%) patients. External factors contribute to gastrointestinal changes: moderate quantities of alcohol consumption, smoking cigarettes, various drugs intake, and non-observance of dietetic regime. These risk factors also contribute to deciding on the performance of proximal endoscopy. The presence of the subjective problems with the digestive tract, along with the objective finding in the patients on chemodialysis are indications for proximal endoscopy aimed at prevention, and early detection of changes in the digestive tract. According to our investigation, the indications for proximal endoscopy in patients undergoing chronic hemodialysis are: patients on dialysis for 0-2 years, frequent digestive problems but not closely associated with uremic toxicity, acute gastrointestinal symptomatology (stomach aches, hematemesis, melena...etc), pretransplantation balance and patients with chronic systemic disease that receive immunosuppressive therapy for 6 months.
The fact that cell death is not ultimately a bad thing came as a surprise to many researchers. Physiological cell death has been observed in various multicellular organisms. Apoptosis or programmed cell death is the predominant form of physiological cell death by which the organism eliminates unnecessary or damaged single cells. It is a major component of normal development and disease. Apoptosis is characterized by membrane blobbing, shrinkage of the cell, nuclear fragmentation and chromatin condensation. Organelles are preserved almost intact. Cell surface molecules change to assure that apoptotic cells will be immediately recognized and engulfed by neighboring cells or phagocytes leading to little or no inflammation. A wide variety of physiological and pathological stimuli can initiate apoptosis. They act via receptor mechanisms, through biochemical agents, or cause DNA and cell membrane damage. Death receptors that initiate apoptosis include the Fas receptor and the TNF receptor systems. After an appropriate stimulus, the first stage of apoptosis or decision phase is the genetic control point of cell death. This is followed by the second stage or execution phase, which is responsible for the morphological change in apoptosis. The third stage is engulfment of the dying cell followed by degradation of the engulfed cell DNA. There are two overlapping signaling pathways leading to apoptosis, termed the intrinsic and extrinsic pathways. In the intrinsic, various stimuli, such as oxidative stress, lead to mitochondrial dysfunction and the release of pro-apoptotic factors. Ligand binding to cell surface death receptors, such as Fas, activates the extrinsic pathway. During the last decades the molecular mechanisms involved in disordered apoptosis were unraveled, suggesting that cancer, chronic disease, and fetal developmental abnormalities can occur as a result of disordered apoptosis.
6The aim of this research was to examine the relationship between inflammatory parameters and markers of cholestasis in patients with choledocholithiasis. All subjects underwent clinical, laboratory and ultrasound examination at the Department of Internal Medicine, Military Hospital Nis, Serbia. Inflammatory parameters and biochemical markers of cholestasis were measured by standard biochemical methods. Most of cholestasis markers showed no significant correlation with inflammatory parameters in blood, except for a weak significant correlation between the number of monocytes with the activity of aspartate aminotransferase (AST) (r=0.37, p<0.05). Hyperbilirubinemia was significantly correlated with the fibrinogen values (r=0.42, p<0.05), while albumin positive values were positively associated with alanine aminotransferase (ALT) activity (r=0.5, p<0.05), and negatively with the alkaline phosphatase (AP) (r=-0.43, p<0.05). In patients with choledocholithiasis, there was a positive correlation between the number of monocytes and the activities of AST, hyperbilirubinemia, and fibrinogen, albumin and ALT, while a negative correlation between albumin and AP was present. Acta Medica Medianae 2014;53(2):28-32.
Summary. Variceal bleeding is the most life-threating complication in liver cirrhosis. The aim of this study was to ascertain the risk factors of bleeding from esophageal varices.52 patients with liver cirrhosis and portal hypertension were included in prospective study. We analyzed the severity of liver dysfunction according to Child's classification, coagulation parameters, and endoscopic parameters: size, color, location of varices, and the presence of red signs. Varices were classified as small, medium and large.Esophageal varices were found in 76.9% of the patients with liver cirrhosis and portal hypertension. Small varices were present in 10%, medium in 25% and large in 65% patients. 55% of them had variceal bleeding. Variceal bleeding was present in 50% patients with medium and in 65.38% patients with large varices. There was no bleeding in patients with small varices.Endoscopy revealed red signs before bleeding in 85% patients with large varices. There was a higher incidence of variceal bleeding in Child's group B. There were no significant differences (p>0.05) of the coagulation parameters in patients with and without variceal bleeding. Rebleeding was present in 86.36% patients. Most of them (52.63%) rebled between 7 weeks and 12 months after the first episode of variceal bleeding. In the patients with the most severe hepatocellular dysfunction (Child's group C) period between the first bleeding and rebleeding was the shortest (mean 20.8 days). Our study revealed association between the first bleeding and large varices and the red signs. Coagulation disorders and hepatic dysfunction were not related to the initial episode of variceal bleeding. The risk of early rebleeding was higher in patients with severe hepatic dysfunction (Child's class C).