Edmund Sabo

Laparoscopic cholecystectomy for acute cholecystitis: can the need for conversion and the probability of complications be predicted? A prospective study.

AbstractBackground: Laparoscopic cholecystectomy (LC) in acute cholecystitis is associated with a relatively high rate of conversion to an open procedure as well as a high rate of complications. The aim of this study was to analyze prospectively whether the need to convert and the probability of complications is predictable. Methods: A total of 215 patients undergoing LC for acute cholecystitis were studied prospectively by analyzing the data accumulated in the process of investigation and treatment. Factors associated with conversion and complications were assessed to determine their predictive power. Results: Conversion was indicated in 44 patients (20.5%), and complications occurred in 36 patients (17%). Male gender and age >60 years were associated with conversion, but these factors had no sensitivity and no positive predictive value. The same factors, together with a disease duration of >96 h, a nonpalpable gallbladder, a white blood count (WBC) of >18,000/cc3, and advanced cholecystitis, predicted conversion with a sensitivity of 74%, a specificity of 86%, a positive predictive value of ∼40%, and a negative predictive value of 96%. However, these data became available only when LC was underway. Male gender and a temperature of >38°C were associated with complications, but these factors had no sensitivity and no positive predictive value. Progression along the stages of admission and therapy did not add predictive factors or improve the predictive characteristics. Male gender, abdominal scar, bilirubin >1 mg%, advanced cholecystitis, and conversion to open cholecystectomy were associated with infectious complications. Their sensitivity and positive predictive value remained 0 despite progression along the stages of admission and therapy. Conclusion: Although certain preoperative factors are associated with the need to convert a LC for acute cholecystitis, they have limited predictive power. Factors with higher predictive power are obtained only during LC. The need to convert can only be established during an attempt at LC. Preoperative and operative factors associated with total and infectious complications have no predictive power.

Anticardiolipin antibodies and acute myocardial infarction in non-systemic lupus erythmatosus patients: A controlled prospective study

PURPOSE To examine the prevalence of anticardiolipin antibodies (ACLA) in relatively young patients with acute myocardial infarction (MI) and their role in subsequent coronary and thromboembolic events in the post-MI period. PATIENTS AND METHODS In 124 relatively young survivors (aged 65 or younger) of acute MI, ACLA were measured in a controlled prospective study on admission and 3 months later. Myocardial reinfarction and thromboembolic events during a mean follow-up period of 19 +/- 3 months were diagnosed by standard tests. RESULTS Seventeen (14%) of the 124 patients were ACLA positive (either IgM or IgG) upon admission compared with 2 out of 76 (3%) of the control group matched for age and coronary risk factors (P < 0.01). The levels of ACLA remained unchanged in all but 1 patient 3 months later. During the follow-up period the rate of thromboembolic events and myocardial reinfarction was significantly higher in the ACLA-positive patients as compared with the ACLA-negative group: 41% versus 4% (P < 0.0001) and 35% versus 10% (P < 0.05), respectively. Using logistic regression, high titer of ACLA was found to be the only independent risk factor for subsequent thromboembolic events or myocardial reinfarction after acute MI. CONCLUSIONS High prevalence of ACLA was found in relatively young survivors of acute MI. The presence of ACLA is a marker for increased risk of subsequent myocardial reinfarction and thromboembolic events after acute MI.

Cancer antigen 125: a sensitive marker of ascites in patients with liver cirrhosis.

ObjectiveCancer antigen 125 (CA 125) is a high molecular mass glycoprotein, usually used for monitoring the course of epithelial ovarian cancer. Recently it has been shown that liver cirrhosis is associated with increased levels of CA 125, particularly in the presence of ascites. The aim of this study was to evaluate CA 125 as a marker for the detection of ascites in patients with chronic liver disease.MethodsA total of 170 patients were studied. All had ultrasound scanning for detection of ascites. Group I consisted of 123 patients with chronic liver disease without ascites; whereas group II consisted of 47 patients with chronic liver disease with ascites. CA 125 levels were measured in all patients and also simultaneously in the ascitic fluid of 31 patients from group II.ResultsOf 47 patients, 46 (97.8%) of group II had elevated serum levels of CA 125 (mean 321 ± 283 U/ml) as compared with only nine of 123 (7.3%) patients of group I [mean 13 ± 15 U/ml]), p < 0.001. The mean CA 125 concentration in the ascitic fluid of 31 cirrhotic patients (group II) was 624 ± 397 U/ml and was always higher than corresponding serum levels (p < 0.01). Serum CA 125 levels correlated with the amount of ascitic fluid (r = 0.78). A profound decrease in serum CA 125 concentration was noted 2–3 and 10 days after large volume paracentesis. CA 125 was more sensitive and preceded ultrasonography in detection of ascites in few cirrhotic patients.ConclusionsCA 125 is a highly sensitive marker to detect ascites in patients with liver cirrhosis. This marker may be useful to detect small to moderate amounts of ascitic fluid in cirrhotic patients when physical examination is difficult or equivocal for ascites.

Peripheral B-cell CD5 expansion and CD81 overexpression and their association with disease severity and autoimmune markers in chronic hepatitis C virus infection

Hepatitis C virus (HCV) infection is associated with immune‐mediated abnormalities and B‐cell lymphoproliferation evolving to an overt lymphoma. Recently, CD81 was identified as an HCV receptor on B‐lymphocytes, providing a mechanism by which B cells are infected and activated by the virus. In addition, expansion of CD5+ B lymphocytes was described to be associated with various non‐HCV related autoimmune disorders. Therefore, we studied the possible role of peripheral B cells CD81 and CD5 over‐expression in the development of HCV‐related autoimmunity and their association with disease severity in chronic HCV infection. Peripheral B cells CD5 expression and mean fluorescence intensity (MFI) of CD81 were determined in 30 HCV‐infected patients, 30 healthy controls and 15 patients with hepatitis B virus infection using fluorescence‐activated cell scan (FACS). We have also investigated the association between peripheral CD5 and CD81 B‐cell over‐expression and markers of autoimmunity and disease severity in patients chronically infected by HCV. CD5+ B‐cells were increased in chronic HCV infection (23·2 ± 7·2%) compared with those of healthy controls (15 ± 5·5%) (P < 0·0001) and chronic HBV infection (19 ± 3·7%) (P = 0·08). CD81 MFI was significantly higher in HCV‐infected compared to HBV‐infected patients and healthy controls. Both increased CD81 MFI and CD5+ B‐cell expansion were associated with the production of rheumatoid factor and mixed cryoglobulins and positively correlated with HCV viral load and histological activity index. The overexpression of CD81 and the expansion of CD5+ peripheral B‐cells in HCV‐infected patients may possibly play a role in the development of HCV‐associated autoimmunity and lymphoproliferation.

Immune aberrations in B and T lymphocytes derived from chronic urticaria patients.

To investigate the pathophysiology of chronic urticaria (CU) in light of the abundant evidences that it is an autoimmune disease and to define some cellular markers in B/T lymphocytes that could be of pathogenic significance, we investigated 14 patients suffering from CU, compared to 7 contact dermatitis patients and 10 normal control individuals. We tested the expression of CD5, B7.1 (CD80), CD23, and CD25 on B cells and of CD40L and CD25 on T cells from all studied individuals. We also tested B cell proliferation upon their activation followed by dexa-methazone induced inhibition of proliferation. The expression of bcl-2 protein in activated lymphocytes from normal individuals was compared to that of contact dermatitis and CU patients. CD40L expression was found significantly higher on in vitro activated CD3 [with phorbol myristate acetate (PMA) and ionomycine Ca2+ at 12 hr of culture] from CU patients compared to that of contact dermatitis and normal individuals. Whereas the proliferation of activated B cells from CU patients was higher, dexamethazone-induced inhibition of B cell proliferation was found statistically similar in both groups yet lower in B cells from most severe CU patients. We demonstrate a higher bcl-2 expression in activated B and T lymphocytes of severe CU patients compared to that of moderate CU and both contact dermatitis and normal individuals. The increased expression of CD40L on activated T cells might play a role in the polyclonal increased B cell proliferation of CU patients. This increased proliferation accompanies the finding that activated B and T lymphocytes from these patients demonstrate increased bcl-2 expression. The resistance of some B cells to dexamethazone-induced inhibition of proliferation encourages us to investigate the possibility that B cells from some CU patients might develop rescue mechanisms from activated cell death. These findings provide further evidence that CU is indeed an autoimmune disease, although its precise nature has yet to be fully elucidated.

The effects of enoxaparin on the reparative processes in experimental osteonecrosis of the femoral head of the rat

The blood supply of one femoral head of 6‐month‐old rats was severed by incising the periosteum of the neck and cutting the ligamentum teres. The rats were killed on the 30th postoperative day and the femoral bones were obtained for semiquantification of the reparative processes in the necrotic heads. Fourteen rats were treated with enoxaparin and 14 untreated animals served as controls. Statistically, the amounts of necrotic bone in the epiphysis were less, the extent of remodeling of the femoral heads was milder, and the articular cartilage degeneration was slighter in the enoxaparin‐treated than untreated rats. There was no significant difference in the quantities of newly formed bone in femoral heads of treated and untreated rats. These findings are in agreement with the known effects of unfractionated and low‐molecular‐weight heparins which enhance osteoclastic bone resorption and angiogenesis and decrease osteoblastic bone formation. The former activities, operative in minimizing the structural distortion of the femoral head, oppose the crucial event in the pathogenesis of post‐osteonecrotic osteoarthritis.

Autosomal‐recessive omodysplasia: Prenatal diagnosis and histomorphometric assessment of the physeal plates of the long bones

Second-semester ultrasonography of a female fetus documented short femora and humeri and dislocation of the radii. Based on the clinical and postmortem radiological findings, autosomal-recessive omodysplasia was diagnosed. The physeal plates of the long tubular bones were assessed by computer-assisted image analysis. The dimensions and orientation of the chondrocytic lacunae in the physeal plates of the omodysplastic fetus were compared with those in the physeal plates of fetuses without gross limb abnormalities (oligohydramnios, n = 2; hydrocephalus, n = 2; Down syndrome, n = 1). The pathological characteristics of the omodysplastic physeal plates were an expanded zone of proliferating cartilage and an increased number of closely packed, small chondrocytes. We propose that a genetic, functional deficiency of the physeal cells, underlying the short-limbed dwarfism of autosomal-recessive omodysplasia, is partially compensated, albeit ineffectively, by an increased number of small chondrocytes in the proliferating zone of the physeal plate.

Colonic ulcers in a patient with hepatitis C virus-associated polyarteritis nodosa

An elderly woman presented with abdominal discomfort, pulmonary infiltrates, acute renal failure, purpura, and massive hematochezia. Numerous colonic ulcers with underlying fibrinoid necrotizing arteritis were found in the colectomy specimen. Anti-hepatitis C virus (HCV) antibodies and HCV RNA were present in the serum. The diagnosis of HCV-associated polyarteritis nodosa was clear. This clinical presentation differs from the more commonly occurring vasculitis complicating HCV infection, which is of the leukocytoclastic type, and is associated with overt liver disease and cryoglobulinemia. In our patient, results of liver tests were normal, there was no cryoglobulinemia, and the vasculitis was of the fibrinoid necrotizing arteritis type. HCV-associated polyarteritis nodosa should be considered in the differential diagnosis of necrotizing fibrinoid arteritis even in a patient with normal liver function test results and in the absence of cryoglobulinemia.

Case Report: Extensive Pulmonary and Aortic Thrombosis and Ectasia

Progressive shortness of breath developed in an elderly woman with a 25-year history of recurrent superficial phlebitis and hemoptysis. Extensive mural thrombosis and ectasia of the large and medium-sized pulmonary arteries and aorta were revealed on echocardiography and computerized tomography. The patient died 2 months later. On autopsy, the gross morphologic findings were similar with those observed by imaging. Histologically, there was mild inflammation in the intima and media of the aorta and the large pulmonary arteries, consistent with nonspecific arteritis. The extensive thrombosis and ectasia of the pulmonary arteries and aorta differ from previously published cases and cannot be assigned to a known nosologic entity. Two alternative explanations are proposed. First, an endothelial disorder was responsible for a diffuse vasculopathy that involved veins, pulmonary arteries, and aorta. Second, a vasculopathy of the Hugh-Stovin type, characterized by phlebitis and pulmonary thromboembolism, caused pulmonary hypertension and low cardiac output. The low flow state favorized aortic thrombosis and, at the site of interaction between the clot and the arterial wall, arteritis developed as an epiphenomenon, which induced arterial dilatation. Combined idiopathic pulmonary artery and aortic thrombosis and ectasia is rare and calls for corroboration of sporadic observations such as the current one.

Morphologic and morphometric study of patellar resurfacing with woven carbon filamentous pads

Abstract Analysis of retrieved woven carbon filamentous pads, used for resurfacing of the patellar joint surface, disclosed a 4-zonal organizational pattern. Zone 1, facing the articular cavity, was devoid of carbon filaments and consisted of fibrous tissue. Foreign body granulation tissue and fibrous tissue occupied about one-third and ∼50%–60% of the interfilamentous space in zones 2 and 3, respectively. Carbon filaments formed 2%–9% of zone 2 and 14%–16% of zone 3. An interfacial membrane-like zone 4 separated the carbon filamentous pads from a trabecular bony shell. The bone volume within the latter was ∼25%. Given that the purpose of articular resurfacing with implants is repopulation of the defect by chondrocytes producing a cartilaginous matrix, the woven carbon filamentous pads did not fulfill this expectation. In an environment of an ongoing foreign body-induced granulomatous reaction, the stem cells permeating the interstices of the woven carbon filamentous pad are apparently incapable of maturing into highly differentiated cells (chondrocytes) synthesizing a highly complex (cartilaginous) matrix.