Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A new non-linear mathematical model was constructed in order to perform in vivo quantification of the RES phagocytic function. This method is based on the same technical facilities as used for the routine liver-spleen scintigraphy with radiocolloids [1, 2]. But kinetic modeling of dynamic Tc-99m-sulfur colloid data produced estimations of the functional RE-parameters: the clearance rate of the colloidal particles, the rate of phagocytosis, and the RES functional volume, which can not be obtained by classical approaches. This non-linear model was designed on the basis of the principal characteristics of particulate material interaction with macrophages (attachment, phagocytosis, digestion) [3, 4, 5]. The theoretically examined behavior of this in vivo mathematical model corresponds with the experimental behavior of the RES. The mathematical expression of the dynamics is the system of non-linear differential equations with constant coefficients that have no analytical solution. Fitting of the normalized heart blood time-activity curve was obtained to identify the unknown model parameters via non-linear regression. For this purpose general interactive PASCAL procedure IDPAR for a PDP-11/34 computer was used (an IBM PC version is also available). Two to three iterations were needed to estimate the set of unknown parameters for any patient study (1-1.5 min). A very good fitting was obtained between experimental and model curves in every case of different pathologies (error of the approximation is about 2-3%). Studies were performed using an in vivo bolus injection of 3.6 mg/80 kg commercially available colloid KOREN labeled with 3m-Ci 99m-Tc (analog of TCK-1). Our method was used to determine the RES functional parameters for patient groups with different levels of the RES dysfunction. Obtained results illustrate the possibilities of our technique to quantitatively estimate not only great pathology (portal cirrhosis), but also small changes of the RE-function (case of hyperlipidemia and ulcer gaster). In all patient groups marked changes of Tc-99m-sulfur colloid turnover were observed. In general, tracer clearance from the circulation was decreased, and the rate of phagocytosis and the RES volume were diminished compared with controls. The effect of a reduction of phagocytosis increases when the RES dysfunction becomes stronger. It can be shown that a non-parametric Wilcoxon-Mann-Whitney test gives a significant difference (P95%) for these patient groups. Further, we represent the possibility of using the model for monitoring changes of the RES-function parameters during and after therapy. The quantitative test of the RES function can significantly enhance the diagnosis and management of different diseases. Serial colloidal studies may document changes in the RES-function for the tumors, cirrhosis, hyperlipidemia, reticulosis, hepatitis, thrombosis, infection, AIDS, burn injury, shock and trauma patients. The technique may be useful for the different RES investigations with laboratory animals. Created computer software can be used as a tool for kinetic models, simulation, and unknown parameters identification.
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PMID:A non-linear mathematical model for the in vivo evaluation of the RES phagocytic function. 859 76

Eighty-six patients were followed for 6.5 years to study the epidemiological, virological, and histological course of chronic delta hepatitis and the relationship of this disease with HIV and HCV infection. Patients were classified into four groups according to simultaneous HCV and/or HIV infection: group 1, HDV infection (20 cases); group 2, HDV and HCV infection (11 cases); group 3, HDV and HIV infection (12 cases), and group 4, HDV, HCV, and HIV infection (43 cases). All but 14 patients were asymptomatic at presentation. Liver histology showed chronic active hepatitis in 53 cases and cirrhosis in 19 cases. During followup, 52 patients remained asymptomatic, 34 developed hepatic dysfunction, 28 died, and 1 received a liver transplant. Among the 28 patients who died, 4 had HDV infection; 3 HDV and HCV infection; 3 HDV and HIV infection; and 18 HDV, HCV, and HIV infection. Death was due to liver failure in 16 (57%), AIDS in 10 (36%), and was unrelated to liver disease in 2 (8%) cases. There results demonstrate that chronic delta hepatitis is a severe disease, especially among drug users with HIV and HCV infection. The high morbidity and mortality of chronic delta hepatitis justifies the use of antiviral therapy to modify the natural course of the disease.
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PMID:Chronic delta hepatitis: is the prognosis worse when associated with hepatitis C virus and human immunodeficiency virus infections? 873 62

Gram negative infections, particularly by E. coli, are usually observed in cirrhotic patients while infections by Cryptococcus neoformans are commonly found in immunosuppressed patients. The case of a cirrhotic patient with hepatitis C virus infection who developed pleural infection by C. neoformans is presented. No disease other than cirrhosis was observed in the patient. The treatment with oral fluconazole was initiated with good clinical response and infection cure. The efficacy of fluconazole in infections by this microorganism has been reported in other cases, mainly in patients with acquired immunodeficiency syndrome. The fact that the patient may be a liver transplant candidate, given the hepatic cirrhosis, leads to speculation as to the need for chronic treatment with fluconazole to avoid reactivation of C. neoformans on initiation of pharmacologic immunosuppression.
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PMID:[Pleural empyema caused by Cryptococcus neoformans in a patient with liver cirrhosis]. 907 99

We report an Hepatitis B Virus reactivation, in a patient with an end-stage Human Immunodeficiency Virus infection who developed a rapidly progressive liver failure in four months. The main histological features include ballooning of hepatocytes and ground glass transformation, without significant inflammation. Immunohistochemical staining showed a high expression of viral antigens. This case can be related to "Fibrosing Cholestatic Hepatitis", first described after liver transplantation for cirrhosis B. The mechanism of hepatocellular damage is likely to be a direct cytotoxicity of hepatitis B virus.
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PMID:[Fibrosing cholestatic hepatitis by B virus reactivation in AIDS]. 876 76

The autopsy findings of 80 human immunodeficiency virus (HIV)-infected adults, who died between 1982-1995, are presented with special emphasis on the risk factor of hemophilia. The study included 23 blood product recipients (hemophiliacs n = 21; non-hemophiliacs n = 2), 34 homosexuals, four intravenous drug abusers, and 19 patients with no known risk factor. Nearly all individuals (93%) showed the late stage of acquired immunodeficiency syndrome (AIDS). Blood product recipients had a significantly lower overall frequency of opportunistic infections (p < 0.05). Homosexuality was associated with the highest overall frequency of opportunistic infections and HIV-associated malignancies, such as Kaposi's sarcoma and malignant non-Hodgkin's lymphoma. Exclusive visceral involvement of Kaposi's sarcoma was frequent, and no decrease of Kaposi's sarcoma was observed during the study period. Pneumocystis infections, atypical mycobacteriosis, and non-Hodgkin's lymphoma showed a significant increase during the last five years (1991-1995) of the observation interval. Opportunistic infections and malignancies were the cause of death in approximately one-half of the patients. In blood product recipients, hepatic failure due to posthepatitic cirrhosis and hemorrhage due to hepatic failure with subsequent coagulopathy and in non-blood product recipients, bacterial bronchopneumonia, and diffuse alveolar damage were additional major causes of death. The data suggest a lower risk for HIV-infected blood product recipients, particularly hemophiliacs, to acquire opportunistic infections and malignant neoplasms.
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PMID:Autopsy findings in patients with human immunodeficiency virus infection with emphasis on the risk factor of hemophilia. 878 Sep 28

We report a case of tuberculous peritonitis in a patient with concomitant HIV infection and liver cirrhosis. A 50-year-old man with viral B and delta liver cirrhosis and AIDS was diagnosed with spontaneous Escherichia coli peritonitis and successfully treated with beta-lactamins. Three months later, ascites reappeared and Mycobacterium tuberculosis was identified in peritoneal fluid cultures. The triple antituberculosis regimen was adjusted to his level of liver failure but the patient died of hepatic encephalopathy. Concomitant HIV infection and liver cirrhosis favour tuberculous peritonitis but they also make its diagnosis extremely difficult. Considering the poor prognosis of this infection when untreated, tuberculous peritonitis should be systematically suspected in such patients.
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PMID:Unusual presentation of a tuberculous peritonitis in a patient with concomitant AIDS and liver cirrhosis. 893 May 71

We identified 54 patients with AIDS and ascites seen over a 4.5-year period at a university hospital. This retrospective study is the largest reported series of patients with AIDS and ascites. Patients with AIDS who are evaluated for ascites should be stratified by the CD4 + cell count and the presence or absence of portal hypertension based upon the serum-ascites albumin gradient and clinical presentation. Awareness of possible surgery-related causes of ascites is crucial, as these patients may not manifest the usual signs and symptoms of peritonitis or abdominal catastrophes seen in immunocompetent hosts. Patients with evidence of portal hypertension due to hepatic cirrhosis and an elevated ascitic neutrophil count should be suspected to be infected with common bacterial pathogens associated with peritonitis unless the CD4 + cell count is below 50 cells/mm3. When the CD4 + cell count declines below this threshold, infections due to Mycobacterium avium complex, cytomegalovirus, and other opportunistic infections should be considered.
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PMID:Ascites and the acquired immunodeficiency syndrome. Report of 54 cases. 896 82

The renal pathologic features of 120 consecutively autopsied patients affected by acquired immunodeficiency syndrome was investigated by light microscopic analysis. Variously associated renal changes were found in 82 patients (68.3%). Glomerular changes were present in 25. The following diagnoses were made: mesangial glomerulonephritis (16 patients), defined by the presence of deposits in the mesangium and/or mesangial cell proliferation; membranous glomerulonephritis (4 patients), cirrhotic glomerulosclerosis (2 patients); and lupuslike glomerulonephritis (3 patients). Glomerular diseases seemed to be significantly associated with chronic hepatitis or liver cirrhosis. Interstitial inflammation was present in 19 cases: chronic pyelonephritis (2 patients), focal nephritis (5 patients), multiple cortical abscesses (7 patients), granulomatous nephritis (5 patients). Cryptococci were found in one and undetermined microorganisms in two cases of multiple cortical abscesses. Atypical mycobacteria were found in two cases of granulomatous nephritis. Mycotic infections were identified in another 6 patients, in whom they did not elicit any inflammatory response. It is worth stressing that, although various generalized infections are common in patients with acquired immunodeficiency syndrome, only cryptococci and atypical mycobacteria also frequently involve the kidney. Focal tubular necrosis was observed in 15 patients. Benign nephrosclerosis was the most common vascular change (27 patients). Changes recalling hemolyticuremic and localized intravascular coagulation were found in three and six patients, respectively. Our data, dealing with a European Caucasian population, considerably differ from those reported in North American literature, in as much as we found no cases of human immunodeficiency virus nephropathy. Conversely, immune-mediated glomerular diseases were frequent, in agreement with recent studies on renal biopsy specimens from AIDS patients with acquired immunodeficiency syndrome. This type of infections, supplies multiple sources of antigens that may stimulate immune complex formation and, therefore, glomerular diseases.
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PMID:Renal changes in patients with acquired immunodeficiency syndrome: a post-mortem study on an unselected population in northwestern Italy. 907 21

Abnormalities in iron metabolism have been reported in patients with acquired immunodeficiency syndrome (AIDS). To assess the frequency of abnormal hepatic iron deposition in these patients and to examine potential causes of iron overload, we analyzed the amount of iron at different cellular sites in liver sections obtained at autopsy of 78 patients with AIDS. Quantitation of serum iron and transferrin levels and estimation of total iron binding capacity was obtained using serum from 63 patients. The number of whole blood/packed red blood cell transfusions and opportunistic infections was recorded. Of the 78 patients, 25 (32%) showed a Grade 3 or 4 (0-4 scale) iron level, distributed in three patterns, i.e., in hepatocytes only, in hepatocytes and Kupffer cells, and in Kupffer cells only. In these 25 livers, 4 had cirrhosis, with no documented cause; the mean number of transfusions was 12.5; and 16 (64%) had Mycobacterium avium-Mycobacterium intracellulare infection. In the 53 livers with little or no iron, 5 had cirrhosis, with 3 of those 5 listing alcoholic liver disease or hepatitis as the cause; the mean number of transfusions was 1.4; and 18 (34%) had Mycobacterium avium-Mycobacterium intracellulare infection. Transferrin saturation was more than 50% in 6 (29%) of 21 cases with increased hepatic iron levels and in 6 (14%) of 42 cases with little or no hepatic iron. These results indicate that hepatic iron overload in patients with AIDS is associated with blood transfusions, an elevated transferrin saturation, and Mycobacterium avium-Mycobacterium intracellulare infection. Significant hepatic iron deposition in patients with AIDS with no other apparent cause of cirrhosis suggests an etiologic role for iron in hepatic injury. The increase in hepatic iron levels in these patients has potentially adverse clinical effects related to the use of transfusions, iron supplements, and iron-containing drugs.
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PMID:Increased hepatic iron in the acquired immunodeficiency syndrome: an autopsy study. 938 70

Alterations of calcium and bone metabolisms have been observed in numerous studies of small groups of male HIV-infected patients. However, our knowledge regarding the manifestation of AIDS-associated hypoparathyroidism in female subjects is limited. In order to investigate the influence of heroin on the calciotropic hormones we performed a cross-sectional study on 45 female patients with proven HIV infection. The following criteria were used for exclusion from the study: age less than 20/ more than 50 years; confinement to bed; wasting symptoms; treatment with agents containing ketoconazole, renal or hepatic insufficiency; clinical or echographic signs of liver cirrhosis; endocrine diseases, or treatment with drugs known to influence calcium metabolism. A reduced parathormone (PTH) level was found among the female HIV-infected patients. Additional long-term use of heroin resulted in a significant increase of PTH compared to sex- and age matched controls and a second group of non-HIV-afflicted heroin dependent females. Significantly lowered serum magnesium concentrations were found in all three groups. Both serum calcium and urinary excretion of calcium were elevated in the group of HIV-infected heroin addicts and were independent from low vitamin D3 levels (1,25-dihydroxycholecalciferol) and alterations of protein metabolism. Therefore, it is concluded that the changes of PTH secretion are mainly due to mechanisms both of the impaired immune defense of HIV-infected females and the additional effect of opiates.
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PMID:Elevated serum-calcium and parathormone-levels in HIV afflicted female heroin addicts. 926 87


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