Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: UMLS:C0021051 (immunodeficiency)
71,517 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To investigate the influence of human immunodeficiency virus (HIV) coinfection on preexisting long-term chronic C hepatitis (HCV) 68 liver biopsies from 22 HIV/HCV-coinfected, 13 HIV- and 33 HCV-monoinfected patients and 71 livers obtained at autopsy from 26 HIV/HCV-coinfected and 45 HIV-monoinfected patients were studied by histo- and immunohistochemistry. All HIV patients had reached the advanced stage of immunodeficiency (stage III CDC), except for 3 haemophilias (stage II CDC). HCV infection was associated with a higher degree of portal, periportal and lobular inflammation-regardless of whether there was concurrent HIV infection. HIV/HCV coinfection was associated with a significantly higher rate of granulocytic cholangiolitis than HCV and HIV monoinfection (P < 0.05), a histological feature uncommon in C hepatitis. In HIV/HCV coinfection cholestasis was a predominant histological feature. HCV monoinfection and HCV/HIV coinfection were associated with the highest fibrosis index. In HIV/HCV coinfection centrilobular fibrosis was significantly more marked than in HCV monoinfection (P < 0.05), suggesting an HIV-associated fibrogenic effect. Patients with chronic C hepatitis showed a significantly increased rate of posthepatitic cirrhosis compared with the patients without HCV infection (P < 0.05). At autopsy, 10 of the 20 HIV/HCV-coinfected haemophiliacs had developed cirrhosis because of chronic C hepatitis, whereas cirrhosis was found in only 2 of 6 HIV/HCV-coinfected non-haemophiliacs (1 case of chronic B and C hepatitis, and 1 case of chronic alcohol abuse). No cirrhosis was observed in the 45 autopsy patients with HIV monoinfection. The findings suggest that HIV coinfection aggravates the course of preceding long-term chronic C hepatitis by a more marked (centrilobular) fibrosis. HIV/HCV-coinfected patients are threatened by a higher rate of posthepatitic cirrhosis-particularly in multitransfused haemophiliacs-and cholestatic hepatopathy.
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PMID:Liver histopathology in patients with concurrent chronic hepatitis C and HIV infection. 913 37

Cholangitis/cholangiopathy associated with the human immunodeficiency virus (HIV) infection is characterized by chronic abdominal pain, low-grade fever, cholestasis, and sometimes areas of focal or diffuse dilatation of the bile ducts that may be apparent on noninvasive imaging studies. Although the etiology of this biliary disease may be multifactorial, it appears to be the result of immunosuppression and/or secondary opportunistic infections rather than a direct cytopathic effect of HIV itself. Various opportunistic pathogens, including cytomegalovirus, Cryptosporidium, Campylobacter fetus, and Candida albicans, have been implicated as causes of HIV-associated cholangitis. We report an unusual case of polymicrobial cholangitis and liver abscess in a patient with HIV infection.
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PMID:Polymicrobial cholangitis and liver abscess in a patient with the acquired immunodeficiency syndrome. 1070 98

Pruritus is a common manifestation of dermatologic diseases, including xerotic eczema, atopic dermatitis, and allergic contact dermatitis. Effective treatment of pruritus can prevent scratch-induced complications such as lichen simplex chronicus and impetigo. Patients, particularly elderly adults, with severe pruritus that does not respond to conservative therapy should be evaluated for an underlying systemic disease. Causes of systemic pruritus include uremia, cholestasis, polycythemia vera, Hodgkin's lymphoma, hyperthyroidism, and human immunodeficiency virus (HIV) infection. Skin scraping, biopsy, or culture may be indicated if skin lesions are present. Diagnostic testing is directed by the clinical evaluation and may include a complete blood count and measurement of thyroid-stimulating hormone, serum bilirubin, alkaline phosphatase, serum creatinine, and blood urea nitrogen levels. Chest radiography and testing for HIV infection may be indicated in some patients. Management of nonspecific pruritus is directed mostly at preventing xerosis. Management of disease-specific pruritus has been established for certain systemic conditions, including uremia and cholestasis.
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PMID:Pruritus. 1452 1

Systemic mycoses, especially pulmonary diseases and septicemia are observed increasingly at intensive care units. Essential risk factors for development of candidosis are the expanded use of antibiotics and immunocompromised patients, caused either as a result of a severe underlying disease or iatrogenically induced after organ transplantation. Candida albicans is the most frequent pathogen in microbiological findings. Blood cultures are only positive in massive fungemia. We report a 50-year-old patient with recurrent Candida-septicemia: rupture of the distal esophagus after dilatation because of cardiac achalasia with mediastinal emphysema and mediastinitis. Severe acute respiratory distress syndrome after aspiration with septic shock and acute renal failure at the beginning. Long-term mechanical ventilation, continuous renal replacement therapy and multifarious antibiotic therapy. Early microbiological samples of several positive blood cultures and bronchoalveolar lavages revealed the presence of Candida albicans. In the further clinical course, detection of Pseudomonas species in bronchoalveolar lavages and Staphylococci as well as Enterococci in a number of positive blood cultures. Later on development of a severe liver dysfunction with test results that showed an intrahepatic cholestasis. Because of coagulation failure commencement of artificial liver support with the MARS-system (molecule adsorbent recirculating system). Decrease of high bilirubin levels was accompanied by improvement of clinical condition of the patient. In the following course, repeated severe systemic infections with phases of septicemia or rather septic shock and detection of Candida in several positive blood cultures and bronchoalveolar lavages. In each case increasing bilirubin levels with signs of intrahepatic cholestasis and each time improvement with antimycotic therapy (voriconazol, caspofungin and fluconazol). The patient showed more and more signs of immunodeficiency in the sequel. The clinical appearance of candidosis is manifold. Systemic Candida infections are frequent in patients with immunodeficiency. A recurrent Candida septicemia with prolonged respiratory failure and severe liver dysfunction in form of cholestatic hepatosis, that improved several times with antimycotic therapy in combination with evidence based intensive care measures and artificial organ support is a comparatively rare event.
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PMID:[Recurrent Candida sepsis with prolonged respiratory failure and severe liver dysfunction]. 1582 96

Cholestasis in a patient with Hodgkin's disease is uncommon, and the causes of cholestasis are mainly direct tumor involvement of the liver, hepatotoxic effects of drugs, viral hepatitis, sepsis and opportunistic infections. Vanishing bile duct syndrome (VBDS) represents a very rare cause for cholestasis in this disease. We report here on a case of a 45-year-old man who developed VBDS during the complete remission stage of Hodgkin's lymphoma. There was no history of hepatitis or intravenous drug abuse, and the patient had negative results for hepatitis A virus, hepatitis B virus, hepatitis C virus, cytomegalovirus, and human immunodeficiency virus. The serological studies for antinuclear antibodies, anti-mitochondrial antibodies and anti-smooth muscle antibodies were also negative. Liver biopsy disclosed the absence of interlobular bile ducts in 9 of 10 portal tracts without any active lymphocyte infiltration and there were no Reed-Sternberg cell in the liver. The patient's cholestasis was in remission and the serum bililrubin level was normalized after two months without treatment, but tumor recurrence was noted at multiple sites of the abdominal lymph nodes on follow-up abdomino-pelvic computed tomogram.
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PMID:[Spontaneous resolution of vanishing bile duct syndrome in Hodgkin's lymphoma]. 1598 Jun 75

X-linked hyper-immunoglobulin M (IgM) syndrome (XHIGM) is a rare genetic primary immunodeficiency disease caused by mutations of the CD40 ligand (CD40L) gene with normal or elevated levels of IgM and markedly decreased serum IgG, IgA, and IgE. Liver disease may occur as a clinical manifestation in XHIGM. This complication appears to increase with age. We report an 18-year-old male patient who had recurrent episodes of acalculous cholecystitis (AC) and sclerosing cholangitis (SC). The diagnosis of XHIGM was confirmed by the finding of CD40L expression < 1% of normal and a tyrosine 169 asparaginase (t526a) mutation in exon 5 (the tumor necrosis factor domain) of the CD40L gene. The patient had direct hyperbilirubinemia (direct bilirubin 5.5 mg/dL, total bilirubin 8.7 mg/dL), cholestasis (alkaline phosphatase 1133 U/L, gamma-glutamyl transferase 1019 U/L) and elevated transaminases (aspartate aminotransferase 70 U/L, alanine aminotransferase 101 U/L). Findings on abdominal ultrasound and abdominal computed tomography were compatible with AC. After the fourth episode of cholecystitis, cholecystectomy and liver biopsy were performed. Operative cholangiography revealed poor opacification of the hepatic duct and proximal common bile duct; the upstream intrahepatic bile ducts were not visualized. The biopsy specimen showed marked fibrosis of the portal areas. Enterococcus species was cultured from the bile. Children or adolescents with recurrent AC and SC should be evaluated for an underlying immunodeficiency syndrome such as XHIGM.
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PMID:Recurrent acalculous cholecystitis and sclerosing cholangitis in a patient with X-linked hyper-immunoglobulin M syndrome. 1603 32

The behavior of hepatitis C in states of immunodeficiency is poorly understood and it is still unclear whether the characteristics of hepatitis C virus (HCV) infection in renal transplant patients differ from those observed in immunocompetent subjects. The aim of this study was to compare the biochemical and histologic characteristics of chronic HCV infection between renal transplant and immunocompetent patients. Forty-one HCV-RNA-positive renal transplant patients and 41 immunocompetent controls matched for gender, age at infection and time of infection were included in the study. The groups were compared regarding laboratory and histologic variables. Renal transplant patients showed lower alanine aminotransferase (ALT) levels (p = 0.005) and higher levels of gamma-glutamyltransferase (p = 0.003), alkaline phosphatase (p < 0.001), and direct bilirubin (p < 0.001) when compared with controls. Histologic analysis revealed less intense portal (p < 0.001) and periportal (p = 0.046) inflammatory infiltrate in renal transplant patients but a larger proportion of cases with confluent necrosis (p = 0.043). No difference in the presence of septal fibrosis, hepatic steatosis, bile duct injury and siderosis was observed. However, there was a difference in the presence of lymphoid aggregates, which were less frequent in the renal transplant group (p < 0.001). In conclusion, the characteristics of hepatitis C in renal transplant patients differ from that observed in immunocompetent patients. In renal transplant patients, HCV infection is biochemically characterized by lower ALT levels and higher frequency of cholestasis. Regarding histology, despite lower frequency of lymphoid aggregates and less intense portal/periportal inflammatory infiltrate, a greater lobular damage was observed. The impact of these differences on the progression of fibrosis remains to be established.
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PMID:Hepatitis C virus infection in renal transplant patients: a comparative study with immunocompetent patients. 1631 22

Drug-induced liver injury (DILI) encompasses a spectrum of clinical disease ranging from mild biochemical abnormalities to acute liver failure. The majority of adverse liver reactions are idiosyncratic, occurring in most instances 5-90 days after the causative medication was last taken. The diagnosis of DILI is clinical, based on history, probability of the suspect medication as a cause of liver injury and exclusion of other hepatic disease. DILI can be hepatocellular (predominant rise in alanine transaminase), cholestatic (predominant rise in alkaline phosphatase) or mixed liver injury. An elevated bilirubin level more than twice the upper limit of normal in patients with hepatocellular liver injury implies severe DILI, with a mortality of approximately 10% and with an incidence rate of 0.7-1.3 per 100,000. Although acute liver failure is rare, 13-17% of all acute liver failure cases are attributed to idiosyncratic drug reactions. Response to drug withdrawal may be delayed up to 1 year with cholestatic liver injury with occasional subsequent progressive cholestasis known as the vanishing bile duct syndrome. Overall, chronic disease may occur in up to 6% even if the offending drug is withdrawn. Antibiotics and NSAIDs are the most common cause of DILI. Statins rarely cause significant liver injury whereas antiretroviral therapy is associated with hepatotoxicity in 10% of treated patients. Multiple mechanisms of DILI have been implicated, including TNF-alpha-activated apoptosis, inhibition of mitochondrial function and neoantigen formation. Risk factors for DILI include age, sex and genetic polymorphisms of drug-metabolising enzymes such as cytochrome P450. In patients with human immunodeficiency virus, the presence of chronic viral hepatitis increases the risk of antiretroviral therapy hepatotoxicity. Over the next decade, the combination of accurate case ascertainment of DILI via clinical networks and the application of genomics and proteomics will hopefully lead to accurate prediction of risk of DILI, so that pharmacotherapy can be optimised with avoidance of adverse hepatic events.
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PMID:Idiosyncratic drug-induced liver injury: an overview. 1796 56

Several experimental studies of obstructive jaundice (OJ) have shown the presence of immunosuppressive state associated with the rise of tumor necrosis factor-alpha (TNF-alpha) concentration in plasma. The present study evaluates the impact of anti-TNF- alpha administration or bile duct drainage on the inflammatory response, liver injury and renal insufficiency in obstructed rats. OJ was induced by the ligation of bile duct in Wistar rats. The parameters were determined at 14 and 21 days after OJ. Two additional groups of animals were treated with anti-TNF-alpha antibodies or submitted to bile duct drainage at 14 days, and sacrificed 21 days after OJ. Cholestasis decreased glucose, and enhanced urea, creatinin, bilirubin and transaminases. Cholestasis increased the number of different inflammatory cells (T and B lymphocytes, and monocytes-macrophages) but reduced the expression of the corresponding cellular activation markers. This low responsiveness of the inflammatory cells was related to a decreased free radical production and phagocytic activity of cells. Anti-TNF-alpha and bile duct drainage reduced tissue injury, and prevented the reduction of the number and activity of T lymphocytes and phagocytic cells observed at the advanced stages of cholestasis. In conclusion, anti-TNF- alpha and bile duct drainage improved cell immunodeficiency, and reduced liver injury, cholestasis and renal insufficiency in experimental OJ.
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PMID:Anti-TNF-alpha treatment and bile duct drainage restore cellular immunity and prevent tissue injury in experimental obstructive jaundice. 1817 61

The primary compromise of the pancreas in lymphomas is uncommon. However, in advanced stages of Non-Hodgkin's lymphomas (LNH) the secondary invasion of the pancreas is observed more frequently. Jaundice due to extrahepatic cholestasis as a presentation form is extremely rare, with only few cases described in the literature. The aim is to present a case of an obstructive jaundice as an expression of Burkitt's lymphoma probably due to a diffuse pancreatic infiltration in an adult without immunodeficiency with a rapid response of cholestasis to low dose of hydrocortisone. Skin tumor simultaneously present with jaundice allowed the histologic diagnosis with skin biopsies. After a unique dose of 100 mg hydrocortisone, jaundice improved and cholestatic enzymes decreased, pancreas became smaller and common bile duct diameter became normal at ultrasound and CT scan, also skin tumors turn pale and diminished in size. There are isolated reports of Burkitt's lymphoma cases with associated obstructive jaundice due to pancreatic infiltration or by compression by lymph nodes of the bile ducts, many of them are pediatric cases or immunodepressed HIV patients. In the case presented, surgical resection of the pancreatic infiltration and biliary drainage, either surgical or endoscopic during the same procedure was not necessary for the histopathologic diagnosis of the illness like is described in the literature. The diagnosis was suspected by the rapid decrease of cholestatic features after a single dose of hydrocortisone and the histology was easy done by a skin biopsy. We think the interest in this case is the quick response to low doses of corticoids, which avoided the necessity of surgical procedure for the diagnosis of the biliary tree obstruction, allowing a quick implementation of the specific chemotherapeutic treatment of the lymphoma without any surgical or endoscopic procedures to heal the jaundice.
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PMID:[Obstructive jaundice associated Burkitt's lymphoma mimicking pancreatic carcinoma]. 1825 63


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