Search PubMed⌕ Search
Home/Archive/PubMed

PubMed · 9411638

[The general practitioner and abnormal liver function tests].

R Hallez
View original source ↗Export metadata ↓

Abstract

In case of abnormal liver function tests, it's necessary to distinguish different situations, starting from this first data. We will successively consider: the high and moderate acute increases of aminotransferase, the chronic increases of aminotransferase, the isolated cholestase picture and the isolated increases of gamma GT or of bilirubine. We will finish with a partial survey about drug-induced liver diseases.

Explore related subjects

Alanine TransaminaseAlkaline PhosphataseAspartate AminotransferasesBilirubinDiagnosis, DifferentialFamily PracticeHumansLiver DiseasesLiver Function Testsgamma-GlutamyltransferaseEnglish AbstractJournal ArticleReview

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

R Hallez. 1997. [The general practitioner and abnormal liver function tests].. https://pubmed.ncbi.nlm.nih.gov/9411638/

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

PubMed2002

Inhibition of haem oxygenase activity increases leukocyte accumulation in the liver following limb ischaemia-reperfusion in mice.

The role of haem oxygenase (HO) in the hepatic accumulation of leukocytes in mice during the initiation of remote organ injury following normotensive limb ischaemia-reperfusion (I-R) was investigated. Remote organ injury was initiated by 1 h bilateral hindlimb ischaemia followed by either 1 or 1.5 h reperfusion (I-R) in male C57BL/6 mice. Mice were randomly assigned to either sham (no I-R, n = 4), I-R (n = 4 for both time points), I-R plus chromium mesoporphyrin (CrMP, n = 4) to inhibit HO or I-R plus haemin (n = 4) to increase HO. Leukocyte accumulation and leukocyte-endothelial interaction were directly measured using fluorescence intravital microscopy. Leukocytes were labelled via an injection of rhodamine 6G. In sinusoids the total number and the number of stationary leukocytes were assessed. In postsinusoidal venules the number of adherent and rolling leukocytes and the velocities of both red blood cells and leukocytes were measured. The total number of leukocytes increased in sinusoids of I-R mice reaching a plateau within 1 h compared with sham animals, while the number of stationary leukocytes progressively increased over the entire study period. Stationary leukocytes in sinusoids increased after 1 and 1.5 h of I-R following CrMP, while they were significantly reduced following haemin treatment compared to animals treated with I-R only. In postsinusoidal venules a progressive increase in adherent leukocytes also occurred. As observed in sinusoids, CrMP significantly increased, while haemin significantly reduced leukocyte adhesion. The number of rolling leukocytes increased after CrMP in both I-R groups (1 and 1.5 h). The velocities of rolling leukocytes declined following 1.5 h of I-R compared with sham. Haemin treatment of 1.5 h I-R animals restored the velocities back to sham levels. The calculated wall shear rates in postsinusoidal venules were significantly lower in all I-R groups in comparison to sham animals. Combination of 1.5 h I-R with CrMP resulted in the lowest shear rates of all I-R groups. The number of stationary leukocytes within sinusoids and adherent leukocytes in postsinusoidal venules were correlated to the corresponding alanine aminotransferase (ALT) levels. In conclusion, endogenous HO reduces leukocyte-endothelial interactions within the liver. Thus, endogenous HO activity provides an important mechanism controlling the hepatic inflammatory response during the initiation of remote organ injury following normotensive limb ischaemia-reperfusion.

Alanine Transaminase↗
PubMed2002

Targeting urokinase-type plasminogen activator receptor on human glioblastoma tumors with diphtheria toxin fusion protein DTAT.

BACKGROUND: The prognosis for patients with brain cancer is poor, and new therapies are urgently needed. Recombinant toxic proteins that specifically target tumor cells appear to be promising. Urokinase-type plasminogen activator (uPA) receptor (uPAR) is expressed on the surface of glioblastoma and some other tumor cells and endothelial cells. We synthesized a recombinant fusion protein, DTAT, which contains the catalytic portion of diphtheria toxin (DT) for cell killing fused to the noninternalizing amino-terminal (AT) fragment of uPA, and investigated its effectiveness in targeting uPAR-positive tumor cells. METHODS: In vitro cytotoxicity of DTAT was measured by cell proliferation assays. For in vivo studies, athymic nude mice (four to five animals/group) bearing uPAR-expressing human glioblastoma (U118MG) cell-induced tumors were injected with DTAT or control protein. Tumor volume was assessed over time, and differences between treatments were analyzed by Student's t test. Effects of DTAT on body organ systems were evaluated in normal, tumor-free C57BL/6 mice histologically and functionally by serum enzyme tests. All statistical tests were two-sided. RESULTS: In vitro, DTAT was highly potent and selective in killing uPAR-expressing glioblastoma cells (U118MG, U373MG, and U87MG) and human umbilical vein endothelial cells. In vivo, compared with mice treated with control proteins, DTAT caused a statistically significant (P =.05) regression of small U118MG cell-induced tumors in all mice. Control fusion proteins that did not react with glioblastoma cells had no effect on tumor growth. DTAT given to tumor-free C57BL/6 mice had little effect on kidney, liver, heart, lung, and spleen histologies. Serum analysis in the same mice showed no elevation in blood urea nitrogen, indicating lack of effect on kidney function but a statistically significant (P =.046), albeit non-life-threatening, elevation in liver alanine aminotransferase levels. CONCLUSION: DTAT may have potential for intracranial glioblastoma therapy because of its ability to target tumor cells and tumor vasculature simultaneously and its apparent lack of systemic effects.

Alanine Transaminase↗
PubMed2002

Promotion of hepatic ischemia/reperfusion injury by IL-12 is independent of STAT4.

BACKGROUND: We have recently demonstrated a role for interleukin-12 (IL-12) in the induction and development of hepatic ischemia/reperfusion injury. IL-12 mediates its effects through the transcription factor, signal transducer and activator of transcription-4 (STAT4). Therefore, we investigated the response to hepatic ischemia/reperfusion in STAT4-deficient mice. METHODS: Wild-type and STAT4-deficient mice were subjected to 90 min of partial hepatic ischemia followed by reperfusion. In some experiments, IL-12 was neutralized with antibody administered intravenously. RESULTS: Wild-type mice demonstrated rapid activation of STAT4 in liver after ischemia/reperfusion, which mirrored hepatic protein expression of IL-12. Interestingly, STAT4-deficient mice were indistinguishable from wild-type mice in their response to hepatic ischemia reperfusion. No differences were observed in serum levels of tumor necrosis factor alpha (TNF-alpha), liver accumulation of neutrophils, or hepatocellular injury. However, blockade of endogenous IL-12 significantly reduced these parameters in STAT4-knockout mice. CONCLUSIONS: These data demonstrate that IL-12 promotes hepatic inflammation in a manner that is independent of STAT4 and implicate a novel mechanism for the pro-inflammatory effects of IL-12.

Alanine Transaminase↗