Tuberculosis Arthritis Genu Sinistra with Drug-Induced Liver Injury, COVID 19 Confirmed

Background. Tuberculosis is still a significant health problem, especially in developing countries. Although pulmonary tuberculosis is the most common form of the disease, extrapulmonary tuberculosis also contributes significantly to morbidity and mortality. 10-15% of extrapulmonary cases are due to tuberculous arthritis. The following is a case report of a 36-year-old woman with a diagnosis of genu Sinistra tuberculosis arthritis and drug-induced hepatotoxic injury due to OAT. Case presentation. A woman, 36 years old, Muslim, addresses Banyuasin. The patient is a housewife, treated at Dr. Moh Hoesin General Hospital since October 11, 2021. The main complaint in the form of pain in the left knee has been getting worse since 1 week before being admitted to the hospital. 4 months before admission the hospital, the patient complained of left knee pain, the pain felt like being stabbed, coming and going, especially when walking. In this patient, there was a complaint of nausea that was felt in the pit of the stomach. The results of laboratory examinations showed an increase in the transaminase enzyme and hyperuricemia, so it was suspected that the patient had DILI due to OAT drugs. Hepatocyte death in DILI can occur through two processes, namely processes mediated by apoptosis or necrosis. In apoptosis, cell shrinkage and fragmentation occur into small pieces with the cell membrane intact. These fragments are cleared by phagocytosis and generally do not stimulate the host immune response. Conclusion. A patient diagnosed with arthritis tuberculosis genu Sinistra with Drug-Induced Liver Injury and Confirmed COVID 19.

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A case of statin-induced liver injury with positive rechallenge with a second statin. Is there a class effect?

Journal of Basic and Clinical Physiology and Pharmacology ◽

10.1515/jbcpp-2021-0013 ◽

2021 ◽

Vol 0 (0) ◽

Author(s):

Giovanna Onfiani ◽

Fabio Nascimbeni ◽

Francesca Carubbi

Keyword(s):

Liver Injury ◽

Clinical Symptoms ◽

High Risk Population ◽

Drug Induced ◽

Case Presentation ◽

Drug Induced Liver Injury ◽

Aged Woman ◽

Cardiovascular Morbidity And Mortality ◽

Middle Aged Woman

Abstract Objectives Statins have proved to reduce cardiovascular morbidity and mortality in high-risk population and are generally well tolerated, although adverse events can occur. Up to 3% of patients develop aminotransferases elevation, which usually normalizes with continued treatment and hardly is associated with clinical symptoms. Serious statin-related liver injury is exceedingly rare. Furthermore, literature regarding rechallenge with a second statin is extremely poor. Some authors caution that re-exposure to these drugs is associated with a more serious liver injury but safe switching to a second statin after drug-induced liver injury (DILI) is also reported. Case presentation We describe a case of a middle-aged woman who developed hepatocellular liver injury after simvastatin dose escalation; a rechallenge with low dose rosuvastatin caused rapid recurrence of DILI. Conclusions In our opinion, clinicians should be very cautious upon rechallenge and closely follow-up patients who experienced statin-induced liver injury when trying re-exposure to another statin.

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Contrasting model mechanisms of alanine aminotransferase (ALT) release from damaged and necrotic hepatocytes as an example of general biomarker mechanisms

10.1101/2019.12.24.887869 ◽

2019 ◽

Author(s):

Andrew K. Smith ◽

Glen E.P. Ropella ◽

Mitchell R. McGill ◽

Preethi Krishnan ◽

Lopamudra Dutta ◽

...

Keyword(s):

Liver Injury ◽

Plasma Levels ◽

Alanine Aminotransferase ◽

Cellular Damage ◽

Virtual Experiment ◽

Drug Induced ◽

Drug Induced Liver Injury ◽

Causal Processes ◽

Model Execution ◽

Hepatocyte Death

AbstractInterpretations of elevated blood levels of alanine aminotransferase (ALT) for drug-induced liver injury often assume that the biomarker is released passively from dying cells. However, the mechanisms driving that release have not been explored experimentally. The usefulness of ALT and related biomarkers will improve by developing mechanism-based explanations of elevated levels that can be expanded and elaborated incrementally. We provide the means to challenge the ability of closely related concretized model mechanisms to generate patterns of simulated hepatic injury and ALT release that scale (or not) to be quantitatively similar to the wet-lab validation targets. The validation targets for this work are elevated measures of plasma ALT following acetaminophen (APAP) exposure in mice. We build on a published model mechanism that helps explain the generation of characteristic spatiotemporal features of APAP hepatotoxicity within hepatic lobules. Discrete event and agent-oriented software methods are most prominent. We instantiate and leverage a small constellation of concrete model mechanisms. Their details during execution help bring into focus ways in which particular sources of uncertainty become entangled within and across several levels with cause-effect details. Monte Carlo sampling and simulations comprise a virtual experiment. Falsification of one (or more) of the model mechanisms provides new knowledge and shrinks the model mechanism constellation incrementally. We challenge the sufficiency of four potentially explanatory theories for ALT release. The first model mechanism tested failed to achieve the initial validation target, but each of the three others succeeded. We scale ALT amounts in virtual mice directly to target plasma ALT measures in individual mice. Results for one of the three model mechanisms matched all target ALT measures quantitatively. We assert that the actual mechanisms responsible for ALT measures in individual mice and the virtual causal processes occurring during model execution are strongly analogous within and among real hepatic lobular levels.Author summaryInterpretations of elevated biomarkers for drug-induced liver injury assume passive release during hepatocyte death, yet indirect evidence indicates that plasma levels can increase absent injury. Limitations on measurements make it infeasible to resolve causal linkages between drug disposition and plasma levels of biomarkers. To improve explanatory knowledge, we instantiate within virtual mice, plausible mechanism-based causal linkages between acetaminophen disposition and alanine aminotransferase (ALT) behavior that enables simulation results to meet stringent quantitative validation prerequisites. We challenge the sufficiency of four model mechanisms by scaling ALT measurements in virtual mice to corresponding plasma values. Virtual experiment results in which ALT release is a combined consequence of lobular-location-dependent hepatocyte death and drug-induced cellular damage, matches all validation targets. We assert that the actual mechanisms responsible for plasma ALT measures in individual mice and the virtual causal processes occurring during model execution are strongly analogous within and among real hepatic lobular levels.

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Aseptic meningitis, hepatitis and cholestasis induced by trimethoprim/sulfamethoxazole: a case report

BMC Pediatrics ◽

10.1186/s12887-021-02820-y ◽

2021 ◽

Vol 21 (1) ◽

Author(s):

J. A. A. van Asperdt ◽

R. A. De Moor

Keyword(s):

Case Report ◽

Side Effects ◽

Liver Injury ◽

Aseptic Meningitis ◽

Cholestatic Hepatitis ◽

Diagnostic Challenge ◽

Drug Induced ◽

Case Presentation ◽

Drug Induced Liver Injury ◽

Inflammatory Drugs

Abstract Background Drug-induced aseptic meningitis is a rare, but challenging diagnosis, most commonly reported with nonsteoroidal anti-inflammatory drugs (NSAIDs) and antibiotics. Trimethoprim/sulfamethoxazole (TMP/SMX) is a sulfonamide that is widely used in clinical practice for the treatment and prophylaxis of various infections. The most common side effects associated with TMP/SMX are generally mild and self-limited, but serious side effects have been reported, including liver injury and aseptic meningitis. Case presentation We report a 2,5 year old Dutch girl with both drug-induced aseptic meningitis and drug-induced liver injury while using TMP/SMX prophylaxis. Ursodeoxycholic acid was started because of cholestatic injury. After cessation of TMP/SMX, full convalescence was reached within weeks. Conclusions This is the first report of a young patient with both aseptic meningitis and drug-induced liver injury caused by TMP/SMX. Drug-induced aseptic meningitis and cholestatic hepatitis constitute a considerable diagnostic challenge to clinicians. In addition to a thorough evaluation for infectious causes, clinicians should be aware of drug-induced aseptic meningitis and cholestatic hepatitis.

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Leberschaden unter oraler Antikoagulation, Statin- und ACE-Hemmertherapie

Praxis ◽

10.1024/1661-8157/a000298 ◽

2010 ◽

Vol 99 (21) ◽

pp. 1259-1265 ◽

Cited By ~ 2

Author(s):

Bruggisser ◽

Terraciano ◽

Rätz Bravo ◽

Haschke

Keyword(s):

Liver Injury ◽

Wird Eine ◽

Drug Induced ◽

Drug Induced Liver Injury

Ein 71-jähriger Patient stellt sich mit Epistaxis und ikterischen Skleren auf der Notfallstation vor. Der Patient steht unter einer Therapie mit Phenprocoumon, Atorvastatin und Perindopril. Anamnestisch besteht ein langjähriger Alkoholabusus. Laborchemisch werden massiv erhöhte Leberwerte (ALAT, Bilirubin) gesehen. Der INR ist unter oraler Antikoagulation und bei akuter Leberinsuffizienz >12. Die weiterführenden Abklärungen schliessen eine Virushepatitis und eine Autoimmunhepatitis aus. Nachdem eine Leberbiopsie durchgeführt werden kann, wird eine medikamentös-toxische Hepatitis, ausgelöst durch die Komedikation von Atorvastatin, Phenprocoumon und Perindopril bei durch Alkohol bereits vorgeschädigter Leber diagnostiziert. Epidemiologie, Pathophysiologie und Klink der medikamentös induzierten Leberschäden (drug induced liver injury, DILI), speziell von Coumarinen, Statinen und ACE-Hemmern werden im Anschluss an den Fallbericht diskutiert.

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