How is klonopin metabolized

Because these abnormalities improved soon after discontinuation of clonazepam, the drug was the most likely cause of these events. He had been advised to reduce alcohol intake and improve his diet. Recently, he noticed mild tremor in his left hand. He was not feverish and had no skin rash. Because specific antibodies for viral hepatitis or specific immunological parameters in autoimmune liver diseases were absent Table 1 , viral hepatitis or autoimmune liver diseases were unlikely to be the cause of the abrupt liver dysfunction.

High glycoalbumin GA level Because the patient showed negative result in anti-glutamic acid decarboxylase GAD antibody test and sufficient postprandial C-peptide level 8. Therefore, we suspected clonazepam as the cause of the sudden emergence of abnormalities and discontinued the drug. Seven days after clonazepam discontinuation, the abnormal levels of triglycerides, liver dysfunction, and glycometabolism improved without any other medical intervention.

Changes in liver function, triglycerides levels, and glycometabolism over the time of clonazepam administration and discontinuation. Drug-induced liver injury DILI is defined as liver injury caused by various medications, herbs, or xenobiotics that results in abnormalities in liver tests.

Although the patient showed negative results in drug lymphocyte-stimulation test DLST , clonazepam was not ruled out as a suspected drug. The patient had been taking fenofibrate and febuxostat regularly, which are potential risk factors for liver dysfunction. The patient had been receiving occasional drip infusion of electrolyte solution for his chronic whiplash-associated disorder.

Based on results of pancreatic function-related blood parameters and repeated CT scans, pancreatic disease was unlikely to have contributed to the events. Although he denied it and this suspicion would not necessarily explain the remarkable glucose elevation, the possibility of a recent binge should be considered for a patient such as ours. Because our patient consumed excessive alcohol regularly, ALDs, such as previously unrecognized alcoholic fatty liver disease, could be a possible reason for liver dysfunction, and this could have triggered and aggravated DILI.

Therefore, we considered that the DILI in our patient was metabolic rather than allergic or hypersensitive. This could have eventually caused DILI in our patient.

After clonazepam initiation, the patient showed exacerbation of dyslipidaemia and developed remarkable fatty liver. DISH is a rare form of DILI that is manifested through the characteristic pathological patterns of intracellular accumulation of lipids in hepatocytes, often accompanied by oxidative stress and hepatic inflammation.

In addition to DILI and DISH, clonazepam was considered a direct or indirect cause of the hyperglycaemic crisis in our patient owing to the medical time course of the initiation and discontinuation of the drug. Broad classes of commonly used drugs, such as the drugs used in hormonal therapy, mTOR inhibitors, tyrosine kinase inhibitors, antihypertensive agents, statins, antipsychotics, antiretroviral agents, and interferon, are known to cause diabetes.

However, we should also consider the effect of DISH on glycometabolism because fatty acids FAs are known to induce a pleiotropic effect on beta-cell function, including changes in cell signalling, insulin secretion, mitochondrial metabolism, and membrane composition.

Another possible explanation for the effect on glycometabolism is mitochondrial dysfunction due to the drug. Mitochondria plays a significant role in regulating insulin secretion in beta-cells by regulating adenosine triphosphate ATP levels responsible for facilitating membrane depolarization and insulin granule exocytosis.

In addition, our findings suggested that caution should be exercised when any drug is initiated in patients with pre-existing metabolic abnormality.

Further investigation on the relationship between DISH and hyperglycaemia in patients will improve our understanding of how lipid and glycaemic metabolism are linked. Ethical approval: All procedures followed were in accordance with the ethical standards of the responsible committee on human experimentation institutional and national and the Helsinki Declaration of , as revised in and Ethical approval to report this case was obtained from Ethics Committee of Sanno Hospital 25 August , approval number: S Informed consent: Written informed consent was obtained from the patient for his anonymized information to be published in this article.

National Center for Biotechnology Information , U. Published online Apr 8. Author information Article notes Copyright and License information Disclaimer. Email: pj. Received Sep 2; Accepted Mar This article has been cited by other articles in PMC. Abstract In this study, we report a case of a year-old Japanese man who had chronic whiplash-associated disorder, hyperlipidaemia, hyperuricacidaemia, and mild liver dysfunction due to excessive alcohol intake.

Keywords: Clonazepam, drug-induced liver dysfunction, drug-induced glycaemic crisis. Introduction Clonazepam 1 , 2 [5- 2-chlorophenyl -1,3-dihydromethylnitro-2H-1,4-benzodiazepinone] is a benzodiazepine structurally related to chlordiazepoxide hydrochloride, diazepam, and nitrazepam. Table 1. Open in a separate window.

Figure 1. Discussion Drug-induced liver injury DILI is defined as liver injury caused by various medications, herbs, or xenobiotics that results in abnormalities in liver tests. References 1. Browne TR. N Engl J Med ; : — Olsson R, Zettergren L. Anticonvulsant-induced liver damage. Am J Gastroenterol ; 83 : — The more fat someone has, the more likely Klonopin and its metabolites will stick to those fat cells while being metabolized.

A large dose of Klonopin will take more time to eliminate than a smaller dose. With constant use, Klonopin can build up in the body. The longer someone takes this drug, the more likely they are to develop a tolerance to it, which can increase how often they take the medication to achieve the same effects.

Taking more than one medication at once can slow down the liver because it has to process more than one substance at the same time. Because the liver is the main organ responsible for breaking down Klonopin, how well it is or is not functioning can play a significant role in how long Klonopin will stay in the body. Some factors may be more influential than others depending on the individual and their unique circumstances.

The detection time for Klonopin in blood, saliva, and urine is between five to six days after consumption. Hair tests, on the other hand, tend to have longer detection times and may detect benzodiazepines for up to four months after the last dose. Call now to be connected with one of our compassionate treatment specialists. Taking too much Klonopin can be considered abuse, and where there is substance abuse, treatment is often necessary if not required.

Abusing benzodiazepines can lead to health issues and raise the risk of overdose, dependence, and addiction. By addressing physical, mental, and spiritual health concerns, individuals are more likely to have extended recovery times. To learn more about Klonopin detection times and addiction treatment, contact a specialist at Vertava Health today. This page does not provide medical advice. Don't Wait. Get Help Now How Is Klonopin Metabolized?