Should I Take Activated Charcoal With Minocycline

[ecstatichamster]

I'm taking mino for a respiratory infection.

I'm feeling a lot of tiredness that I think is die-off.

Should I take AC between dosages?

I'm taking 100mg of minocycline twice a day.

 

[aquaman]

I find splitting charcoal, tetracyline and cascara through the day helps clear things out. I think the Charcoal by itself adds to the blockage even though it may soak up nasties. The cascara helps blast it all out!

 

[Tarmander]

I find splitting charcoal, tetracyline and cascara through the day helps clear things out. I think the Charcoal by itself adds to the blockage even though it may soak up nasties. The cascara helps blast it all out!

"Aquaman's patented butt blaster formula."

 

[ecstatichamster]

my only concern was adsorbing the minocycline or something. Man this stuff does a number on my gut. But I am persevering. Will take some charcoal tomorrow between dosages. I'm getting a lot of endotoxin reactions. Hopefully the AC will help.

 

[ecstatichamster]

I just quite minocyclin. First, it wasn't working. Second, it was making me fell so sick in my stomach and gut. Ugh.

I took charcoal yesterday and some probiotics and these make me feel a bit better. Hopefully it will all come back. My gut hurts.

 

[Koveras]

I'm taking mino for a respiratory infection.

I'm feeling a lot of tiredness that I think is die-off.

Should I take AC between dosages?

I'm taking 100mg of minocycline twice a day.

Minocycline is a bacteriostatic antibacterial - meaning it inhibits bacterial replication, but it does not kill them. Hence - no die off or increased endotoxin. It has a variety of other effects though - including potential liver injury.

J Pediatr Gastroenterol Nutr. 2011 Aug;53(2):182-9. doi: 10.1097/MPG.0b013e31821d6cfd.
Characteristics of idiosyncratic drug-induced liver injury in children: results from the DILIN prospective study.
Molleston JP1, Fontana RJ, Lopez MJ, Kleiner DE, Gu J, Chalasani N; Drug-Induced Liver Injury Network.

BACKGROUND:
The spectrum and severity of idiosyncratic drug-induced liver injury (DILI) in children are not well established.
PATIENTS AND METHODS:
The DILIN (Drug-Induced Liver Injury Network) Prospective Study is a longitudinal multicenter study designed to determine the etiologies, risk factors, and outcomes of suspected DILI. Between September 2004 and September 2009, 30 children ages 2 to 18 years with suspected DILI who met eligibility criteria were enrolled and studied for at least 6 months.
RESULTS:
Mean age was 14 years; 70% were girls. Antimicrobial (50%) and central nervous system agents (40%) were the most commonly implicated drug classes, with minocycline (4), isoniazid (3), azithromycin (3), atomoxetine (3), and lamotrigine (3) the leading agents. Median time from drug initiation to symptom onset was 32 days. Peak (median) liver chemistries were aspartate aminotransferase 503  U/L, alanine aminotransferase 727  U/L, alkaline phosphatase 331  U/L, and total bilirubin 3.9  mg/dL. Autoantibodies were common (64%). Liver injury pattern was hepatocellular 78%, cholestatic 13%, and mixed 9%. The DILI episode was scored: mild 32%, moderate 44%, severe 20%, and fatal (within 6 months) 4%. Causality assessment was definite 36%, very likely 36%, probable 16%, possible 8%, and unlikely 4%. Seven percent had persistent liver test abnormalities at 6-month follow-up suggesting chronic DILI. Liver biopsies from 12 children most frequently demonstrated chronic hepatitis or bile duct injury.
CONCLUSIONS:
Idiosyncratic DILI in children is most commonly caused by antimicrobial or central nervous system agents and usually presents with a hepatocellular injury pattern. The majority of patients recover, but morbidity and infrequent mortality are seen.

Rev Esp Enferm Dig. 2010 Nov;102(11):668.
Acute hepatitis caused by minocycline.
Casella G, Villanacci V, Di Bella C, Drera E, Baldini V, Bassotti G.

Eur J Gastroenterol Hepatol. 2008 Aug;20(8):796-9. doi: 10.1097/MEG.0b013e3282f493c5.
Minocycline hepatitis.
Ford TJ1, Dillon JF.

Minocycline is an effective antibiotic widely used in the treatment of acne vulgaris. We report a previously well 20-year-old woman who developed liver dysfunction with jaundice and malaise following a 1 year course of minocycline for acne vulgaris. Serum antinuclear antibody was strongly positive (1 : 2560) and liver transaminases were grossly deranged. All other causes of liver disease were excluded. Both the clinical symptoms and laboratory abnormalities resolved spontaneously on stopping the drug. We review the three different types of hepatotoxicity associated with minocycline and draw evidence to support the diagnosis of minocycline-induced autoimmune hepatitis. This case supports the call to monitor patients on minocycline therapy for autoimmune disease of the liver and highlights the need for a multicentre prospective trial of the risks and benefits of long-term minocycline therapy.

Neth J Med. 2004 Feb;62(2):62-4.
Interstitial pneumonia and hepatitis caused by minocycline.
Rikken NE1, Klinkhamer PJ, Haak HR.

A 28-year-old patient is described who presented with progressive dyspnoea and jaundice due to interstitial pneumonia and hepatitis. The most likely cause is a drug-related reaction to minocycline. We discuss the different kinds of drug-related reactions that are most likely involved.

Am J Gastroenterol. 2000 Oct;95(10):2993-5.
Minocycline-induced hepatitis.
Nietsch HH, Libman BS, Pansze TW, Eicher JN, Reeves JR, Krawitt EL.
PMID: 11051393 DOI: 10.1111/j.1572-0241.2000.03222.x

Med Clin (Barc). 1997 Apr 19;108(15):596.
[Acute hepatitis associated with treatment with minocycline].
[Article in Spanish]
Bruguera M, Padrós J.

Am J Gastroenterol. 1996 Aug;91(8):1641-3.
Minocycline-induced liver injury.
Malcolm A1, Heap TR, Eckstein RP, Lunzer MR.

Tetracycline may cause fatty infiltration of the liver; more recently, it has been reported to cause intrahepatic cholestasis with bile duct depletion. However, minocycline, a derivative of tetracycline, is not generally recognized to be hepatotoxic. We report a series of six cases of presumed minocycline-induced liver injury; five of these patients had acute hepatitic illness, whereas one had a more prolonged course with histological evidence of chronic hepatitis. In addition, three patients demonstrated abnormal anti-nuclear antibody levels, and one had positive double-stranded DNA.

Clin Exp Dermatol. 1996 May;21(3):244-5.
Minocycline and hepatitis.
Hardman CM, Leonard JN, Thomas HC, Goldin R.
PMID: 8914374

Gastroenterol Clin Biol. 1995 Jun-Jul;19(6-7):640-1.
[Acute hepatitis induced by minocycline].
[Article in French]
Castex F, Canva-Delcambre V, Maunoury V, Talbodec N, Wolchies E, Paris JC.
PMID: 7590035

Pharmacotherapy. 1992;12(1):68-71.
Acute hepatic failure associated with oral minocycline: a case report.
Min DI1, Burke PA, Lewis WD, Jenkins RL.

A 39-year-old woman was evaluated for possible liver transplantation due to rapidly developing hepatic failure 4 weeks after initiation of oral minocycline 100 mg twice a day for the treatment of acne. The patient developed a maculopapular rash, malaise, fever, nausea, and vomiting 2 weeks prior to admission to the hospital. On admission, her symptoms rapidly progressed to liver failure characterized by rapidly rising liver enzyme levels, worsening encephalopathy, and coagulopathy. Viral hepatitis serologies and blood cultures were all negative. After intensive supportive care for 2 weeks, the patient's condition gradually improved and she was discharged with mildly elevated liver enzyme levels and pruritus, without need of liver transplantation. Minocycline-induced hepatic injury is an idiosyncratic reaction with a sensitization period that appears to be 3-4 weeks in duration. The characteristic features include rash, fever, lymphadenopathy, and eosinophilia, as well as severe alterations in liver function. The high liver enzyme levels and the significant prolongation of the prothrombin time suggest massive hepatocellular damage. In light of the profound liver damage that occurs with this adverse reaction, care should be taken in administering minocycline to patients who have concomitant liver disease. It is recommended that patients should be instructed as to the possible signs and symptoms of toxicity and be monitored for evidence of idiosyncratic reaction or liver failure.

Antimicrob Agents Chemother. 1991 Jul;35(7):1434-6.
Evaluation of the hepatotoxic potential of minocycline.
Böcker R1, Estler CJ, Ludewig-Sandig D.

Minocycline (25 to 100 micrograms/g) dose dependently increased serum glutamic oxalacetic transaminase, urea, and bilirubin levels, and the hepatic triglyceride content in mice. In animals pretreated with phenobarbital to enhance minocycline metabolism, the effects on liver triglycerides were attenuated, while the changes in serum glutamic oxalacetic transaminase, urea, and bilirubin were enhanced. It is concluded that part of the toxic effects of minocycline may be produced by a metabolite of minocycline.

 

[ecstatichamster]

Thank you so much @Koveras

 

[tomisonbottom]

I just quite minocyclin. First, it wasn't working. Second, it was making me fell so sick in my stomach and gut. Ugh.

I took charcoal yesterday and some probiotics and these make me feel a bit better. Hopefully it will all come back. My gut hurts.

I just did the same; had to quit because it was making me sick.

I'm thinking it must be liver issues. Have you tried a lower dose?

 

[ecstatichamster]

I just did the same; had to quit because it was making me sick.

I'm thinking it must be liver issues. Have you tried a lower dose?

I haven’t had any infection for a year since I wrote this. So no. I have not.

 

[ddjd]

Why does charcoal make me so tired? Which stress hormone is it reducing?