About INH

INH, or isoniazid is the preferred treatment for LTBI, although there are alternatives for those who are allergic, or react strongly to INH.

Some side effects of INH:
  • Nausea and vomiting.
  • Constipation.
  • Dry mouth.
  • Fever.
  • Difficulty urinating.
  • Dizziness or spinning sensation (vertigo).
  • Inflammation of the nerves (neuritis), which may cause pins and needles sensations, muscle weakness or blurred vision. Your doctor may prescribe you pyridoxine (vitamin B6) supplements to help prevent this side effect.
  • Inflammation of the liver (hepatitis).
  • Seizures (convulsions).
  • Loss of contact with reality (psychosis).
  • Blood disorders.
  • Skin reactions.
  • Raised blood sugar levels (hyperglycaemia).


There are an overwhelming number of studies on INH, dealing with the liver.  I'm copying all of the below information directly from this website

The Drug:

Isoniazid kills actively growing tubercle bacilli by inhibiting the biosynthesis of mycolic acids which are major components of the cell wall of Mycobacterium tuberculosis.


Image from Drug Label ContentIsoniazid is the hydroxide of isonicotinic acid. It is a colorless or white crystalline powder or white crystals. It is odorless and slowly affected by exposure to air and light. It is freely soluble in water, sparingly soluble in alcohol and slightly soluble in chloroform and in ether. Its molecular weight is 137.14 and its chemical formula is C6H7N3O.
The chemical name for isoniazid is 4-pyridinecarboxylic acid, hydrazide and its structural formula is:


After oral administration, isoniazid is readily absorbed from the GI tract and produces peak blood levels within 1 to 2 hours. It diffuses readily into all body fluids (cerebrospinal, pleural, and ascitic fluids), tissues, organs, and excreta (saliva, sputum, and feces). Isoniazid is not substantially bound to plasma proteins. The drug also passes through the placental barrier and into milk in concentrations comparable to those in the plasma. The plasma half-life of isoniazid in patients with normal renal and hepatic function ranges from 1–4 hours, depending on the rate of metabolism. From 50% to 70% of a dose of isoniazid is excreted in the urine within 24 hours, mostly as metabolites.

Isoniazid is metabolized in the liver mainly by acetylation and dehydrazination. The rate of acetylation is genetically determined. Approximately 50% of African Americans and Caucasians are "slow inactivators" and the rest are "rapid inactivators"; the majority of Eskimos and Asians are "rapid inactivators." The rate of acetylation does not significantly alter the effectiveness of isoniazid. However, slow acetylation may lead to higher blood levels of the drug, and thus, an increase in toxic reactions.

Pyridoxine (B6) deficiency is sometimes observed in adults with high doses of isoniazid and is probably due to its competition with pyridoxal phosphate for the enzyme apotryptophanase.

Isoniazid has been reported to inhibit the metabolism of the following drugs: anticonvulsants (eg, carbamazepine, phenytoin, primidone, valproic acid), benzodiazepines (eg, diazepam), haloperidol, ketoconazole, theophylline, and warfarin. Daily ingestion of alcohol may be associated with a higher incidence of isoniazid hepatitis.

Isoniazid may produce hyperglycemia and lead to loss of glucose control in patients on oral hypoglycemics.
Fast acetylation of isoniazid may produce high concentrations of hydrazine that facilitate deflorination of enflurane

Because isoniazid has some monoamine oxidase inhibiting activity, an interaction with tyramine-containing foods (cheese, red wine) may occur. Diamine oxidase may also be inhibited, causing exaggerated response (eg, headache, sweating, palpitations, flushing, hypotension) to foods containing histamine (eg, skipjack, tuna, other tropical fish).

Isoniazid has been reported to induce pulmonary tumors in a number of strains of mice.

Isoniazid overdosage produces signs and symptoms within 30 minutes to 3 hours. Nausea, vomiting, dizziness, slurring of speech, blurring of vision, and visual hallucinations (including bright colors and strange designs) are among the early manifestations. With marked overdosage, respiratory distress and CNS depression, progressing rapidly from stupor to profound coma, are to be expected along with severe, intractable seizures. Severe metabolic acidosis, acetonuria, and hyperglycemia are typical laboratory findings.



DISCLAIMER:  I am not a medical professional.  All information on this page is credited to its source; please feel free to review sources and come to your own conclusions!