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Isoniazod

(5)

(Max:300)

(好友:

ethionamide)                                                        

prodrug,被分枝桿菌的Kat-G活化,阻止mycolic acid合成

1.代謝由N-acetyltransferase進行乙醯化(*注意slow acylator)

2.為強效CYP2C9/CYP2C19/CYP2E1抑制劑

-周邊神經病變:因結構和pyridoxine相似,會促B6排除(和INH劑量無關)

-發燒/皮疹

-肝炎(AST/ALT↑) :N/V,黃疸,腹痛→不用停藥,停藥後恢復正常

-乳酸中毒

Rifampin

(10)

(Max:600)

為rifamycin半合成衍生物,和細菌的DNA-dependent RNA polymerase結合,抑制RNA生成

1.若單獨使用抗藥性易被篩選出

2.殺菌性

-rifabutin為低酵素誘導劑，較適合AIDS患者使用

-橘色體液

-...

Isoniazid: An overview

Adverse reactions — Adverse reactions to INH include hepatotoxicity and neurologic reactions.

Neurologic reactions — INH competes with vitamin B6 (pyridoxine) in its action as a cofactor in the synthesis of synaptic neurotransmitters. Resulting dose-related neurologic side effects include peripheral neuropathy, ataxia, and paresthesia. Such side effects are uncommon in the absence of risk factors. (See "Overview of acquired peripheral neuropathies in children", section on 'Vitamin B6 (pyridoxine) deficiency'.)

Patients at increased risk for INH-induced neurotoxicity...

Isoniazid: An overview

Adverse reactions — Adverse reactions to INH include hepatotoxicity and neurologic reactions.

Neurologic reactions — INH competes with vitamin B6 (pyridoxine) in its action as a cofactor in the synthesis of synaptic neurotransmitters. Resulting dose-related neurologic side effects include peripheral neuropathy, ataxia, and paresthesia. Such side effects are uncommon in the absence of risk factors. (See "Overview of acquired peripheral neuropathies in children", section on 'Vitamin B6 (pyridoxine) deficiency'.)

Patients at increased risk for INH-induced neurotoxicity include:

●Older adults

●Pregnant or breastfeeding women

●Children

●Individuals who are malnourished

●Individuals with alcohol use disorder

●Individuals with chronic liver disease

●Individuals with HIV infection

●Individuals with renal failure

●Individuals with diabetes

Hepatotoxicity — INH-induced hepatotoxicity is probably related to metabolites of INH and is not correlated with serum concentrations of the parent compound. This is most likely due to genetic polymorphisms that affect the metabolic rates of drug enzymes responsible for the production of toxic metabolites [23,24]. The onset of INH-induced hepatotoxicity is observed within the first two months of therapy in approximately 50 percent of patients.