Chemistry of this pair. Hydrocolloids raise luminal viscosity and physically entrap co-administered drug molecules, delaying and reducing absorption.

Class mechanism. Cardenolide- and bufadienolide-bearing plants are themselves Na+/K+-ATPase inhibitors, so co-administration is pharmacological overdose. Several also inhibit intestinal P-glycoprotein, raising digoxin exposure, and cross-react with digoxin immunoassays so that serum levels become uninterpretable.

Expected

Nausea, xanthopsia, bradyarrhythmia, AV block, ventricular tachycardia and death; falsely reassuring or falsely high assay results.

Management

Treat as an absolute contraindication. If exposure has occurred, manage on ECG and clinical grounds, not on assay values, and consult toxicology about digoxin-specific Fab.

Onset

rapid

Evidence

B - reviewed clinical column, source pending

Matched on

“cardiac glycoside”

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Chemistry of this pair. Hydrocolloids raise luminal viscosity and physically entrap co-administered drug molecules, delaying and reducing absorption.

Class mechanism. Hypoglycaemic botanicals act through insulin secretagogue, insulin-sensitising, alpha-glucosidase-inhibiting or glucose-transport routes. Added to a titrated pharmacological regimen the effects summate rather than plateau.

Expected

Symptomatic hypoglycaemia, sweating, tremor, confusion; severe events reported with insulin and sulfonylureas.

Management

Increase self-monitoring frequency for 2 weeks after starting or stopping. Anticipate a downward dose adjustment of insulin or sulfonylurea.

Onset

rapid

Evidence

B - reviewed clinical column, source pending

Matched on

“antidiabetic”

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Class mechanism. Enzyme-inducing botanicals lower plasma anticonvulsant concentrations, while GABAergic constituents add sedation and a few (thujone, camphor, beta-asarone, pinene-rich oils) are directly proconvulsant and lower seizure threshold.

Expected

Breakthrough seizures, status epilepticus, or additive sedation and ataxia.

Management

Measure anticonvulsant levels before and 2-4 weeks after any change. Avoid proconvulsant essential oils entirely in epilepsy.

Onset

delayed

Evidence

B - reviewed clinical column, source pending

Matched on

“antiepileptic”

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Chemistry of this pair. Hydrocolloids raise luminal viscosity and physically entrap co-administered drug molecules, delaying and reducing absorption.

Class mechanism. Tannins, phytates, oxalates and mucilage form insoluble complexes with divalent and trivalent cations in the gut lumen, reducing absorption of both the mineral and any co-administered chelating drug.

Expected

Failure of iron-deficiency correction, unexplained non-response to oral iron or calcium.

Management

Separate mineral doses from tannin- and fibre-rich botanicals by at least 2 hours; take iron with ascorbate instead.

Onset

unspecified

Evidence

B - reviewed clinical column, source pending

Matched on

“iron supplement”

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Chemistry of this pair. Hydrocolloids raise luminal viscosity and physically entrap co-administered drug molecules, delaying and reducing absorption.

Class mechanism. Cation- and tannin-rich botanicals chelate tetracyclines and fluoroquinolones; efflux-pump-inhibiting and CYP-modulating constituents alter macrolide, rifamycin and azole exposure. Anthelmintic botanicals add to praziquantel and albendazole effect.

Expected

Treatment failure from subtherapeutic antibiotic concentrations, or raised toxicity of azoles and macrolides.

Management

Separate doses by 2-3 hours. Do not rely on botanical antimicrobials in place of an indicated antibiotic.

Onset

unspecified

Evidence

D - in silico rule prediction only

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Chemistry of this pair. Hydrocolloids raise luminal viscosity and physically entrap co-administered drug molecules, delaying and reducing absorption.

Class mechanism. Guggulsterone stimulates thyroid function and T4-to-T3 conversion; goitrogenic glucosinolates and lithospermic acid suppress it; high-fibre and cation-rich botanicals bind levothyroxine in the gut and reduce absorption.

Expected

Iatrogenic hyper- or hypothyroidism, unexplained TSH drift, loss of euthyroid control.

Management

Separate levothyroxine from fibre and mineral products by 4 hours. Recheck TSH 6-8 weeks after any botanical change.

Onset

unspecified

Evidence

D - in silico rule prediction only

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