Chemistry of this pair. Phenylpropanoids inhibit platelet aggregation and thromboxane synthesis and are direct mucosal irritants; some deplete hepatic glutathione at high dose.

Class mechanism. Coumarin-, salicylate- and coumestan-bearing botanicals add to vitamin-K-antagonist effect; several also compete for CYP2C9 and CYP3A4, raising S-warfarin exposure. Botanicals rich in vitamin K1 act in the opposite direction and blunt anticoagulation.

Expected

INR destabilisation in either direction; ecchymosis, epistaxis, gum bleeding, GI or intracranial haemorrhage.

Management

Do not start or stop the botanical without INR cover. Check INR at 3-5 days and again at 2 weeks. Document the product, batch and dose in the anticoagulation record.

Onset

rapid

Evidence

B - reviewed clinical column, source pending

Matched on

“anti-coagulants”

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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

“anti-diabetic”

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Chemistry of this pair. Phenylpropanoids inhibit platelet aggregation and thromboxane synthesis and are direct mucosal irritants; some deplete hepatic glutathione at high dose.

Class mechanism. Organosulfur compounds, gingerols, salicylates, ginkgolides and eugenol inhibit thromboxane A2 synthesis, platelet aggregation and PAF-mediated activation, duplicating the pharmacology of aspirin and P2Y12 blockers.

Expected

Prolonged bleeding time, surgical and post-procedural bleeding, bruising, haematuria.

Management

Stop the botanical 7-14 days before elective surgery or neuraxial anaesthesia. Record it on the pre-operative medicines list.

Onset

rapid

Evidence

B - reviewed clinical column, source pending

Matched on

“anti-platelet drugs”

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Chemistry of this pair. Phenylpropanoids inhibit platelet aggregation and thromboxane synthesis and are direct mucosal irritants; some deplete hepatic glutathione at high dose.

Class mechanism. Pyrrolizidine alkaloids, high-dose anthraquinones, kava constituents and germander-type diterpenes cause hepatocellular or sinusoidal injury that adds to the risk from paracetamol, isoniazid, methotrexate, azoles and statins.

Expected

Transaminase elevation, cholestasis, sinusoidal obstruction syndrome, acute liver failure.

Management

Baseline and 4-weekly ALT and bilirubin. Stop the botanical at any transaminase rise above three times the upper reference limit.

Onset

unspecified

Evidence

D - in silico rule prediction only

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Chemistry of this pair. Phenylpropanoids inhibit platelet aggregation and thromboxane synthesis and are direct mucosal irritants; some deplete hepatic glutathione at high dose.

Class mechanism. Salicylate-, coumarin- and eugenol-bearing botanicals add both antiplatelet activity and direct gastric mucosal irritation to cyclo-oxygenase inhibition; several also reduce renal prostaglandin-dependent perfusion.

Expected

Peptic ulceration, upper GI bleeding, acute kidney injury in volume-depleted patients.

Management

Avoid in ulcer history. Add gastroprotection where the combination is unavoidable, and monitor renal function in the elderly.

Onset

rapid

Evidence

D - in silico rule prediction only

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