Senna leaf

Sennae folium, senna leaf.  

Senna leaf consists of the dried leaflets (pinnulae) of Cassia senna L.  ( C.  acutifolia Del.) [Fam.  Fabaceae], known as Alexandrian or Khartoum senna, or of C.  angustifolia Vahl [Fam.  Fabaceae], known as Tinnevelly senna, as well as their preparations in effective dosage.  

[Ed.  note:Currently accepted nomenclature for all three cultivars is Senna alexandrina Miller . ]

The leaves contain anthranoids, mainly of the bi-anthrone type.  The content of anthranoids of the emodin and aloe-emodin type is usually higher in senna fruit.  

The drug must conform to the currently valid pharmacopeia.  

Pharmacological Properties, Pharmacokinetics, Toxicology

1,8-dihydroxy-anthracene derivatives have a laxative effect.  This effect is due to the sennosides, specifically, their active metabolite in the colon, rheinanthrone.  The effect is primarily caused by the influence on the motility of the colon by inhibiting stationary and stimulating propulsive contractions.  This results in an accelerated intestinal passage and, because of the shortened contact time, a reduction in liquid absorbed through the lumen.  In addition, stimulation of active chloride secretion increases water and electrolyte content of the contents of the intestine.  

Systematic studies pertaining to the kinetics of senna leaf preparations are not available.  However, it must be supposed that the aglycones contained in the drug are absorbed in the upper small intestine.  The -glycosides are prodrugs that are neither absorbed nor cleaved in the upper gastrointestinal tract.  They are degraded in the colon by bacterial enzymes to rheinanthrone.  Rheinanthrone is the laxative metabolite.  The systemic availability of rheinanthrone is very low.  Animal experiments reveal that less than 5 percent is passed in the urine in the oxidized form and/or in conjugated form as rhein and sennodine.  The major amount of rheinanthrone (more than 90 percent) is bound to the feces in the colon and excreted as a polymer.  

Active metabolites, such as rhein, infiltrate in small amounts into the milk ducts.  A laxative effect on nursing infants has not been observed.  The placental permeability for rhein is very small, as was observed in animal experiments.  

Drug preparations have a higher general toxicity than the pure glycosides, presumably due to the content of aglycones.  Experiments with senna leaf preparations are not available.  A senna extract showed mutagenic toxicity in vitro.  The pure substance, sennoside A, B, showed no mutagenic toxicity in vitro.  An in vivo study with a defined extract of senna fruit revealed no mutagenicity.  Preparations with an anthranoid content of 1.4 - 3.5 percent (calculated as the sum of specific individual compounds) were used.  These were potentially equivalent to 0.9 - 2.9 percent rhein, 0.05 - 0.15 percent aloe-emodin and 0.001 - 0.006 percent emodin.  The results appear to be also applicable for specific senna leaf preparations.  Some positive results have been observed for aloe-emodin and emodin.  A study for carcinogenicity was performed with an enriched sennoside fraction containing about 40.8 percent anthranoids, of which 35 percent were sennosides (calculated as the sum of the individually determined compounds), equivalent to about 25.2 percent of the calculated potential rhein, 2.3 percent potential aloe-emodin and 0.007 percent potential emodin.  The tested substance contained 142 ppm free aloe-emodin and 9 ppm free emodin.  The study was conducted over 104 weeks, rats received up to 25 mg/kg body weight and showed no substance-dependent increase of tumors.  

Clinical Data

Uses

Constipation.  

Contraindications

Intestinal obstruction, acute intestinal inflammation, e.g., Crohn's disease, colitis ulcerosa, appendicitis, abdominal pain of unknown origin.  Children under 12 years of age.  

Side Effects

In single incidents, cramp-like discomforts of the gastrointestinal tract.  These cases require a dosage reduction.  

With chronic use or abuse:

• Disturbance of electrolyte balance, especially potassium deficiency, albuminuria and hematuria.  Pigment implantation into the intestinal mucosa ( pseudomelanosis coli ) is harmless and usually reverses on discontinuation of the drug.  Potassium deficiency can lead to disorders of heart function and muscular weakness, especially with concurrent use of cardiac glycosides, diuretics, or corticosteroids.  

Stimulating laxatives must not be used over a long period (more than 1 - 2 weeks) without medical advice.  

Due to insufficient toxicological investigation, this herb should not be used during pregnancy or lactation.

In cases of chronic use or abuse, loss of potassium may potentiate cardiac glycosides and have an effect on anti-arrhythmic medications.  

Potassium deficiency may be exacerbated by simultaneous administration of thiazide diuretics, corticoadrenal steroids, or licorice root.  

Comminuted herb, powder or dried extracts for teas, decoctions, cold macerates, or elixirs.  Liquid or solid forms of medication exclusively for oral use.  

Unless otherwise prescribed:

• 20 - 30 mg hydroxyanthracene derivatives daily, calculated as sennoside B.  

The individually correct dosage is the smallest dose necessary to maintain a soft stool.  

Note:The form of administration should be smaller than the daily dose.  

Electrolyte and fluid imbalance.  

Use of a stimulating laxative for longer than the recommended period can cause intestinal sluggishness.  

This preparation should be used only if no effects can be obtained through changes in diet or the use of bulk-forming products.  

None known.