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Uva Ursi
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Uva Ursi/Bearberry
(English) Arctostaphylos uva ursi (Botanical) Ericaceae (Plant
Family) Uvae ursi folium (Pharmacopeial)
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Overview |
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Uva ursi is a trailing evergreen shrub indigenous to northern temperate
zones. It is now distributed throughout regions as diverse as the Iberian
peninsula, Europe, North America, Siberia, and the Himalayas. Uva ursi
flourishes in alpine coniferous forests, and it is widespread in the Scottish
Highlands. Like other members of the heath family, it thrives in humus-rich
soils.
This plant has a long history of medicinal use dating back to Galen around
the 2nd century A.D. The leaves (rather than the berries) of uva ursi were
frequently employed as an astringent, mild diuretic, and treatment for urinary
tract infections. Native Americans extolled its virtues for remedying
inflammation of the urinary tract, including cystitis. In 19th century America,
uva ursi was a popular therapy for painful urinary tract disorders. Until the
advent of sulfa drugs and antibiotics, uva ursi remained the treatment of choice
for bladder infections in the United States.
Pharmacological studies show unequivocally that uva ursi has bacteriostatic
properties. Structure-function studies reveal that arbutin, the chief active
compound in uva ursi, hydrolyzes in the intestinal tract to form hydroquinone.
The antiseptic and astringent effects of this plant are due to the hydroquinone
derivatives of arbutin. These compounds exhibit urinary antiseptic effects only
if the urine is alkaline. Maintaining an alkaline urine with uva ursi, however,
requires adherence to a strict diet of vegetables, potatoes, and nonacidic
fruits and juice.
A triterpenoid and flavonoid are responsible for diuretic activity, although
the diuretic action of this plant is actually minimal. Nonetheless, the research
findings as a whole provide a compelling pharmaceutical rationale for the
efficacy of uva ursi in treating various bladder and kidney infections.
Hydroquinone is potentially poisonous, however. Consequently, uva ursi should
be consumed in limited quantities and only for a duration of a few days. The
potential toxicity, in concert with dietary restrictions, places a limit on the
utilization of uva ursi as a practical drug for urinary tract infections.
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Macro Description |
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Uva ursi is adwarf, evergreen perennial that grows up to a elevations of
3,000 m. A single long, fibrous main root gives off short, creeping, red-brown
branches that coalesce in a dense mat. The small leaves are alternate, obovate
to spatulate, entire-margined, and broadened at the tips. The leaves have a
characteristic leathery texture with a dark green upperside. The underside is
defined by distinctive reticulate veins. The pink or white flowers are small and
bell-shaped, and appear in sparse terminal clusters that bloom in spring. The
fruits are shiny, bright red or pink globose pea-sized berries. Though edible,
they are sour to the taste. |
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Part Used/Pharmaceutical
Designations |
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Constituents/Composition |
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Flavonoids (e.g., myricetin, quercetin, plus their glycosides, including
hyperin, isoquercitrin, myricitrin, and quercitrin; iridoids (monotropein,
putatively asperuloside); quinones (principally arbutin and methyl-arbutin
[glycosides]); smaller amounts of piceoside, free hydroquinone, free
methoxyphenol; hydrolysable-type tannins; ellagic and gallic acids; terpenoids;
malic and quinic acids; allantoin; resin; volatile oil (trace);
wax. |
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Commercial
Preparations |
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Available as crushed leaf or powder preparations containing 400 to 840 mg
water-free arbutin per 10 to 12 g drug. |
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Medicinal
Uses/Indications |
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Traditional uses: Cystitis, urinary antiseptic, astringent, diuretic
Conditions: Infections and inflammatory conditions of the urinary tract
Clinical applications: Urinary antiseptic and astringent |
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Pharmacology |
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Most of the pharmacological investigations of uva ursi have centered on
arbutin. In several studies, however, whole-plant extracts were shown to exhibit
greater antibacterial action than arbutin alone. This presumably occurred
because arbutin, when administered as a single agent, is degraded in the
intestines before it can be absorbed. It cannot be converted into its active
aglycon form, hydroquinone, until it is absorbed intact from the intestinal
tract. Crude plant extracts may enhance the absorption of arbutin by inhibiting
cleavage of its glucosidase in the intestines before it can be metabolized.
In in vivo studies, uva ursi elicited antimicrobial activity against
Proteus vulgaris, Escherichia coli, Ureaplasma urealyticum, Mycoplasma hominis,
Staphylococcus aureus, Pseudomonas aeruginosa, Friedlander's pneumonia,
Enterococcus faecalis, Streptococcus strains, and Candida albicans.
The minimal inhibitory concentration calculated for arbutin against
microorganisms such as these is 0.4 to 0.8%. While these studies support the
urinary antiseptic activity of uva ursi, human research is needed to assess its
clinical benefits.
In other in vivo research, uva ursi produced anti-inflammatory effects in rat
paw edema tests. However, it had no effect on uterotonic activity in vitro.
In another study, hydroquinone was more cytotoxic to rat hepatoma cells than
agents like azauridin or colchicine, but less cytotoxic than valtrate from
valerian (Valeriana officinalis). |
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Dosage Ranges and Duration of
Administration |
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- Standard dose: 10 to 12 g crushed leaf or powder (400 to 840 mg
hydroquinone derivatives as water-free arbutin) daily
- Dry extract: 100 to 210 mg hydroquinone derivatives (as water-free
arbutin) daily to qid
- Fluid extract (1:1 g/ml): 3 ml (corresponding to 400 to 840 mg
arbutin) daily to qid
- Tincture (1:5): 3 ml tid to
qid
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Side
Effects/Toxicology |
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Uva ursi is considered generally safe when administered in standard
therapeutic dosages. Side effects have been reported, however, and include
irritability, motor restlessness, insomnia, nausea, vomiting, headaches, urinary
complaints, and tachycardia. Higher doses can lead to drug dependence and marked
elevations in cardiac arrhythmia. Excessive dosage can also cause inflammatory
and irritable conditions of the bladder and urinary tract mucous membranes. Uva
ursi may produce concomitant problems of hepatotoxicity, especially in children,
related to the release of hydroquinones during the metabolic conversion of
arbutin. |
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Warnings/Contraindications/Precautions |
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Uva ursi is contraindicated for lactating women because arbutin and
hydroquinone may be released into breast milk; further research is needed to
confirm that this actually occurs. Uva ursi is also contraindicated in pregnant
women and children under 12 years of age. The tannin levels in this plant may
predispose individuals with gastric sensitivity to nausea and vomiting.
Uva ursi should also be avoided by individuals with anxiety, hypertension,
glaucoma, impaired cerebral circulation, benign prostate tumor with residual
urine accumulation, pheochromocytoma (adrenal medulla or sympathetic paraganglia
tumor), and thyrotoxicosis (Graves' disease).
Long-term may be contraindicated because of the possible toxicity of
hydroquinone. Uva ursi tea is contraindicated for prolonged periods unless taken
under the supervision of a qualified health care provider. Preparations
containing arbutin should be limited to a maximum duration of one week for no
more than five times a year.
Because uva ursi is efficacious only in alkaline urine, persons taking oral
preparations of uva ursi should not consume highly acidic foods, including
acidic fruits and fruit juices. |
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Interactions |
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Dexamethasone;
Prednisolone
Uva ursi (100 mg/kg 50% methanolic extract po) increased the inhibitory
effect of prednisolone on picryl chloride-induced swelling in mice (Kubo et al.
1990). Arbutin, a compound isolated from the leaves of uva ursi, may be
responsible for the anti-inflammatory effects of this herb. In another mouse
study, arbutin (10 or 50 mg/kg) potentiated the effects of prednisolone and
dexamethasone on picryl chloride-induced contact dermatitis (Matsuda et al.
1990). Similar results were obtained with a water extract of uva ursi that also
enhanced the ability of dexamethasone ointment (0.005 or 0.025%) to inhibit
picryl-chloride-induced contact dermatitis in mice (Matsuda et al. 1992).
Indomethacin
Arbutin (50 mg/kg po) increased the anti-inflammatory activity of
indomethacin on picryl chloride-induced contact dermatitis, sheep red cell
delayed type hypersensitivity, carrageenin-induced edema, and adjuvant-induced
arthritis in mice (Matsuda et al. 1991). Clinical studies are needed to confirm
whether uva ursi could potentiate the effects of anti-inflammatory medications
in humans. |
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Regulatory and Compendial
Status |
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In Britain, uva ursi is an entry on the General Sale List, Schedule 2. It is
approved by the German Commission E and accepted for specified indications in
France. |
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References |
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Jahodar L, et al. Antimicrobial action and the extracts from the leaves of
Arctostaphylos uva-ursi in vitro. Cekoslov Farm. 1985;34:174-178.
Kubo M, Ito M, Nakata H, Matsuda H. Pharmacological studies on leaf of
arctostaphylos uva-ursi (L.) Spreng. I. Combined effect of 50% methanolic
extract from Arctostaphylos uva-ursi (L.) Spreng. (bearberry leaf) and
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Zasshi–J Pharm Soc Jpn.
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Matsuda H, Tanaka T, Kubo M. Pharmacological studies on leaf of
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indomethacin on immuno-inflammation. Yakugaku Zasshi.
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Copyright © 2000 Integrative Medicine
Communications This publication contains
information relating to general principles
of medical care that should not in any event be construed as specific
instructions for individual patients. The publisher does not accept any
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interactions, and contraindications before administering any drug, herb, or
supplement discussed herein. | |