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SAW PALMETTO

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Classification   |    Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

    A) Saw palmetto is an herbal product consisting of the partially dried, ripe fruit of Serenoa repens (Bartr.), a member of the family Palmae, and known to have anti-androgenic properties. It is most commonly used for the management of genitourinary problems and is used for the treatment of benign prostatic hypertrophy. The liposterolic extract of the fruit appears to be the active formulation in saw palmetto.

Specific Substances

    1) American dwarf palm
    2) Cabbage palm
    3) PA-109
    4) Permixon
    5) Sabal
    6) Sabal palmetto
    7) Sabal serrulata
    8) Serenoa repens
    9) Serenoa repens small

Available Forms Sources

    A) FORMS
    1) Saw palmetto is available as a berry extract tea, liquid extract from the berries, and as tablets or capsules containing a liposterolic extract of saw palmetto berries which are standardized to contain between 85% and 95% fatty acids and sterols. Tablets and capsules contain 80 mg of the berry extract ((Anon, 1998)) .
    B) SOURCES
    1) A liposterolic extract of Serenoa replens berries, standardized to contain between 85% and 95% fatty acids and sterols, is used in saw palmetto preparations ((Anon, 1998)).
    2) In Europe, the most studied form of saw palmetto is Permixon, which is a hexane extract of the American dwarf palm tree. The extract contains free (90%) and esterified (7%) fatty acids in addition to small amounts of sterols, polyprenic compounds, flavonoids and other substances (Gerber, 2000).
    C) USES
    1) In the early 1900's, saw palmetto was used as a mild diuretic and as a therapy for prostatic enlargement. Other traditional uses have been for the management of genitourinary problems, to increase sperm production, to increase breast size and stimulate lactation, and as a sexual stimulant. This product was included in the National Formulary of the United States from 1906 to 1950, before falling into disuse following World War II (Tyler, 1994; (Anon, 1998)).
    2) Currently, saw palmetto has found a niche in the short and long term treatment of benign prostatic hypertrophy, where it appears to increase urinary flow, reduces residual urine, increases ease in initiating micturition, and decreases urinary frequency (Tyler, 1994; Champault et al, 1984; Gerber et al, 1998; (Anon, 1998); Brown, 1995). It has been termed the "plant catheter" because of its effect on the bladder neck and the prostate in males ((Anon, 1998)).

Overview

Life Support

    A) This overview assumes that basic life support measures have been instituted.

Clinical Effects

    0.2.1) SUMMARY OF EXPOSURE
    A) USES: Saw palmetto is an herbal product consisting of the partially dried, ripe fruit of Serenoa repens (W. Bartram) Small, a member of the family Palmae, and known to have antiandrogenic properties. It is most commonly used for the management of genitourinary (ie, lower urinary tract symptoms) problems and the treatment of benign prostatic hypertrophy.
    B) PHARMACOLOGY: The liposterolic (ie, steroidal compounds and sitosterol) extract of the fruit appears to be the active formulation in saw palmetto. Although the mechanism for saw palmetto is not fully understood, it has been suggested that it inhibits 5 alpha-reductase, it has antiandrogenic effects, anti-inflammatory and anti-edema effects. It may also act to increase the metabolism and excretion of dihydrotestosterone by inhibition of cellular and nuclear receptor binding.
    C) EPIDEMIOLOGY: Saw palmetto is widely available over-the-counter. Use is common, but severe toxicity with saw palmetto intake is unlikely.
    D) WITH THERAPEUTIC USE
    1) ADVERSE EVENTS: COMMON: Adverse effects are usually mild; serious adverse events are not usually associated with saw palmetto. Gastrointestinal effects, including diarrhea, nausea, and abdominal pain are commonly observed.
    2) Other frequently reported events include: fatigue, headache, dizziness, rhinitis, dry mouth, tachycardia, angina, decreased libido and testicular pain.
    3) There have been infrequent reports of acute pancreatitis and liver injury following saw palmetto use.
    E) WITH POISONING/EXPOSURE
    1) Events are anticipated to be similar to adverse events reported with saw palmetto therapy. No known cases of overdose have been reported.
    0.2.20) REPRODUCTIVE
    A) Due to the estrogenic actions of saw palmetto, it should probably not be used during pregnancy.

Laboratory Monitoring

    A) Monitor vital signs in symptomatic patients.
    B) Routine laboratory studies are not necessary after overdose unless otherwise clinically indicated.

Treatment Overview

    0.4.2) ORAL/PARENTERAL EXPOSURE
    A) MANAGEMENT OF MILD TO MODERATE TOXICITY
    1) At the time of this review, saw palmetto is a widely used herbal product with limited reports of adverse events in human or animal studies. Significant toxicity is not expected after overdose. Treatment is symptomatic and supportive.
    B) MANAGEMENT OF SEVERE TOXICITY
    1) Treatment is symptomatic and supportive. Serious toxicity is not anticipated following saw palmetto only.
    C) DECONTAMINATION
    1) PREHOSPITAL: Decontamination is generally NOT required.
    2) HOSPITAL: Decontamination is generally NOT required. Consider activated charcoal in those with significant coingestants.
    D) AIRWAY MANAGEMENT
    1) Airway management is unlikely to be necessary following a saw palmetto exposure.
    E) ANTIDOTE
    1) None.
    F) PATIENT DISPOSITION
    1) HOME CRITERIA: An asymptomatic adult or child with an inadvertent minor exposure (eg, a single dietary supplement ingested by a young child) may be monitored at home.
    2) OBSERVATION CRITERIA: Patients with a deliberate self-harm ingestion should be evaluated in a healthcare facility and monitored for symptoms. Patients may be discharged to home, if no symptoms develop.
    3) ADMISSION CRITERIA: Patients with persistent symptoms should be admitted for further treatment.
    4) CONSULT CRITERIA: Contact a medical toxicologist or poison center for assistance in managing patients with severe toxicity or in whom the diagnosis is unclear. Patients with a deliberate self-harm ingestion should be evaluated by a mental health specialist.
    G) PHARMACOKINETICS
    1) Biological half-life of Serenoa repens, following a single 320 mg dose in volunteers, was reported to be 1.69 hours (range, 1.26 to 2.15 hours). Elimination half-life, following a single 320 mg dose in volunteers, was reported to be 1.9 hours. The mean peak plasma concentration following a single 320 mg dose of Serenoa repens in volunteers was 2.58 mcg/mL (range, 2.3 to 2.9 hours). Saw palmetto reportedly has both estrogenic and antiandrogenic effects via direct stimulation of estrogen receptors and inhibition of testosterone-5-alpha-reductase, it has been theorized that cholestatic hepatitis may result from known estrogenic and antiandrogenic effects.
    H) PITFALLS
    1) Saw palmetto is often taken in older men who may be on multiple medications and have significant comorbidities. Lack of adequate history to determine other coingestants.

Range Of Toxicity

    A) TOXICITY: No acute overdoses have been reported with saw palmetto. Adverse effects appear to be minor, as reported in clinical trials. In a randomized clinical trial, saw palmetto doses up to 960 mg daily (usual dose 320 mg/day) for an 18-month period did not result in any evidence of toxicity.
    B) ANIMAL DATA: In animal studies, LD50 values could not be determined. Doses greater than 50 g/kg in rats exhibited no adverse clinical effects.

Clinical Effects

Summary Of Exposure

    A) USES: Saw palmetto is an herbal product consisting of the partially dried, ripe fruit of Serenoa repens (W. Bartram) Small, a member of the family Palmae, and known to have antiandrogenic properties. It is most commonly used for the management of genitourinary (ie, lower urinary tract symptoms) problems and the treatment of benign prostatic hypertrophy.
    B) PHARMACOLOGY: The liposterolic (ie, steroidal compounds and sitosterol) extract of the fruit appears to be the active formulation in saw palmetto. Although the mechanism for saw palmetto is not fully understood, it has been suggested that it inhibits 5 alpha-reductase, it has antiandrogenic effects, anti-inflammatory and anti-edema effects. It may also act to increase the metabolism and excretion of dihydrotestosterone by inhibition of cellular and nuclear receptor binding.
    C) EPIDEMIOLOGY: Saw palmetto is widely available over-the-counter. Use is common, but severe toxicity with saw palmetto intake is unlikely.
    D) WITH THERAPEUTIC USE
    1) ADVERSE EVENTS: COMMON: Adverse effects are usually mild; serious adverse events are not usually associated with saw palmetto. Gastrointestinal effects, including diarrhea, nausea, and abdominal pain are commonly observed.
    2) Other frequently reported events include: fatigue, headache, dizziness, rhinitis, dry mouth, tachycardia, angina, decreased libido and testicular pain.
    3) There have been infrequent reports of acute pancreatitis and liver injury following saw palmetto use.
    E) WITH POISONING/EXPOSURE
    1) Events are anticipated to be similar to adverse events reported with saw palmetto therapy. No known cases of overdose have been reported.

Cardiovascular

    3.5.2) CLINICAL EFFECTS
    A) CONDUCTION DISORDER OF THE HEART
    1) WITH THERAPEUTIC USE
    a) In a saw palmetto clinical trial for treatment of benign prostatic hypertrophy, 305 patients completed the trial. Adverse effects were reported in 5% of patients and included tachycardia, angina pectoris, extrasystole, and angiopathy (Braeckman, 1994). Minor hypertension was reported as an adverse reaction (Plosker & Brogden, 1996). None of the reactions were serious.

Neurologic

    3.7.2) CLINICAL EFFECTS
    A) HEADACHE
    1) WITH THERAPEUTIC USE
    a) Headache was reported in clinical trials as a minor adverse effect (Champault et al, 1984; Plosker & Brogden, 1996).
    B) CENTRAL NERVOUS SYSTEM FINDING
    1) WITH THERAPEUTIC USE
    a) CNS adverse effects, reported in less than 5% of patients (n=305) in a clinical trial, included dizziness, fatigue, and insomnia (Braeckman, 1994). Adverse effects were not serious.

Gastrointestinal

    3.8.2) CLINICAL EFFECTS
    A) NAUSEA AND VOMITING
    1) WITH THERAPEUTIC USE
    a) Minor gastrointestinal symptoms, including abdominal pain, dry mouth, nausea and vomiting, have been reported following therapeutic use (McGuffin et al, 1997; Braeckman, 1994; Plosker & Brogden, 1996).
    b) INCIDENCE: In a meta-analysis review of clinical studies of saw palmetto in males, 1.3% of participants were reported to have gastrointestinal adverse effects (Wilt et al, 1998).
    c) INCIDENCE: In a clinical trial studying a twice daily dose of 160 mg Serenoa repens, with 305 patients completing, 25 (5%) experienced adverse effects to saw palmetto. Gastrointestinal symptoms, including gastritis, nausea, vomiting, constipation and diarrhea, were reported in 50% of these patients (Braeckman, 1994).
    B) DIARRHEA
    1) WITH THERAPEUTIC USE
    a) Diarrhea has been reported in a small number of patients as an adverse effect (Marks et al, 2000; Hung et al, 1998; Braeckman, 1994).
    C) ACUTE PANCREATITIS
    1) WITH THERAPEUTIC USE
    a) CASE REPORT: A 65-year-old man with a history of BPH, diabetes, hypertension, hyperlipidemia, gout, Barrett esophagitis and chronic gastritis developed acute pancreatitis after taking a saw palmetto herbal product (160 mg twice daily) for 1 week for urinary hesitancy. Lipase (2697 units/L {0 to 160 units/L}) and amylase (626 units/L {30 to 220 units/L}) were elevated; liver function tests and triglycerides were normal. A CT of the abdomen revealed an edematous pancreas without fluid collection consistent with early pancreatitis. An esophagogastroduodenoscopy was also performed due to the patient's history and showed antral gastritis but no new clinical findings. Signs and symptoms improved with supportive care and the patient was started on tamsulosin for urinary retention and advised to avoid saw palmetto. At follow-up one month later, clinical symptoms were completely resolved with normal amylase and lipase concentrations (Wargo et al, 2010).
    b) CASE REPORT: A 61-year-old man with benign prostatic hyperplasia and gastrointestinal reflux developed epigastric pain with nausea (up to 36 hours) prior to presentation. He had been taking saw palmetto for 3 years; other daily medications included lansoprazole and multivitamins. Serum amylase and lipase concentrations were elevated; liver function and a CBC were normal. A CT of the abdomen showed peripancreatic inflammatory changes consistent with acute pancreatitis. Following supportive care and pain management the patient recovered with normal pancreatic enzymes by day 4. The patient was advised to discontinue saw palmetto (Bruminhent et al, 2011).
    c) CASE REPORT: A 55-year-old man with benign prostatic hypertrophy and no history of cholelithiasis, developed severe non-radiating epigastric pain associated with nausea and vomiting following intermittent use of saw palmetto. Laboratory studies revealed a serum amylase of 2152 mmol/L and lipase 39,346 mmol/L and elevated liver enzymes. An abdominal ultrasound and magnetic resonance cholangiography revealed sludge without stones. Signs and symptoms acute pancreatitis and hepatitis improved following the withdrawal of saw palmetto. He had had two previous episodes of pancreatitis while taking saw palmetto in the preceding 14 months, both of which improved with discontinuation of saw palmetto. The patient remained well 8 months after complete abstinence (Jibrin et al, 2006).

Hepatic

    3.9.2) CLINICAL EFFECTS
    A) CHOLESTATIC HEPATITIS
    1) WITH THERAPEUTIC USE
    a) CASE REPORT: A 58-year-old man with symptoms of BPH developed acute liver damage after taking a commercially available preparation of saw palmetto (3 capsules/day {900 mg of dried extract and 660 mg of berry powder}) for approximately a week. At the time of admission, he complained of asthenia and severe right upper abdominal pain. Laboratory studies revealed elevated liver enzymes and virus markers were negative with the exception of a positive anti-CMV IgG. A further blood test was negative for CMV. All symptoms resolved over the next few weeks and laboratory studies returned to normal. Analysis of the saw palmetto tablets was positive for the herb only (ie, an absence of any other herb, or synthetic and/or chemical contaminants) (Lapi et al, 2010).
    b) CASE REPORT: After using an unreported dose of saw palmetto-containing product for 2 weeks for treatment of nocturia and urinary hesitancy, a 65-year-old man developed cholestatic hepatitis. He discontinued the herbal medication after the onset of jaundice and severe pruritus. Serum laboratory values on admission were as follows: bilirubin 8.2 mg/dL, AST 1238 IU/L, ALT 1364 IU/L, and alkaline phosphatase 179 IU/L. Liver biopsy, taken 2 months later, showed a parenchymal infiltrate of neutrophils and lymphocytes involving the portal tracts, early bridging, and mild periportal fibrosis. Liver function returned to normal 3 months after stopping saw palmetto (Hamid et al, 1997). Cholestasis may be a hormonal related incident due to the mechanism of action of saw palmetto.
    c) CASE REPORT: A 55-year-old man with BPH and no history of cholelithiasis, developed severe non-radiating epigastric pain associated with nausea and vomiting following intermittent use of saw palmetto. Laboratory studies revealed ALT 1232 Units/L, AST 1265 Units/L and ALP 185 Units/L and elevated serum amylase and lipase levels. A hepatic indole diacetic acid scan was negative. Signs and symptoms of acute hepatitis and pancreatitis improved following the withdrawal of saw palmetto. The patient remained well 8 months after complete abstinence (Jibrin et al, 2006).
    B) CHOLECYSTITIS
    1) WITH THERAPEUTIC USE
    a) Cholecystitis was reported as a severe adverse reaction in a patient receiving saw palmetto. The relation of the herbal medication to cholecystitis could not be causally established (Plosker & Brogden, 1996).

Genitourinary

    3.10.2) CLINICAL EFFECTS
    A) FUNCTIONAL DISORDER OF PENIS
    1) WITH THERAPEUTIC USE
    a) Erectile dysfunction was reported in 1.1% of men taking saw palmetto in a meta-analysis of saw palmetto treatment studies for males (Wilt et al, 1998a). Testicular pain and vesical tenesmus were reported in a small number of patients following therapeutic use of saw palmetto in a clinical trial (Braeckman, 1994).
    B) DISORDER OF PROSTATE
    1) WITH THERAPEUTIC USE
    a) Acute prostatitis was reported as a serious adverse event in a patient receiving saw palmetto therapy. A definite causal relationship could not be established (Plosker & Brogden, 1996).

Hematologic

    3.13.2) CLINICAL EFFECTS
    A) HEMORRHAGE
    1) WITH THERAPEUTIC USE
    a) CASE REPORT: Intraoperative hemorrhage (about 2000 cc of blood loss) was reported in a 53-year-old man who was taking saw palmetto. Prolonged bleeding time normalized over 5 days after discontinuing saw palmetto. Preoperative and postoperative PT and PTT were reported as normal. No other predisposing factors for hemorrhage were reported (Cheema et al, 2001). The authors speculated that the prolonged bleeding time was due to platelet dysfunction resulting from saw palmetto's inhibition of cyclooxygenase.

Dermatologic

    3.14.2) CLINICAL EFFECTS
    A) ITCHING OF SKIN
    1) WITH THERAPEUTIC USE
    a) Pruritus, which spontaneously cleared, has been reported as an adverse effect of saw palmetto (Grasso et al, 1995).

Musculoskeletal

    3.15.2) CLINICAL EFFECTS
    A) MUSCLE PAIN
    1) WITH THERAPEUTIC USE
    a) Muscle pain has been reported as a minor adverse effect in a small percentage of patients in clinical trials (Braeckman, 1994; Plosker & Brogden, 1996).

Reproductive

    3.20.1) SUMMARY
    A) Due to the estrogenic actions of saw palmetto, it should probably not be used during pregnancy.
    3.20.2) TERATOGENICITY
    A) ANIMAL STUDIES
    1) LACK OF EFFECT
    a) Animal studies conducted in Italy found no teratogenic effects with doses up to 600 mg/kg in rats ansd rabbits (USP,2000).
    3.20.3) EFFECTS IN PREGNANCY
    A) LACK OF INFORMATION
    1) Due to the estrogenic actions of saw palmetto, it should probably not be used during pregnancy.
    2) At the time of this review, no data were available to assess the potential effects of exposure to this agent during pregnancy or lactation.
    3.20.4) EFFECTS DURING BREAST-FEEDING
    A) LACK OF INFORMATION
    1) At the time of this review, no data were available to assess the potential effects of exposure to this agent during pregnancy or lactation.

Carcinogenicity

    3.21.3) HUMAN STUDIES
    A) CYTOTOXICITY
    1) Biologically active acylglycerides from the berries of saw palmetto were found to have borderline cytotoxicity against human prostatic (PC-3) cells (Shimada et al, 1997).

Laboratory Monitoring

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) Monitor vital signs in symptomatic patients.
    B) Routine laboratory studies are not necessary after overdose unless otherwise clinically indicated.
    4.1.2) SERUM/BLOOD
    A) BLOOD/SERUM CHEMISTRY
    1) Monitor electrolytes and fluid status as indicated in patients with vomiting or diarrhea.
    2) Monitor liver enzymes and lipase in patients with abdominal pain.
    4.1.4) OTHER
    A) OTHER
    1) MONITORING
    a) Monitor vital signs in all symptomatic patients.

Methods

    A) CHROMATOGRAPHY
    1) De Bernardi et al (1994) describe a validated high performance liquid chromatographic (HPLC) assay for the quantitative determination of Serenoa repens in human plasma. Sensitivity was reported equivalent to 0.01 mcg/mL.
    B) SPECTROSCOPY/SPECTROMETRY
    1) Electrospray ionization/mass spectrometry (ES-MS) technique is described by van Berkel et al (1998) for the detection of alcohols in mixtures of saw palmetto fruit extract. Spectroscopic methods are described by Shimada et al (1997) to study the components of Serenoa repens.

Treatment

Life Support

    A) Support respiratory and cardiovascular function.

Patient Disposition

    6.3.1) DISPOSITION/ORAL EXPOSURE
    6.3.1.1) ADMISSION CRITERIA/ORAL
    A) Patients with persistent symptoms should be admitted for further treatment.
    6.3.1.2) HOME CRITERIA/ORAL
    A) An asymptomatic adult or child with an inadvertent minor exposure (eg, a single dietary supplement ingested by a young child) may be monitored at home.
    6.3.1.3) CONSULT CRITERIA/ORAL
    A) Contact a medical toxicologist or poison center for assistance in managing patients with severe toxicity or in whom the diagnosis is unclear. Patients with a deliberate self-harm ingestion should be evaluated by a mental health specialist.
    6.3.1.5) OBSERVATION CRITERIA/ORAL
    A) Patients with a deliberate self-harm ingestion should be evaluated in a healthcare facility and monitored for symptoms. Patients may be discharged to home, if no symptoms develop.

Monitoring

    A) Monitor vital signs in symptomatic patients.
    B) Routine laboratory studies are not necessary after overdose unless otherwise clinically indicated.

Oral Exposure

    6.5.1) PREVENTION OF ABSORPTION/PREHOSPITAL
    A) SUMMARY
    1) Decontamination is generally NOT required. Consider gastric decontamination in symptomatic patients and those with significant coingestants.
    B) ACTIVATED CHARCOAL
    1) PREHOSPITAL ACTIVATED CHARCOAL ADMINISTRATION
    a) Consider prehospital administration of activated charcoal as an aqueous slurry in patients with a potentially toxic ingestion who are awake and able to protect their airway. Activated charcoal is most effective when administered within one hour of ingestion. Administration in the prehospital setting has the potential to significantly decrease the time from toxin ingestion to activated charcoal administration, although it has not been shown to affect outcome (Alaspaa et al, 2005; Thakore & Murphy, 2002; Spiller & Rogers, 2002).
    1) In patients who are at risk for the abrupt onset of seizures or mental status depression, activated charcoal should not be administered in the prehospital setting, due to the risk of aspiration in the event of spontaneous emesis.
    2) The addition of flavoring agents (cola drinks, chocolate milk, cherry syrup) to activated charcoal improves the palatability for children and may facilitate successful administration (Guenther Skokan et al, 2001; Dagnone et al, 2002).
    2) CHARCOAL DOSE
    a) Use a minimum of 240 milliliters of water per 30 grams charcoal (FDA, 1985). Optimum dose not established; usual dose is 25 to 100 grams in adults and adolescents; 25 to 50 grams in children aged 1 to 12 years (or 0.5 to 1 gram/kilogram body weight) ; and 0.5 to 1 gram/kilogram in infants up to 1 year old (Chyka et al, 2005).
    1) Routine use of a cathartic with activated charcoal is NOT recommended as there is no evidence that cathartics reduce drug absorption and cathartics are known to cause adverse effects such as nausea, vomiting, abdominal cramps, electrolyte imbalances and occasionally hypotension (None Listed, 2004).
    b) ADVERSE EFFECTS/CONTRAINDICATIONS
    1) Complications: emesis, aspiration (Chyka et al, 2005). Aspiration may be complicated by acute respiratory failure, ARDS, bronchiolitis obliterans or chronic lung disease (Golej et al, 2001; Graff et al, 2002; Pollack et al, 1981; Harris & Filandrinos, 1993; Elliot et al, 1989; Rau et al, 1988; Golej et al, 2001; Graff et al, 2002). Refer to the ACTIVATED CHARCOAL/TREATMENT management for further information.
    2) Contraindications: unprotected airway (increases risk/severity of aspiration) , nonfunctioning gastrointestinal tract, uncontrolled vomiting, and ingestion of most hydrocarbons (Chyka et al, 2005).
    6.5.2) PREVENTION OF ABSORPTION
    A) SUMMARY
    1) At the time of this review, clinical studies have reported no or mild adverse events following saw palmetto exposure. Gastrointestinal decontamination is generally NOT necessary. Consider decontamination in those with significant coingestants.
    B) ACTIVATED CHARCOAL
    1) CHARCOAL ADMINISTRATION
    a) Consider administration of activated charcoal after a potentially toxic ingestion (Chyka et al, 2005). Administer charcoal as an aqueous slurry; most effective when administered within one hour of ingestion.
    2) CHARCOAL DOSE
    a) Use a minimum of 240 milliliters of water per 30 grams charcoal (FDA, 1985). Optimum dose not established; usual dose is 25 to 100 grams in adults and adolescents; 25 to 50 grams in children aged 1 to 12 years (or 0.5 to 1 gram/kilogram body weight) ; and 0.5 to 1 gram/kilogram in infants up to 1 year old (Chyka et al, 2005).
    1) Routine use of a cathartic with activated charcoal is NOT recommended as there is no evidence that cathartics reduce drug absorption and cathartics are known to cause adverse effects such as nausea, vomiting, abdominal cramps, electrolyte imbalances and occasionally hypotension (None Listed, 2004).
    b) ADVERSE EFFECTS/CONTRAINDICATIONS
    1) Complications: emesis, aspiration (Chyka et al, 2005). Aspiration may be complicated by acute respiratory failure, ARDS, bronchiolitis obliterans or chronic lung disease (Golej et al, 2001; Graff et al, 2002; Pollack et al, 1981; Harris & Filandrinos, 1993; Elliot et al, 1989; Rau et al, 1988; Golej et al, 2001; Graff et al, 2002). Refer to the ACTIVATED CHARCOAL/TREATMENT management for further information.
    2) Contraindications: unprotected airway (increases risk/severity of aspiration) , nonfunctioning gastrointestinal tract, uncontrolled vomiting, and ingestion of most hydrocarbons (Chyka et al, 2005).
    6.5.3) TREATMENT
    A) SUPPORT
    1) In cases of saw palmetto overdose ingestions, treatment is SYMPTOMATIC and SUPPORTIVE. Severe toxicity is not anticipated following saw palmetto only; evaluate for coingestants.
    B) MONITORING OF PATIENT
    1) No routine laboratory studies are necessary unless otherwise clinically indicated.

Enhanced Elimination

    A) SUMMARY
    1) Enhanced elimination, including hemodialysis, is not anticipated to be necessary.

Range Of Toxicity

Summary

    A) TOXICITY: No acute overdoses have been reported with saw palmetto. Adverse effects appear to be minor, as reported in clinical trials. In a randomized clinical trial, saw palmetto doses up to 960 mg daily (usual dose 320 mg/day) for an 18-month period did not result in any evidence of toxicity.
    B) ANIMAL DATA: In animal studies, LD50 values could not be determined. Doses greater than 50 g/kg in rats exhibited no adverse clinical effects.

Therapeutic Dose

    7.2.1) ADULT
    A) DISEASE STATE
    1) BENIGN PROSTATIC HYPERTROPHY (BPH): The dose most commonly used in males to treat symptoms of BPH is 160 mg orally twice daily for 1 to 6 months (De Bernardi et al, 1994) Braekman, 1994; (Anon, 1998a; Grasso et al, 1995; Gerber et al, 1998; Plosker & Brogden, 1996). Generally within 6 to 8 weeks clinical results may be seen. Dosing with 320 mg once daily has also been advocated (De Bernardi et al, 1994). Onset of therapeutic effect has been reported to occur after 30 to 45 days (Braeckman, 1994). The dosage refers to mg of the plant extract administered.
    a) As a tincture, a dose of 1 to 2 mL orally 3 times daily has been suggested ((Hoffman, 1997)).
    b) RANDOMIZED CONTROL TRIAL: In a double-blind, multicenter, placebo-controlled randomized trial of 369 men aged 45 years or older with a peak urinary flow rate of at least 4 mL/s were treated with 1, 2 and 3 saw palmetto doses (320 mg/capsule) or placebo with dose increases at 24 and 48 weeks. Saw palmetto extract was found to be no more effective than placebo in reducing lower urinary tract symptoms. No adverse events attributable to saw palmetto were reported (Barry et al, 2011).
    B) DOSE EQUIVALENCY
    1) A dose of 320 mg of liposterolic extract is comparable to 3 grams of dried fruit (USP,2000).

Maximum Tolerated Exposure

    A) RANDOMIZED CONTROL TRIAL
    1) In a randomized control trial (Complementary and Alternative Medicine for Urological Symptoms {CAMUS trial}), 357 men were treated with ethanolic saw palmetto extract at 320 (usual daily dose), 640 and 960 mg daily or placebo. There was no evidence of toxicity at doses up to 3 times the usual dose for an 18-month period. Of the 8 patients that developed serious adverse events during the course of the study, none of these events could be associated or were related to saw palmetto use (Avins et al, 2008; Avins et al, 2013).

Toxicity Information

    7.7.1) TOXICITY VALUES
    A) LD50- (ORAL)RAT:
    1) > 50 g/kg (USP,2000)

Pharmacology Toxicology

Pharmacologic Mechanism

    A) The hexane extract of saw palmetto berries has been shown to have antiestrogenic and antiandrogenic properties through a direct action on the estrogen receptors and by inhibiting the enzyme testosterone-5-alpha-reductase (Champault et al, 1984; Di Silverio et al, 1998; Di Silverio et al, 1992; Iehle et al, 1995). Ravenna et al (1996) have shown a role for androgen receptors in mediating effects of saw palmetto in the prostatic cell line LNCaP (lymph node carcinoma of the prostate).
    1) Additionally, the extract has been shown to prevent the conversion of testosterone to dihydrotestosterone (DHT) as well as to inhibit DHT binding at the androgen receptors and 5-alpha-reductase activity on testosterone, both mechanisms thought to be influential in the management of benign prostatic hypertrophy (BPH) (Sultan et al, 1984; Iehle et al, 1995; Di Silverio et al, 1992). The metabolism and excretion of DHT is also increased.
    B) Hormonal effects were studied in men with benign prostatic hypertrophy (BPH) given saw palmetto for 3 months prior to operation. Results showed saw palmetto displayed an estrogenic and antiprogesterone effect as determined by estrogen and progesterone receptor activity in prostatic tissue, thus relieving voiding symptoms (Di Silverio et al, 1998).
    1) A decrease in epidermal growth factor (EGF) was also noted and was associated with DHT reduction. The authors speculate that reduction of DHT and EGF is involved with clinical improvement of obstructive symptoms of BPH during therapy with saw palmetto.
    C) Serum prostate-specific antigen (PSA) concentration is not modified by taking saw palmetto (Braeckman, 1994; Gerber et al, 1998; Gerber, 2000; Marks et al, 2000), thus reducing the chance of masking potential prostate cancer.
    D) Prostate epithelial contraction, particularly in the transition zone (p<0.01), was noted after 6 months of therapy with saw palmetto herbal blend in males with symptomatic benign prostatic hyperplasia. The authors noted that the mechanism of action appeared to be non-hormonal. No histological changes in carcinoma tissue were seen with saw palmetto herbal blend therapy (Marks et al, 2000).
    E) Saw palmetto extracts inhibit alpha 1 adrenergic receptors in a non-competitive, dose-dependent manner in vitro. Extract oils were more active than extract powders (Goepel et al, 1999).

Toxicologic Mechanism

    A) HEPATITIS - Since saw palmetto has estrogenic and antiandrogenic effects via direct stimulation of estrogen receptors and inhibition of testosterone-5-alpha-reductase, it has been theorized that cholestatic hepatitis may result from known estrogenic and antiandrogenic effects (Hamid et al, 1997).

Physicochemical

Physical Characteristics

    A) Saw palmetto capsules and tablets are the powdered, dried n-hexane lipidosterolic extract of the berries from Serenoa repens (Di Silverio et al, 1998; Shimada et al, 1997).

Molecular Weight

    A) Not available

References

General Bibliography

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