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MIGLITOL

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Classification   |    Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

    A) Miglitol is an absorbable alpha-glucosidase inhibitor used in the management of type 2 diabetes mellitus. Miglitol is a desoxynojirimycin derivative that delays the digestion of ingested carbohydrates.

Specific Substances

    1) BAY-m-1099
    2) Miglitoli
    3) Miglitolum
    4) CAS 72432-03-2

Available Forms Sources

    A) FORMS
    1) Miglitol is available in the United States as 25, 50, and 100 mg film-coated tablets (Prod Info GLYSET(R) oral film coated tablet, 2010).
    B) USES
    1) Miglitol is used as an adjunct to diet and exercise to improve glycemic control in patients with type 2 diabetes mellitus (Prod Info GLYSET(R) oral film coated tablet, 2010).

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: Miglitol is used as an adjunct to diet and exercise to improve glycemic control in patients with type 2 diabetes mellitus.
    B) PHARMACOLOGY: By reversibly inhibiting alpha-glucoside hydrolase enzymes which are located in the brush border of the small intestine, miglitol delays the hydrolysis of ingested complex sugars. By slowing the breakdown of oligosaccharides and disaccharides into monosaccharides, this action slows the absorption of glucose into the bloodstream and thus reduces postprandial hyperglycemia. Miglitol has minor inhibitory activity against lactase but is not expected to cause lactose intolerance.
    C) TOXICOLOGY: Based on its mechanism of action, miglitol when administered alone should NOT cause hypoglycemia in the fasted or postprandial state. Miglitol given in combination with a sulfonylurea or insulin can cause a further lowering of blood glucose; it may increase the hypoglycemic potential of these agents.
    D) EPIDEMIOLOGY: Overdose is rare.
    E) WITH THERAPEUTIC USE
    1) COMMON: Flatulence, diarrhea, abdominal pain. OTHER EFFECTS: Nausea, vomiting, indigestion, low serum iron (not associated with reductions in hemoglobin or other hematologic indices). HYPOGLYCEMIA: Based on its mechanism of action, miglitol should NOT cause hypoglycemia when administered alone in the fasting or postprandial state. Miglitol when given in combination with sulfonylurea agents or insulin may cause a further lowering of blood glucose and increase the hypoglycemic potential of these medications.
    F) WITH POISONING/EXPOSURE
    1) Overdose data are limited. Miglitol overdose will not cause hypoglycemia. However, transient increases in flatulence, diarrhea, and abdominal discomfort may occur.
    0.2.20) REPRODUCTIVE
    A) Miglitol is classified as FDA pregnancy category B. In rat and rabbit studies, there was no evidence of teratogenicity; however, there was evidence of maternal and/or fetal toxicity. Miglitol is secreted in human milk to a limited degree.
    0.2.21) CARCINOGENICITY
    A) At the time of this review, the manufacturer does not report any carcinogenic potential in humans.

Laboratory Monitoring

    A) Monitor blood glucose if miglitol is taken in overdose along with another agent that can cause hypoglycemia (eg sulfonylureas or insulin).
    B) Monitor serum electrolytes in patients with significant vomiting and/or diarrhea.

Treatment Overview

    0.4.2) ORAL/PARENTERAL EXPOSURE
    A) MANAGEMENT OF MILD TO MODERATE TOXICITY
    1) Treatment is symptomatic and supportive. Miglitol alone does not cause hypoglycemia; however, concomitant administration of miglitol and other antidiabetic agents (eg, insulin, sulfonylureas) may increase the risk of hypoglycemia. Monitor blood glucose frequently in these patients.
    B) MANAGEMENT OF SEVERE TOXICITY
    1) Treatment is symptomatic and supportive. Severe toxicity is not expected after overdose of miglitol. Correct any significant fluid and/or electrolyte abnormalities in patients with severe diarrhea. Miglitol alone does not cause hypoglycemia; however, concomitant administration of miglitol and other antidiabetic agents (eg, insulin, sulfonylureas) may increase the risk of hypoglycemia. Monitor blood glucose frequently in these patients. Refer to "SULFONYLUREA AND RELATED AGENTS" for specific treatment information.
    C) DECONTAMINATION
    1) PREHOSPITAL: Severe toxicity is not expected, GI decontamination is generally not indicated unless other more toxic co-ingestants are involved.
    2) HOSPITAL: Severe toxicity is not expected, GI decontamination is generally not indicated unless other more toxic co-ingestants are involved.
    D) AIRWAY MANAGEMENTS
    1) Should not be required in these cases. COMBINATION OVERDOSE: The airway may need to be protected in patients with coma that persists after serum glucose correction.
    E) ANTIDOTE
    1) None.
    F) HYPOGLYCEMIA
    1) Miglitol alone does not cause hypoglycemia; however, concomitant administration of miglitol and other antidiabetic agents (eg, insulin, sulfonylureas) may increase the risk of hypoglycemia. Monitor blood glucose frequently in these patients. Intravenous dextrose will initially reverse hypoglycemia (if symptomatic or BS less 60 mg/dL; 50 mL of 50% dextrose in adults; in children 0.5 to 1 g/kg of 25% dextrose in water (D25W 2 to 4 mL/kg/dose)). Refer to "SULFONYLUREA AND RELATED AGENTS" for specific treatment information.
    G) ENHANCED ELIMINATION
    1) Severe toxicity is not expected therefore hemodialysis is not indicated. Miglitol has a protein binding of less than 4% and a volume of distribution of 0.18 L/kg (consistent with distribution primarily into the extracellular fluid). Theoretically, hemodialysis would be effective at clearing miglitol.
    H) PATIENT DISPOSITION
    1) HOME CRITERIA: A patient with an inadvertent exposure, that remains asymptomatic can be managed at home.
    2) OBSERVATION CRITERIA: Patients with a deliberate overdose, and those who are symptomatic, need to be monitored for several hours to assess electrolyte and fluid balance and gastrointestinal function. Patients that remain asymptomatic can be discharged.
    3) ADMISSION CRITERIA: Patients should be admitted for severe vomiting, profuse diarrhea, severe abdominal pain, dehydration, and electrolyte abnormalities.
    4) CONSULT CRITERIA: Consult a poison center or medical toxicologist for assistance in managing patients with severe toxicity or in whom the diagnosis is not clear.
    I) PITFALLS
    1) When managing a suspected miglitol overdose, the possibility of a coingestant(s) should be considered. Clinical manifestations of hypoglycemia can easily be mistaken for intoxication with ethanol or other substances of abuse.
    J) PHARMACOKINETICS
    1) Miglitol absorption is saturable at high doses (25 mg is completely absorbed whereas a dose of 100 mg is only 50 to 70% absorbed). Protein binding: Minimal (less than 4%). Vd: 0.18 L/kg (consistent with distribution primarily into the extracellular fluid). In studies with humans and animals, miglitol was not metabolized. Elimination half-life: approximately 2 hours. Excretion: 95% of the dose was recovered in the urine within 24 hours following a 25-mg dose.
    K) DIFFERENTIAL DIAGNOSIS
    1) In cases of combination overdose, consider any condition that can cause hypoglycemia including sulfonylurea overdose, starvation, alcoholism, insulinoma, or sepsis.

Range Of Toxicity

    A) TOXICITY: A minimum toxic dose has not been established. During one clinical trial, miglitol 200 mg 3 times daily improved glycemic control, but increased the incidence of gastrointestinal symptoms.
    B) THERAPEUTIC DOSE: ADULTS: INITIAL: 25 mg given orally 1 to 3 times daily. MAINTENANCE: After 4 to 8 weeks of initial therapy, 50 mg 3 times daily for approximately 3 months. MAXIMUM DOSE: 100 mg 3 times daily. CHILDREN: Safety and effectiveness of miglitol use in pediatric patients have not been established.

Clinical Effects

Summary Of Exposure

    A) USES: Miglitol is used as an adjunct to diet and exercise to improve glycemic control in patients with type 2 diabetes mellitus.
    B) PHARMACOLOGY: By reversibly inhibiting alpha-glucoside hydrolase enzymes which are located in the brush border of the small intestine, miglitol delays the hydrolysis of ingested complex sugars. By slowing the breakdown of oligosaccharides and disaccharides into monosaccharides, this action slows the absorption of glucose into the bloodstream and thus reduces postprandial hyperglycemia. Miglitol has minor inhibitory activity against lactase but is not expected to cause lactose intolerance.
    C) TOXICOLOGY: Based on its mechanism of action, miglitol when administered alone should NOT cause hypoglycemia in the fasted or postprandial state. Miglitol given in combination with a sulfonylurea or insulin can cause a further lowering of blood glucose; it may increase the hypoglycemic potential of these agents.
    D) EPIDEMIOLOGY: Overdose is rare.
    E) WITH THERAPEUTIC USE
    1) COMMON: Flatulence, diarrhea, abdominal pain. OTHER EFFECTS: Nausea, vomiting, indigestion, low serum iron (not associated with reductions in hemoglobin or other hematologic indices). HYPOGLYCEMIA: Based on its mechanism of action, miglitol should NOT cause hypoglycemia when administered alone in the fasting or postprandial state. Miglitol when given in combination with sulfonylurea agents or insulin may cause a further lowering of blood glucose and increase the hypoglycemic potential of these medications.
    F) WITH POISONING/EXPOSURE
    1) Overdose data are limited. Miglitol overdose will not cause hypoglycemia. However, transient increases in flatulence, diarrhea, and abdominal discomfort may occur.

Gastrointestinal

    3.8.2) CLINICAL EFFECTS
    A) GASTROENTERITIS
    1) WITH THERAPEUTIC USE
    a) Most adverse effects of miglitol are limited to the gastrointestinal tract secondary to carbohydrate malabsorption. The most common adverse effects are flatulence, diarrhea, abdominal pain or cramps, abdominal distension, and meteorism. Less frequent effects include nausea, vomiting and indigestion (Kingma et al, 1992; Samad et al, 1988; Scott & Tattersall, 1988; Johnston et al, 1994; Requejo et al, 1990).
    b) In placebo-controlled trials, the incidence of abdominal pain, diarrhea and flatulence were 11.7%, 28.7% and 41.5%, respectively (placebo results were 4.7%, 10.0% and 12.0%, respectively in 603 patients) in 962 patients treated with miglitol at doses of 25 to 100 milligrams three times daily (Prod Info GLYSET(R) oral film coated tablet, 2010).
    c) In a relatively large controlled study (n=192), gastrointestinal symptoms frequently occurred and appeared dose related (Johnston et al, 1994).
    1) Of the 192 volunteers, flatulence occurred most frequently in 48% and 60% of patients treated with 50 mg/day and 100 mg/day, respectively. Diarrhea occurred in 20% and 49% at respective doses and the incidence of abdominal pain were 8% and 19% (Johnston et al, 1994).
    2) Adverse symptoms resulting in discontinuation of therapy occurred in 5% of patients receiving 50 mg/day and 15% treated with 100 mg/day (Johnston et al, 1994).
    d) Symptoms of carbohydrate malabsorption (diarrhea, abdominal pain and flatulence) were more pronounced following an increase in dietary sucrose versus a high-starch diet (Lembcke et al, 1990).
    2) WITH POISONING/EXPOSURE
    a) Miglitol overdose may cause transient increases in flatulence, diarrhea, and abdominal discomfort (Prod Info GLYSET(R) oral film coated tablet, 2010).

Hepatic

    3.9.2) CLINICAL EFFECTS
    A) LIVER ENZYMES ABNORMAL
    1) WITH THERAPEUTIC USE
    a) LACK OF EFFECT: Although other alpha-glucosidase inhibitors (acarbose) have reported elevations in liver enzymes, short-term studies with miglitol indicate NO association with abnormal liver function studies (Prod Info GLYSET(R) oral film coated tablet, 2010).
    1) At the time of this review, NO elevations in serum transaminase levels have been reported (Johnston et al, 1994; Holt et al, 1988; Scott & Tattersall, 1988; Kingma et al, 1992; Kennedy & Gerich, 1987). However, no long-term studies have been conducted.

Hematologic

    3.13.2) CLINICAL EFFECTS
    A) ANEMIA
    1) WITH THERAPEUTIC USE
    a) Miglitol does appear to lower serum iron concentrations in some patients (9.2%) versus 4.2% in the placebo group; however, the effects were not associated with reductions in hemoglobin or other hematologic indices (Prod Info GLYSET(R) oral film coated tablet, 2010).
    b) In a small study (n=12), a decrease in hemoglobin by 5.8 g/L was reported, but did not result in drug discontinuation (Arends & Willms, 1986).

Endocrine

    3.16.2) CLINICAL EFFECTS
    A) HYPOGLYCEMIA
    1) WITH THERAPEUTIC USE
    a) Based on its mechanism of action, miglitol should NOT cause hypoglycemia when administered alone in the fasting or postprandial state. Miglitol when given in combination with sulfonylurea agents or insulin may cause a further lowering of blood glucose and increase the hypoglycemic potential of these medications (Prod Info GLYSET(R) oral film coated tablet, 2010).
    b) LACK OF EFFECTS: Hypoglycemic episodes were NOT reported during clinical studies with miglitol at therapeutic dose (Johnston et al, 1994; Kingma et al, 1992; Scott & Tattersall, 1988; Holt et al, 1988).
    c) POTENTIAL EFFECTS: In a small study (n=9) with healthy volunteers, however, miglitol produced a significant depression of post-peak blood glucose compared to placebo or acarbose (Joubert et al, 1990).

Reproductive

    3.20.1) SUMMARY
    A) Miglitol is classified as FDA pregnancy category B. In rat and rabbit studies, there was no evidence of teratogenicity; however, there was evidence of maternal and/or fetal toxicity. Miglitol is secreted in human milk to a limited degree.
    3.20.2) TERATOGENICITY
    A) LACK OF INFORMATION
    1) At the time of this review, the manufacturer does not report any teratogenic potential in humans (Prod Info GLYSET(R) oral tablets, 2009).
    B) ANIMAL STUDIES
    1) RATS: There was no evidence of fetal harm when rats were exposed to miglitol at doses up to 4 times the human exposure. Developmental toxicology studies performed in rats at doses of 50, 150, and 450 mg/kg (1.5, 4, and 12 times, respectively, the maximum recommended human exposure based on body surface area) revealed no evidence of fetal malformations attributable to miglitol (Prod Info GLYSET(R) oral tablets, 2009).
    2) RABBITS: There was no evidence of fetal harm when rabbits were exposed to miglitol at doses up to 3 times the human exposure. Miglitol doses of 10, 45, and 200 mg/kg (0.5, 3, and 10 times the human exposure, respectively) did not cause fetal malformations (Prod Info GLYSET(R) oral tablets, 2009).
    3.20.3) EFFECTS IN PREGNANCY
    A) LACK OF INFORMATION
    1) At the time of this review, the manufacturer does not report any potential effects of exposure to this agent during pregnancy in humans (Prod Info GLYSET(R) oral tablets, 2009).
    B) PREGNANCY CATEGORY
    1) The manufacturer has classified miglitol as FDA pregnancy category B (Prod Info GLYSET(R) oral tablets, 2009).
    C) ANIMAL STUDIES
    1) RATS: Doses of 450 mg/kg did promote maternal and/or fetal toxicity. There was a slight but significant reduction in fetal weight when pregnant rats were exposed to miglitol. In the peri-postnatal study in rats, the NOAEL (No Observed Adverse Effect Level) was 100 mg/kg (about 4 times the human exposure, based on body surface area). In the same rat study, there was an increase in stillborn progeny at 300 mg/kg. In the delivery portion of the rat developmental toxicity study, there was not an increase in stillbirths (Prod Info GLYSET(R) oral tablets, 2009).
    2) RABBITS: Doses of 200 mg/kg did promote maternal and/or fetal toxicity. There was a slight reduction in fetal weight, delayed ossification of the fetal skeleton, and increased frequency of nonviable fetuses (Prod Info GLYSET(R) oral tablets, 2009).
    3.20.4) EFFECTS DURING BREAST-FEEDING
    A) BREAST MILK
    1) Miglitol is secreted in human milk to a limited degree. Total excretion into milk accounted for 0.02% of a 100-mg maternal dose; estimated exposure to a nursing infant is approximately 0.4% of the maternal dose (Prod Info GLYSET(R) oral tablets, 2009).
    3.20.5) FERTILITY
    A) LACK OF INFORMATION
    1) At the time of this review, the manufacturer does not report any potential effects on fertility from exposure to this agent (Prod Info GLYSET(R) oral tablets, 2009).
    B) ANIMAL STUDIES
    1) RATS: A fertility study in Wistar rats treated with an oral miglitol dose of 300 mg/kg of body weight (approximately 8 times the maximum human exposure based on body surface area) did not indicate a negative effect on fertility or reproduction.(Prod Info GLYSET(R) oral tablets, 2009).

Carcinogenicity

    3.21.2) SUMMARY/HUMAN
    A) At the time of this review, the manufacturer does not report any carcinogenic potential in humans.
    3.21.4) ANIMAL STUDIES
    A) LACK OF EFFECT
    1) MICE: There was no evidence of carcinogenicity in mice that were given oral miglitol doses as high as approximately 500 mg/kg body weight (greater than 5 times the exposure in humans based on AUC) for 21 months (Prod Info GLYSET(R) oral tablets, 2009).
    2) RATS: There was no evidence of carcinogenicity in rats that were given miglitol (doses comparable to the exposure in humans based on AUC) in a 2-year study (Prod Info GLYSET(R) oral tablets, 2009)

Genotoxicity

    A) Miglitol was not mutagenic in the AMES test and the eukaryotic forward mutation assay (CHO/HGPRT). There was no evidence of clastogenic effects in vivo in the mouse micronucleus test or heritable mutations detected in dominant lethal assay (Prod Info GLYSET(R) oral tablets, 2009).

Laboratory Monitoring

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) Monitor blood glucose if miglitol is taken in overdose along with another agent that can cause hypoglycemia (eg sulfonylureas or insulin).
    B) Monitor serum electrolytes in patients with significant vomiting and/or diarrhea.

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 should be admitted for severe vomiting, profuse diarrhea, severe abdominal pain, dehydration, and electrolyte abnormalities.
    6.3.1.2) HOME CRITERIA/ORAL
    A) A patient with an inadvertent exposure, that remains asymptomatic can be managed at home.
    6.3.1.3) CONSULT CRITERIA/ORAL
    A) Consult a poison center or medical toxicologist for assistance in managing patients with severe toxicity or in whom the diagnosis is not clear.
    6.3.1.5) OBSERVATION CRITERIA/ORAL
    A) Patients with a deliberate overdose, and those who are symptomatic, need to be monitored for several hours to assess electrolyte and fluid balance and gastrointestinal function. Patients that remain asymptomatic can be discharged.

Monitoring

    A) Monitor blood glucose if miglitol is taken in overdose along with another agent that can cause hypoglycemia (eg sulfonylureas or insulin).
    B) Monitor serum electrolytes in patients with significant vomiting and/or diarrhea.

Oral Exposure

    6.5.1) PREVENTION OF ABSORPTION/PREHOSPITAL
    A) Severe toxicity is not expected, therefore GI decontamination is generally not necessary unless co-ingestants are involved.
    6.5.2) PREVENTION OF ABSORPTION
    A) SUMMARY: Severe toxicity is not expected, GI decontamination is generally not indicated unless other more toxic co-ingestants are involved.
    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) MONITORING OF PATIENT
    1) Monitor blood glucose in patients with concomitant overdose with miglitol along with sulfonylureas or insulin.
    2) Monitor serum electrolytes in patients with significant vomiting and/or diarrhea.
    B) HYPOGLYCEMIA
    1) MIGLITOL does NOT cause hypoglycemia (even in the fasted state), however, when combined with sulfonylurea agents or insulin, it may cause hypoglycemic symptoms (Prod Info GLYSET(R) oral film coated tablet, 2010).
    2) Miglitol inhibits the hydrolysis of sucrose to glucose and fructose. Oral glucose (dextrose or d-glucose; NOT sucrose) whose absorption is not inhibited by miglitol should be used in mild to moderate hypoglycemia. Intravenous glucose infusion or glucagon injection may be necessary in severe hypoglycemia (Prod Info GLYSET(R) oral film coated tablet, 2010).
    3) Monitor blood glucose hourly in symptomatic patients, those who may have been fasting and those with combined overdose with insulin or other oral hypoglycemic agents.

Enhanced Elimination

    A) HEMODIALYSIS
    1) Severe toxicity is not expected therefore hemodialysis is not indicated. .
    2) Miglitol has a protein binding of less than 4% and a volume of distribution of 0.18 L/kg (consistent with distribution primarily into the extracellular fluid) (Prod Info GLYSET(R) oral film coated tablet, 2010). Theoretically, hemodialysis would be effective in clearing miglitol.

Range Of Toxicity

Summary

    A) TOXICITY: A minimum toxic dose has not been established. During one clinical trial, miglitol 200 mg 3 times daily improved glycemic control, but increased the incidence of gastrointestinal symptoms.
    B) THERAPEUTIC DOSE: ADULTS: INITIAL: 25 mg given orally 1 to 3 times daily. MAINTENANCE: After 4 to 8 weeks of initial therapy, 50 mg 3 times daily for approximately 3 months. MAXIMUM DOSE: 100 mg 3 times daily. CHILDREN: Safety and effectiveness of miglitol use in pediatric patients have not been established.

Therapeutic Dose

    7.2.1) ADULT
    A) INITIAL: The recommended starting dose is 25 mg given orally 3 times daily at the start of each main meal. To minimize gastrointestinal effects, an initial dose of 25 mg once daily may be beneficial (Prod Info GLYSET(R) oral tablets, 2012).
    B) MAINTENANCE: 50 mg orally 3 times daily with meals; some patients may benefit from 100 mg 3 times daily. The maximum dose is 100 mg orally 3 times a day (Prod Info GLYSET(R) oral tablets, 2012).
    7.2.2) PEDIATRIC
    A) Safety and effectiveness of miglitol use in pediatric patients have not been established (Prod Info GLYSET(R) oral tablets, 2012).

Maximum Tolerated Exposure

    A) During one clinical trial, miglitol 200 mg 3 times daily improved glycemic control, but increased the incidence of gastrointestinal symptoms (Prod Info GLYSET(R) oral film coated tablet, 2010).

Physicochemical

Physical Characteristics

    A) Miglitol is a white to pale-yellow powder with solubility in water (Prod Info Glyset(R), miglitol, 2001).

Molecular Weight

    A) 207.2 (Prod Info Glyset(R), miglitol, 2001).

References

General Bibliography

    1) Arends J & Willms BHL: Smoothing effect of a new alpha-glucosidase inhibitor BAY m 1099 on blood glucose profiles of sulfonylurea-treated type II diabetic patients. Horm Metabol res 1986; 18:761-764.
    2) Chyka PA, Seger D, Krenzelok EP, et al: Position paper: Single-dose activated charcoal. Clin Toxicol (Phila) 2005; 43(2):61-87.
    3) Elliot CG, Colby TV, & Kelly TM: Charcoal lung. Bronchiolitis obliterans after aspiration of activated charcoal. Chest 1989; 96:672-674.
    4) FDA: Poison treatment drug product for over-the-counter human use; tentative final monograph. FDA: Fed Register 1985; 50:2244-2262.
    5) Golej J, Boigner H, Burda G, et al: Severe respiratory failure following charcoal application in a toddler. Resuscitation 2001; 49:315-318.
    6) Graff GR, Stark J, & Berkenbosch JW: Chronic lung disease after activated charcoal aspiration. Pediatrics 2002; 109:959-961.
    7) Harris CR & Filandrinos D: Accidental administration of activated charcoal into the lung: aspiration by proxy. Ann Emerg Med 1993; 22:1470-1473.
    8) Holt PR, Thea D, & Yang MY: Intestinal and metabolic responses to an alpha-glucosidase inhibitor in normal volunteers. Metabolism 1988; 37:1163-1170.
    9) Johnston PS, Coniff RF, & Hoogwerf BJ: Effects of the carbohydrase inhibitor miglitol in sulfonylurea-treated NIDDM patients. Diabetes Care 1994; 17:20-29.
    10) Joubert PH, Venter HL, & Foukaridis GN: The effect of miglitol and acarbose after an oral glucose load: A novel hypoglycemic mechanism?. Br J Clin Pharm 1990; 30:391-396.
    11) Kennedy FP & Gerich JE: A new alpha-glucosidase inhibitor (Bay-m-1099) reduces insulin requirements with meals in insulin-dependent diabetes mellitus. Clin Pharm Ther 1987; 42:455-458.
    12) Kingma PJ, Menheere P, & Sels JP: Alpha-glucosidase inhibition by miglitol in NIDDM patients. Diabetes Care 1992; 15:478-483.
    13) Lembcke B, Diederich M, & Folsch UR: Postprandial glycemic control, hormonal effects and carbohydrate malabsorption during long-term administration of the alpha-glucosidase inhibitor miglitol. Digestion 1990; 47:47-55.
    14) None Listed: Position paper: cathartics. J Toxicol Clin Toxicol 2004; 42(3):243-253.
    15) Pollack MM, Dunbar BS, & Holbrook PR: Aspiration of activated charcoal and gastric contents. Ann Emerg Med 1981; 10:528-529.
    16) Product Information: GLYSET(R) oral film coated tablet, miglitol oral film coated tablet. Pharmacia & Upjohn Co., New York, NY, 2010.
    17) Product Information: GLYSET(R) oral tablets, miglitol oral tablets. Pfizer (per FDA), New York, NY, 2012.
    18) Product Information: GLYSET(R) oral tablets, miglitol oral tablets. Pharmacia & Upjohn Company, New York, NY, 2009.
    19) Product Information: Glyset(R), miglitol. Bayer Corporation, West Haven, CT, 2001.
    20) Rau NR, Nagaraj MV, Prakash PS, et al: Fatal pulmonary aspiration of oral activated charcoal. Br Med J 1988; 297:918-919.
    21) Requejo F, Uttenthal LO, & Bloom SR: Effects of alpha-glucosidase inhibition and viscous fibre on diabetic control and postprandial gut hormone responses. Diabetic Med 1990; 7:515-520.
    22) Reuser AJJ & Wisselaar HA: An evaluation of the potential side-effects of alpha-glucosidase inhibitors used for the managEment of diabetes mellitus. Eur J Clin Inves 1994; 24(Suppl 3):19-24.
    23) Samad AHB, Ty Willing TS, George K, et al: Effects of BAYm 1099, new alpha-glucosidase inhibitor, on acute metabolic responses and metabolic control in NIDDM over 1 mo. Diabetes Care 1988; 11:337-344.
    24) Scott AR & Tattersall RB: Alpha glucosidase inhibition in the treatment on non-insulin-dependent diabetes mellitus. Diabetic Med 1988; 5:42-46.