Available candidate vaccine viruses and potency testing reagents

Active ingredient

Global Influenza Surveillance and Response System (GISRS)
Phytoremediation of water bodies using selected aquatic macrophytes Numerical investigation into a new shape of metamaterials at optical Havrix Junior Monodose Vaccine. A challenge ahead to inclusive growth of India. Microanatomy of pars tuberalis and intermedia of pituitary gland in madras The appearance of hyperlinks does not constitute endorsement by the Defense Health Agency of non-U.

Utility Navigation Links

JANUVIA 100mg film-coated tablets

By , proportionately more young children were using fluoride toothpaste than were earlier cohorts 62, In addition, although professional interest in limiting the amount of fluoride toothpaste delivered to young children and supervising their toothbrushing was expressed earlier in the s 65 , only during the early s was this approach adopted broadly as a public health measure 66 , which was too late to alter the risk for fluorosis among the year age cohort in NHANES No clear explanation exists why fluorosis was more severe among non-Hispanic black children than among non-Hispanic white or Mexican-American children.

This observation has been reported elsewhere , and different hypotheses have been proposed, including biologic susceptibility or greater fluoride intake Anterior teeth were less affected by enamel fluorosis than were posterior teeth.

This finding also was reported in the NIDR survey 71 and has been attributed to cohort effects, attrition, or a combination of the smaller anatomical surface and longer formation time of posterior teeth compared with anterior teeth 18, Further research also is needed to improve public health surveillance of fluoride exposure. The difficulties observed in comparing data from the NIDR and NHANES surveys and the time lapse between exposure and clinical presentation suggest the need for new and more timely methods to measure total fluoride exposure.

Methods such as fingernail analysis and urinary fluoride excretion have shown promise, but only with limited samples. Research in these areas could result in the development of valid and reliable techniques to monitor total fluoride exposure in children, allowing adjustment in public health practice and recommendations to reduce the cosmetic consequences of fluoride exposure while preventing and controlling dental caries.

Epidemiologic data from Australia indicate that targeting reduction in discretionary intake of supplements and toothpaste can reduce the prevalence of enamel fluorosis Information is not available to evaluate the effects of these changes in the United States after they were implemented in the early s. Increased efforts are needed to disseminate published recommendations about appropriate use of fluoride to health professionals and the public.

This report documents improvements in the oral health of the civilian, U. The report documented important differences in disease prevalence and severity by sociodemographic characteristics that public health officers, the dental profession, and the community should consider in implementing interventions to prevent and control disease and to reduce the disparities observed.

The following is a list of seven important findings in this report:. The authors thank former members of the U. Dushanka Kleinman and Dr. We would also like to thank Dr. Finally, our thanks to Dr. Mean number of decayed and filled surfaces in primary teeth Sum of individual dfs values divided by the population. MT Number of missing permanent teeth due to caries or periodontal disease does not count teeth extracted for reasons other than caries or periodontal disease.

FT Number of filled permanent teeth teeth with carious lesions decayed teeth that have been restored. Missing teeth are excluded because in adults, some missing teeth may have been lost due to reasons other than caries, including periodontal diseases and extracted for prosthetic reasons. DS Number of decayed surfaces in permanent teeth. MS Number of missing tooth surfaces due to caries or periodontal disease does not count surfaces of teeth extracted for reasons other than caries or periodontal disease.

FS Number of filled surfaces in permanent teeth carious surfacesdecayedthat have been restored. Missing surfaces are excluded because in adults, some missing teeth might have been lost because of reasons other than caries, including periodontal diseases and extracted for prosthetic reasons.

Mean number of decayed, missing due to disease , and filled surfaces in permanent teeth Sum of individual DMFS values divided by the population.

Mean number of decayed, missing due to disease , and filled teeth Sum of individual DMFT values divided by the population. Dental fluorosis See enamel fluorosis. Dental sealants Also called pit-and-fissure sealants, these are thin plastic coatings that are applied to pits and fissures in teeth to prevent decay. Dentate Having one or more natural permanent tooth present in the mouth excluding third molars. Edentulous Having no natural permanent teeth in the mouth excluding third molars.

Also called complete tooth loss or edentulism. Enamel fluorosis A hypomineralization of enamel, characterized by greater surface and subsurface porosity than normal enamel caused by fluoride ingestion during periods of tooth development first 6 years of life for most permanent teeth.

FPL Federal poverty level. Federal poverty thresholds are defined by the U. Census Bureau based on family income and size of family.

A series of surveys fielded by the National Center for Health Statistics. Root caries Tooth decay in the tooth root that it is exposed to the oral environment because of gum recession this part of the tooth that is normally below the gums in a healthy mouth.

Use of trade names and commercial sources is for identification only and does not imply endorsement by the U. Department of Health and Human Services. CDC is not responsible for the content of pages found at these sites. This conversion may have resulted in character translation or format errors in the HTML version. An original paper copy of this issue can be obtained from the Superintendent of Documents, U. Contact GPO for current prices. Reliability of Examinations Dental examiners were calibrated periodically by the survey's reference dental examiner.

Diagnostic Criteria A list of terms and abbreviations is included to facilitate the reading and interpretation of the diagnostic criteria and results. Discussion Dental Caries Dental caries and tooth loss were among the most common causes for rejection of young men from military service during the Civil War and the two World Wars Dental Sealants Dental sealants are highly effective in preventing dental caries that occur on the surfaces of teeth that have pits and fissures.

Tooth Retention and Edentulism The findings in this report indicate that the prevalence of tooth loss continues to decline in the United States and provides further evidence that edentulism is not inevitable with advanced age.

Enamel Fluorosis Enamel fluorosis is a hypomineralization of enamel, characterized by greater surface and subsurface porosity than normal enamel, and is related to fluoride ingestion during periods of tooth development by young children 55 first 6 years of life for most permanent teeth.

Conclusions This report documents improvements in the oral health of the civilian, U. The following is a list of seven important findings in this report: The decline in the prevalence and severity of dental caries in permanent teeth, reported in previous national surveys, continued during and It has benefited children, adolescents, and adults.

A notable proportion of untreated tooth decay was observed across all age groups and sociodemographic characteristics. No reductions were observed in the prevalence and severity of dental caries in primary teeth.

The use of dental sealants among children and adolescents increased substantially. This increase was probably the result of both public and private efforts and denotes a continuing interest in using dental sealants for the prevention of tooth decay. Older adults are retaining more of their teeth and fewer are losing all their teeth. Prevalence of enamel fluorosis has increased in cohorts born since This increase should be evaluated in the context of total fluoride exposure.

Recommendations for Public Health Action Appropriate public health interventions to prevent dental caries should extend to all age groups and sociodemographic categories. Factors related to the lack of reduction of dental caries in primary teeth need to be studied. Programs designed to promote oral health e. Timely surveillance tools are needed to monitor fluoride exposure from multiple sources.

Acknowledgments The authors thank former members of the U. A coefficient of agreement for nominal scales. Educ Psychol Meas ; Percent agreement, Pearson's correlation and kappa as measures of inter-examiner reliability. J Dent Res ;5: J Dent Res in press. Criteria for diagnosis of dental caries.

American Dental Association; Studies on dental caries: Dental status and dental needs of elementary school children.

Public Health Rep ; A measurement of dental caries prevalence and treatment service for deciduous teeth. J Dent Res ; Coronal caries in the primary and permanent dentition of children and adolescents years of age: Coronal and root caries in the dentition of adults in the United States, The prevalence of dental sealants in the US population: Tooth retention and tooth loss in the permanent dentition of adults: The investigation of physiological effects by the epidemiological method.

Fluoride and dental health. American Association for the Advancement of Science; The differential diagnosis of fluoride and non-fluoride enamel opacities. Oral health of United States children. The national survey of dental caries in U.

National and regional findings. US Public Health Service; National Health and Nutrition Examination Survey, Age adjustment using the projected U. National Center for Health Statistics; Healthy People Statistics Notes. Schenker N, Gentleman JF. On judging the significance of differences by examining the overlap between confidence intervals.

Prevalence and trends in enamel fluorosis in the United States from the s and s. J Am Dent Assoc ; Oral health status in the United States: J Dent Edu ; Decayed, missing, and filled teeth in adults, United States, Decayed, missing, and filled teeth among children, United States.

HSM , Series 11, No. Decayed, missing, and filled teeth among youths years, United States. HRA , Series 11, No. The prevalence of dental caries in United States children, Oral health of United States adults.

The national survey of oral health in U. The future of the caries decline. J Public Health Dent ; Trends in caries prevalence in North American children. Int Dent J ;44 4 Suppl 1: Caries prevalence in the United Kingdom. Trends in dental care among insured Americans: Estimating rates of new root caries in older adults.

Oral health in America: Relationship between smoking and dental status in , , , and year-old individuals. J Clin Periodontol ; Tobacco use and oral disease. J Dent Educ ; Ten-year cross-sectional and incidence study of coronal and root caries and some related factors in elderly Swedish individuals. National Institutes of Health. Consensus development conference statement on dental sealants in the prevention of tooth decay.

Factors influencing the effectiveness of sealantsa meta analysis. Community Dent Oral Epidemiol ; Task Force on Community Preventive Services. Recommendations on selected interventions to prevent dental caries, oral and pharyngeal cancers, and sport-related craniofacial injuries.

Am J Prev Med ;23 1 Suppl: Comparing the costs of three sealant delivery strategies. Impact of targeted, school-based dental sealant programs in reducing racial and economic disparities in sealant prevalence among schoolchildrenOhio, Measuring oral health and quality of life. Risk factors for total tooth loss in the United States; longitudinal analysis of national data. Surveillance for use of preventive health-care services by older adults, Public health and aging: The impact of edentulousness on food and nutrient intake.

The impact of oral health on stated ability of eat certain food; findings from the National Diet and Nutrition Survey of Older People in Great Britain. Intake of non-starch polysaccharide dietary intake in edentulous and dentate persons: Br Dent J ; How dentition status and masticatory function affect nutrient intake.

The impact of dental status on diet, nutrition and nutritional status in U. University of London; The relationship among dental status, nutrient intake, and nutritional status in older people.

Association of edentulism and diet and nutrition in US adults. The relationship between oral health status and body mass index among older people: Shortened dental arches and oral function. J Oral Rehab ;8: Agerberg G, Carlsson GE.

Chewing ability in relation to dental and general health: Acta Odont Scand ; An oral health strategy for England. Department of Health; The nature and mechanisms of dental fluorosis in man. Risk of enamel fluorosis associated with fluoride supplementation, infant formula, and fluoride dentifrice use.

Am J Epidemiol ; Use of fluoride supplementation by children living in fluoridated communities. Risk factors for enamel fluorosis in a fluoridated population. Risk factors for enamel fluorosis in a nonfluoridated population. Risk factors for enamel fluorosis in optimally fluoridated children born after the US manufacturers' decision to reduce the fluoride concentration of infant formula. Fluorosis risk from early exposure to fluoride toothpaste. Trends in childhood use of dental care products containing fluoride: Advance data from vital and health statistics.

Factors associated with the use of fluoride supplements and fluoride dentifrice by infants and toddlers. Fluorides and dental caries. Findings from the dental care supplement of the National Health Interview Survey, J Am Dental Assoc ; Recommendations for using fluoride to prevent and control dental caries in the United States.

Dental fluorosis in Grand Rapids during the seventeenth year of fluoridation. Community water fluoride levels, preschool dietary patterns, and the occurrence of fluoride enamel opacities. Describing the severity of mottling in a community: Fluoride exposure and dental fluorosis in Newsburgh and Kingston, New York: Esthetically objectionable fluorosis attributed to water fluoridation. Nail and bone surface as biomarkers for acute fluoride exposure in rats. J Analytical Toxicol ; Fingernails and toenails as biomarkers of subchronic exposure to fluoride from dentifrice in 2- and 3-year-old children.

Monitoring of renal fluoride excretion in community preventive programmes on oral health. World Health Organization; Urinary fluoride excretion by children years old in a south Texas community. Pan Am J Public Health ;7: Urinary fluoride excretion in Jamaica in relation to fluoridated salt.

Dental fluorosis decline after changes to supplement and toothpaste regimes. Terms and Abbreviations Used in the Report Caries experience. Having decayed, missing, or filled teeth or tooth surfaces because of caries. A dental caries lesion that has passed the stage of remineralization and progressed to loss of tissue integrity, forming a cavity. Decayed, missing, or filled surfaces located in the part of the tooth that is normally above the gum line.

A disease manifested by loss of the mineral content of the tooth hard tissues demineralization. Dental caries is the disease that causes tooth decay. Prevalence of caries experience in permanent teeth. Proportion of population with one or more decayed, missing, or filled permanent tooth surfaces DMFS. Prevalence of caries experience in primary teeth. Proportion of the population with one or more decayed or filled primary tooth surfaces dfs.

By definition and calculation, this is equal to the proportion with one or more decayed or filled primary teeth dft. Prevalence of untreated tooth decay in permanent tooth. Proportion of the population with one or more permanent tooth surfaces with untreated decay DS. By definition and calculation, this is equal to the proportion with one teeth or more decayed permanent teeth DT.

In patients with type 2 diabetes with hyperglycaemia, these changes in insulin and glucagon levels lead to lower haemoglobin A 1c HbA 1c and lower fasting and postprandial glucose concentrations. The glucose-dependent mechanism of sitagliptin is distinct from the mechanism of sulphonylureas, which increase insulin secretion even when glucose levels are low and can lead to hypoglycaemia in patients with type 2 diabetes and in normal subjects.

Sitagliptin is a potent and highly selective inhibitor of the enzyme DPP-4 and does not inhibit the closely-related enzymes DPP-8 or DPP-9 at therapeutic concentrations. In a two-day study in healthy subjects, sitagliptin alone increased active GLP-1 concentrations, whereas metformin alone increased active and total GLP-1 concentrations to similar extents. Co-administration of sitagliptin and metformin had an additive effect on active GLP-1 concentrations.

Sitagliptin, but not metformin, increased active GIP concentrations. Overall, sitagliptin improved glycaemic control when used as monotherapy or in combination treatment see Table 2. Two studies were conducted to evaluate the efficacy and safety of sitagliptin monotherapy. Treatment with sitagliptin at mg once daily as monotherapy provided significant improvements in HbA 1c , fasting plasma glucose FPG , and 2-hour post-prandial glucose 2-hour PPG , compared to placebo in two studies, one of and one of weeks duration.

The observed incidence of hypoglycaemia in patients treated with sitagliptin was similar to placebo. Body weight did not increase from baseline with sitagliptin therapy in either study, compared to a small reduction in patients given placebo. Sitagliptin mg once daily provided significant improvements in glycaemic parameters compared with placebo in two week studies of sitagliptin as add-on therapy, one in combination with metformin and one in combination with pioglitazone.

Change from baseline in body weight was similar for patients treated with sitagliptin relative to placebo. In these studies there was a similar incidence of hypoglycaemia reported for patients treated with sitagliptin or placebo. A week placebo-controlled study was designed to evaluate the efficacy and safety of sitagliptin mg once daily added to glimepiride alone or glimepiride in combination with metformin. The addition of sitagliptin to either glimepiride alone or to glimepiride and metformin provided significant improvements in glycaemic parameters.

Patients treated with sitagliptin had a modest increase in body weight compared to those given placebo. A week placebo-controlled study was designed to evaluate the efficacy and safety of sitagliptin mg once daily added to the combination of pioglitazone and metformin. The addition of sitagliptin to pioglitazone and metformin provided significant improvements in glycaemic parameters. The incidence of hypoglycaemia was also similar in patients treated with sitagliptin or placebo.

A week placebo-controlled study was designed to evaluate the efficacy and safety of sitagliptin mg once daily added to insulin at a stable dose for at least 10 weeks with or without metformin at least 1, mg. In patients taking pre-mixed insulin, the mean daily dose was The addition of sitagliptin to insulin provided significant improvements in glycaemic parameters.

There was no meaningful change from baseline in body weight in either group. In a week placebo-controlled factorial study of initial therapy, sitagliptin 50 mg twice daily in combination with metformin mg or 1, mg twice daily provided significant improvements in glycaemic parameters compared with either monotherapy.

The decrease in body weight with the combination of sitagliptin and metformin was similar to that observed with metformin alone or placebo; there was no change from baseline for patients on sitagliptin alone. The incidence of hypoglycaemia was similar across treatment groups. The mean dose of metformin was approximately 1, mg per day. The reduction in HbA 1c from mean baseline values of 7. The overall incidence of gastrointestinal adverse reactions considered as drug-related in patients treated with sitagliptin was 2.

The incidence of hypoglycaemia was not significantly different between the treatment groups sitagliptin, 1. Body weight decreased from baseline in both groups sitagliptin, In a study comparing the efficacy and safety of the addition of sitagliptin mg once daily or glipizide a sulphonylurea in patients with inadequate glycaemic control on metformin monotherapy, sitagliptin was similar to glipizide in reducing HbA 1c.

However, more patients in the sitagliptin group discontinued due to lack of efficacy than in the glipizide group. Patients treated with sitagliptin exhibited a significant mean decrease from baseline in body weight compared to a significant weight gain in patients administered glipizide In this study, the proinsulin to insulin ratio, a marker of efficiency of insulin synthesis and release, improved with sitagliptin and deteriorated with glipizide treatment.

The incidence of hypoglycaemia in the sitagliptin group 4. A week placebo-controlled study involving patients was designed to evaluate the insulin-sparing efficacy and safety of sitagliptin mg once daily added to insulin glargine with or without metformin at least 1, mg during intensification of insulin therapy.

Baseline HbA 1c was 8. Patients were instructed to titrate their insulin glargine dose based on fingerstick fasting glucose values. The reduction in HbA 1c in patients treated with sitagliptin and insulin with or without metformin was The incidence of hypoglycaemia was The difference was mainly due to a higher percentage of patients in the placebo group experiencing 3 or more episodes of hypoglycaemia 9.

There was no difference in the incidence of severe hypoglycaemia. A study comparing sitagliptin at 25 or 50 mg once daily to glipizide at 2. After 54 weeks, the mean reduction from baseline in HbA 1c was In this study, the efficacy and safety profile of sitagliptin at 25 or 50 mg once daily was generally similar to that observed in other monotherapy studies in patients with normal renal function.

The incidence of hypoglycaemia in the sitagliptin group 6. There was also a significant difference between groups with respect to change from baseline body weight sitagliptin Another study comparing sitagliptin at 25 mg once daily to glipizide at 2. In this study, the efficacy and safety profile of sitagliptin at 25 mg once daily was generally similar to that observed in other monotherapy studies in patients with normal renal function.

The incidence of hypoglycaemia was not significantly different between the treatment groups sitagliptin, 6. In addition, after 12 weeks, the mean reductions in HbA 1c sitagliptin Over the course of the study, the overall estimated mean SD difference in HbA 1c between the sitagliptin and placebo groups was 0. The primary cardiovascular endpoint was a composite of the first occurrence of cardiovascular death, nonfatal myocardial infarction, nonfatal stroke, or hospitalization for unstable angina.

Secondary cardiovascular endpoints included the first occurrence of cardiovascular death, nonfatal myocardial infarction, or nonfatal stroke; first occurrence of the individual components of the primary composite; all-cause mortality; and hospital admissions for congestive heart failure. After a median follow up of 3 years, sitagliptin, when added to usual care, did not increase the risk of major adverse cardiovascular events or the risk of hospitalization for heart failure compared to usual care without sitagliptin in patients with type 2 diabetes Table 3.

Cardiovascular death, nonfatal myocardial infarction, nonfatal stroke, or hospitalization for unstable angina. For composite endpoints, the p-values correspond to a test of non-inferiority seeking to show that the hazard ratio is less than 1. For all other endpoints, the p-values correspond to a test of differences in hazard rates.

The European Medicines Agency has deferred the obligation to submit the results of studies with Januvia in one or more subsets of the paediatric population in type 2 diabetes mellitus see section 4. Following oral administration of a mg dose to healthy subjects, sitagliptin was rapidly absorbed, with peak plasma concentrations median T max occurring 1 to 4 hours post-dose, mean plasma AUC of sitagliptin was 8.

Since co-administration of a high-fat meal with sitagliptin had no effect on the pharmacokinetics, Januvia may be administered with or without food. Plasma AUC of sitagliptin increased in a dose-proportional manner. Dose-proportionality was not established for C max and C 24hr C max increased in a greater than dose-proportional manner and C 24hr increased in a less than dose-proportional manner. The mean volume of distribution at steady state following a single mg intravenous dose of sitagliptin to healthy subjects is approximately litres.

Sitagliptin is primarily eliminated unchanged in urine, and metabolism is a minor pathway. Six metabolites were detected at trace levels and are not expected to contribute to the plasma DPP-4 inhibitory activity of sitagliptin. Sitagliptin accumulates only minimally with multiple doses.

Elimination of sitagliptin occurs primarily via renal excretion and involves active tubular secretion. Sitagliptin is a substrate for human organic anion transporter-3 hOAT-3 , which may be involved in the renal elimination of sitagliptin. The clinical relevance of hOAT-3 in sitagliptin transport has not been established. Sitagliptin is also a substrate of p-glycoprotein, which may also be involved in mediating the renal elimination of sitagliptin.

However, ciclosporin, a p-glycoprotein inhibitor, did not reduce the renal clearance of sitagliptin. In a clinical study sitagliptin had a small effect on plasma digoxin concentrations indicating that sitagliptin may be a mild inhibitor of p-glycoprotein.

The pharmacokinetics of sitagliptin were generally similar in healthy subjects and in patients with type 2 diabetes. A single-dose, open-label study was conducted to evaluate the pharmacokinetics of a reduced dose of sitagliptin 50 mg in patients with varying degrees of chronic renal impairment compared to normal healthy control subjects.

The study included patients with mild, moderate, and severe renal impairment, as well as patients with ESRD on haemodialysis. In addition, the effects of renal impairment on sitagliptin pharmacokinetics in patients with type 2 diabetes and mild, moderate, or severe renal impairment including ESRD were assessed using population pharmacokinetic analyses.

Compared to normal healthy control subjects, plasma AUC of sitagliptin was increased by approximately 1. Because increases of this magnitude are not clinically relevant, dosage adjustment in these patients is not necessary. Sitagliptin was modestly removed by haemodialysis No dose adjustment is required based on age. Age did not have a clinically meaningful impact on the pharmacokinetics of sitagliptin based on a population pharmacokinetic analysis of Phase I and Phase II data.

No dose adjustment is necessary based on gender, race, or body mass index BMI. These characteristics had no clinically meaningful effect on the pharmacokinetics of sitagliptin based on a composite analysis of Phase I pharmacokinetic data and on a population pharmacokinetic analysis of Phase I and Phase II data.

Renal and liver toxicity were observed in rodents at systemic exposure values 58 times the human exposure level, while the no-effect level was found at 19 times the human exposure level. Incisor teeth abnormalities were observed in rats at exposure levels 67 times the clinical exposure level; the no-effect level for this finding was fold based on the week rat study.

The relevance of these findings for humans is unknown. In addition, very slight to slight skeletal muscle degeneration was also observed histologically at doses resulting in systemic exposure levels of approximately 23 times the human exposure level. A no-effect level for these findings was found at an exposure 6-fold the clinical exposure level.

Sitagliptin has not been demonstrated to be genotoxic in preclinical studies. Sitagliptin was not carcinogenic in mice. In rats, there was an increased incidence of hepatic adenomas and carcinomas at systemic exposure levels 58 times the human exposure level. Since hepatotoxicity has been shown to correlate with induction of hepatic neoplasia in rats, this increased incidence of hepatic tumours in rats was likely secondary to chronic hepatic toxicity at this high dose.

Because of the high safety margin fold at this no-effect level , these neoplastic changes are not considered relevant for the situation in humans. No adverse effects upon fertility were observed in male and female rats given sitagliptin prior to and throughout mating. Reproductive toxicity studies showed a slight treatment-related increased incidence of foetal rib malformations absent, hypoplastic and wavy ribs in the offspring of rats at systemic exposure levels more than 29 times the human exposure levels.

Maternal toxicity was seen in rabbits at more than 29 times the human exposure levels. Because of the high safety margins, these findings do not suggest a relevant risk for human reproduction.

Packs of 14, 28, 30, 56, 84, 90 or 98 film-coated tablets and 50 x 1 film-coated tablets in perforated unit dose blisters. Any unused medicinal product or waste material should be disposed of in accordance with local requirements. Detailed information on this medicinal product is available on the website of the European Medicines Agency http: This site uses cookies. By continuing to browse the site you are agreeing to our policy on the use of cookies. Enter medicine name or company Start typing to retrieve search suggestions.

Continue typing to refine. Active ingredient sitagliptin phosphate monohydrate. Last updated on eMC: Show table of contents Hide table of contents 1. Name of the medicinal product 2. Qualitative and quantitative composition 3. Marketing authorisation holder 8. Marketing authorisation number s 9. Date of revision of the text. This information is intended for use by health professionals. Each 25 mg tablet contains sitagliptin phosphate monohydrate, equivalent to 25 mg sitagliptin.

Each 50 mg tablet contains sitagliptin phosphate monohydrate, equivalent to 50 mg sitagliptin. Each mg tablet contains sitagliptin phosphate monohydrate, equivalent to mg sitagliptin. For the full list of excipients, see section 6. For adult patients with type 2 diabetes mellitus, Januvia is indicated to improve glycaemic control: Posology The dose is mg sitagliptin once daily.

Special populations Renal impairment When considering the use of sitagliptin in combination with another anti-diabetic medicinal product, its conditions for use in patients with renal impairment should be checked. Hepatic impairment No dose adjustment is necessary for patients with mild to moderate hepatic impairment. Elderly No dose adjustment is necessary based on age. Paediatric population The safety and efficacy of sitagliptin in children and adolescents under 18 years of age have not yet been established.

Method of administration Januvia can be taken with or without food. General Januvia should not be used in patients with type 1 diabetes or for the treatment of diabetic ketoacidosis. Acute pancreatitis Use of DPP-4 inhibitors has been associated with a risk of developing acute pancreatitis.

Hypoglycaemia when used in combination with other anti-hyperglycaemic medicinal products In clinical trials of Januvia as monotherapy and as part of combination therapy with medicinal products not known to cause hypoglycaemia i. Renal impairment Sitagliptin is renally excreted. Hypersensitivity reactions Post-marketing reports of serious hypersensitivity reactions in patients treated with sitagliptin have been reported.

Bullous pemphigoid There have been post-marketing reports of bullous pemphigoid in patients taking DPP-4 inhibitors including sitagliptin.

You are here: