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Background
Insulin-producing beta cells in the pancreas are destroyed by type 1 diabetes mellitus, an autoimmune condition. Insulin is a crucial anabolic hormone that influences the development and metabolism of carbohydrates, lipids, proteins, and minerals.
Importantly, insulin promotes the storage of glucose as glycogen and the synthesis of fatty acids in the liver, permits glucose to enter muscle and adipose cells, stimulates the uptake of amino acids, prevents the breakdown of fat in adipose tissue, and promotes the uptake of potassium into cells.
Insulin replacement therapy is necessary for life for those with T1DM. Without insulin, Diabetic ketoacidosis (DKA), a potentially fatal condition, develops.
Epidemiology
Although it can begin at any age, T1DM is one of the most common chronic disorders in children. The incidence and prevalence of T1DM, which accounts for 5 to 10% of adults with diabetes, have steadily increased. T1DM currently affects an estimated 1.24 million Americans, and by 2050, that figure is projected to reach 5 million.
The most typical age of presentation is in the early stages of life, between the ages of 4 and 6. Additionally, there is a significant geographic difference in occurrence around the globe.
With rates around 400 times higher than those recorded in Venezuela and China, which have the lowest documented incidence, Finland and other Northern European countries have the highest reported incidences. The non-Hispanic white population in the United States has the most significant rate of T1DM, which affects both genders relatively equally.
Anatomy
Pathophysiology
T1DM progresses through three stages. Asymptomatic stage 1 is characterized by greater than or equivalent to 2 pancreatic autoantibodies, normal fasting glucose, and normal glucose tolerance. The presence of more than two pancreatic autoantibodies, dysglycemia, impaired glucose tolerance, or glucose tolerance with a 2-hour PG of 140 to 199 mg/dL, or a Hemoglobin A1c between 5.7% and 6.4%, are all required for stage 2 diagnosis. In stage 3, diabetes or hyperglycemia, two or more pancreatic autoantibodies, and clinical symptoms present.
T1DM manifests in children as hyperglycemic symptoms, with DKA occurring in one-third of cases. Symptoms may appear abruptly, especially in young adults. It can develop into a medical emergency if not assessed and treated immediately. Patients most frequently have polydipsia, polyuria, and polyphagia when hyperglycemic. Osmotic diuresis, which is brought on by hyperglycemia, is a secondary cause of polyuria. Infants and young children may exhibit nocturnal enuresis.
Regarding individuals with T1DM, the onset of symptoms can vary greatly. HbA1c and plasma glucose tests can be used to diagnose diabetes. The HbA1c level should not be used for diagnosis if the patient has just developed symptoms because the patient’s average glucose levels during the previous two to three months may be normal. T1DM can be identified in patients with the characteristic symptoms when their random plasma glucose level is greater than or equal to 200 mg/dl.
Etiology
In T1DM, the pancreatic islets’ beta cells are gradually destroyed by the immune system over time, leading to an ultimate lack of insulin. Researchers consider there is a genetic predisposition for T1DM, with a solid relationship to HLA alleles, particularly DRB103-DQB10201 and DRB 10401. The exact cause of T1DM is yet unknown. Many additional genes influence heritability. An affected mother’s offspring have a risk of 1 to 4%, an affected father’s offspring has a chance of 3 to 8%, and an offspring of affected parents have a risk of up to 30% of having T1DM.
Pancreatic autoantibodies in the blood may indicate that an individual has T1DM or is at risk for developing it. Islet cell cytoplasmic antibodies, antibodies to glutamic acid decarboxylase, antibodies to insulin, antibodies to insulinoma-associated 2 or protein tyrosine phosphatase, and zinc transporter 8 are some of the pancreatic antibodies. The risk of developing T1DM increases with the number of detected antibodies and their titers.
Toxins present in the environment have also been proposed as a factor. According to the hygiene thesis, more significant sanitization is associated with an uptick in autoimmune-mediated illnesses. It is hypothesized that inadequate immune system development results from the loss of childhood exposure to infectious pathogens. According to a recent study, ingestion of cow’s milk proteins increases the likelihood of developing islet autoimmunity in those with low to moderate-risk HLA-DR genotypes but not significantly in people with high-risk genotypes.
Genetics
Prognostic Factors
High mortality and morbidity are linked to type 1 DM. About 50% of patients will experience a significant complication throughout their lifetime. The prognosis is favorable for individuals who survive over the first 20 years.
The condition is incurable; over time, the patient may experience vision loss, neuropathy, premature coronary artery disease, and foot ulcers. The quality of life is low for many type 1 diabetic patients due to maintaining euglycemia for the rest of life.
Clinical History
Physical Examination
Age group
Associated comorbidity
Associated activity
Acuity of presentation
Differential Diagnoses
Laboratory Studies
Imaging Studies
Procedures
Histologic Findings
Staging
Treatment Paradigm
by Stage
by Modality
Chemotherapy
Radiation Therapy
Surgical Interventions
Hormone Therapy
Immunotherapy
Hyperthermia
Photodynamic Therapy
Stem Cell Transplant
Targeted Therapy
Palliative Care
Medication
Subcutaneous injection:
Initial dose: 0.2-0.4 units/kg/day divided every 8 hours subcutaneous
Maintenance dose: 0.5-1 unit/kg/day divided every 8 hours subcutaneous
Insulin pump
Use the proper rapid-acting insulin formulation, which combines a patient-controlled premeal bolus dose and a basal continuous insulin infusion rate
Infusion IV over 30 minutes every day up to 14 consecutive days
Dosage regimen:
Day 1: 65 mcg/m2
Day 2: 125 mcg/m2
Day 3: 250 mcg/m2
Day 4: 500 mcg/m2
Days 5-14: 1,030 mcg/m2
0.2
unit/kg
Solution
Subcutaneous (SC)
once a day
increase the dose as required
insulin degludec/insulin aspart
Insulin-naive patients' starting dose
:
Subcutaneous (SC)
1/3 to 1/2 of the total daily insulin dose
The remaining daily insulin dosage should be distributed between each meal as a short- or rapid-acting insulin
0.2-0.4 units/kg
insulin isophane human/insulin regular human
0.5 - 0.7
unit/kg
Suspension
Subcutaneous (SC)
once a day
0.2 - 0.4
unit/kg
Solution
Subcutaneous (SC)
every 8 hrs
Start off with one-third to half of the total dose. The remaining of total insulin dose should be divided equally as short acting in between the meals
Initial dose ranges from 0.2-0.4 units/kg subcutaneously in the patients who were not on insulin therapy previously
For the patients who have not taken insulin therapy before
Start with one-third of the total dose of insulin, utilize the remaining of the two-third as a short acting
0.2-0.4 units/kg as an initial range
It may take 5 days to completely manifest the initial dose
The initial insulin dose may be incapable of covering the metabolic requirements in the prior 24 hours
An initial targeted dose of 0.4-0.5 units/kg is subcutaneously divided on the daily basis
0.2-0.4 units/kg subcutaneously, divided daily can be considered to bypass hypoglycemia
Maintenance Dose
0.4 to 1 unit/kg subcutaneously divided on the daily basis
Basal insulin- 40-50% of the targeted dose as a single or 2 divided doses
subcutaneously
Prandial insulin- the left out 50-60% dose of the targeted dose is divided daily around the meals
Dose Adjustments
Dose before any surgery, requires reduction
For an evening surgery- reduce the insulin detemir by 10-25% before the procedure
For morning surgery- administer half or two thirds of the morning dose (prandial+basal)
0.5-1 unit/kg/day subcutaneously divided into doses
Slim people may need 0.4-0.6 unit/kg/day
Whereas, obese may need 0.8-1.2 units/kg/day
Intermediate/Long-acting insulin- Around 1/3rd of the total day to day dose is injected subcutaneously
Rapid/Short-acting insulin- Insulin before the meal should satisfy the remnant of the day to day insulin
0.5-1 unit/kg subcutaneously, each day. It includes total dose (prandial+basal)
For intravenous dose- 0.05 to 1 unit/ml in NS. Closely monitor the serum potassium and blood glucose during administration
Beginning dose- 0.5-1 unit/kg/day subcutaneously in divided doses
Healthy individuals may require 0.4-0.6 unit/kg/day, and for healthy individuals, it is 0.8-1.2 units/kg/day
Subcutaneous injection:
Initial dose: 0.2-0.4 units/kg/day divided every 8 hours subcutaneous Maintenance dose: 0.5-1 unit/kg/day divided every 8 hours subcutaneous
Infusion IV over 30 minutes every day up to 14 consecutive days
Dosage regimen:
Day 1: 65 mcg/m2
Day 2: 125 mcg/m2
Day 3: 250 mcg/m2
Day 4: 500 mcg/m2
Days 5-14: 1,030 mcg/m2
0.2
unit/kg
Solution
Subcutaneous (SC)
once a day
increase the dose as required
insulin degludec/insulin aspart
Insulin-naive patients' starting dose
:
0.2 - 0.4
units/kg
Subcutaneous (SC)
daily once
≥1 year: Type 1 diabetes mellitus: 1/3 to 1/2 of the total daily insulin dose
The remaining daily insulin dosage should be distributed between each meal as a short- or rapid-acting insulin
insulin isophane human/insulin regular human
0.5 - 0.7
unit/kg
Suspension
Subcutaneous (SC)
once a day
0.1
unit/kg
Intravenous (IV)
The dose is meant for children and adolescents less than 17 years
For less than 1 year, safety and efficacy are not seen
Start off with one-third to half of the total dose. The remaining of total insulin dose should be divided equally as short acting in between the meals
The dose ranges from 0.2-0.4 units/kg subcutaneously
For more than 6 years- 1/3rd of the total insulin daily, utilize remaining 2/3rd as short acting or before the meals
Safety and efficacy not seen in children below 3 years
For more than 3 years- 0.4-1 unit/kg each day subcutaneously of the total insulin dose
If required use adult dosing of 0.5-1 unit/kg each day
For more than 2 years- 1/3rd of the total daily dose of insulin subcutaneously
Maintenance dose is less than 1.2 units/kg each day during the growth rush
For less than 12 years- Safety and efficacy are not seen
For more than 12 years- 0.5-1 unit/kg/day subcutaneously
Maintain the dose at less than 1.2 units/kg/day
Future Trends
References
https://www.ncbi.nlm.nih.gov/books/NBK507713/
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» Home » CAD » Endocrinology » Diabetes Mellitus » Diabetes Mellitus Type 1
Insulin-producing beta cells in the pancreas are destroyed by type 1 diabetes mellitus, an autoimmune condition. Insulin is a crucial anabolic hormone that influences the development and metabolism of carbohydrates, lipids, proteins, and minerals.
Importantly, insulin promotes the storage of glucose as glycogen and the synthesis of fatty acids in the liver, permits glucose to enter muscle and adipose cells, stimulates the uptake of amino acids, prevents the breakdown of fat in adipose tissue, and promotes the uptake of potassium into cells.
Insulin replacement therapy is necessary for life for those with T1DM. Without insulin, Diabetic ketoacidosis (DKA), a potentially fatal condition, develops.
Although it can begin at any age, T1DM is one of the most common chronic disorders in children. The incidence and prevalence of T1DM, which accounts for 5 to 10% of adults with diabetes, have steadily increased. T1DM currently affects an estimated 1.24 million Americans, and by 2050, that figure is projected to reach 5 million.
The most typical age of presentation is in the early stages of life, between the ages of 4 and 6. Additionally, there is a significant geographic difference in occurrence around the globe.
With rates around 400 times higher than those recorded in Venezuela and China, which have the lowest documented incidence, Finland and other Northern European countries have the highest reported incidences. The non-Hispanic white population in the United States has the most significant rate of T1DM, which affects both genders relatively equally.
T1DM progresses through three stages. Asymptomatic stage 1 is characterized by greater than or equivalent to 2 pancreatic autoantibodies, normal fasting glucose, and normal glucose tolerance. The presence of more than two pancreatic autoantibodies, dysglycemia, impaired glucose tolerance, or glucose tolerance with a 2-hour PG of 140 to 199 mg/dL, or a Hemoglobin A1c between 5.7% and 6.4%, are all required for stage 2 diagnosis. In stage 3, diabetes or hyperglycemia, two or more pancreatic autoantibodies, and clinical symptoms present.
T1DM manifests in children as hyperglycemic symptoms, with DKA occurring in one-third of cases. Symptoms may appear abruptly, especially in young adults. It can develop into a medical emergency if not assessed and treated immediately. Patients most frequently have polydipsia, polyuria, and polyphagia when hyperglycemic. Osmotic diuresis, which is brought on by hyperglycemia, is a secondary cause of polyuria. Infants and young children may exhibit nocturnal enuresis.
Regarding individuals with T1DM, the onset of symptoms can vary greatly. HbA1c and plasma glucose tests can be used to diagnose diabetes. The HbA1c level should not be used for diagnosis if the patient has just developed symptoms because the patient’s average glucose levels during the previous two to three months may be normal. T1DM can be identified in patients with the characteristic symptoms when their random plasma glucose level is greater than or equal to 200 mg/dl.
In T1DM, the pancreatic islets’ beta cells are gradually destroyed by the immune system over time, leading to an ultimate lack of insulin. Researchers consider there is a genetic predisposition for T1DM, with a solid relationship to HLA alleles, particularly DRB103-DQB10201 and DRB 10401. The exact cause of T1DM is yet unknown. Many additional genes influence heritability. An affected mother’s offspring have a risk of 1 to 4%, an affected father’s offspring has a chance of 3 to 8%, and an offspring of affected parents have a risk of up to 30% of having T1DM.
Pancreatic autoantibodies in the blood may indicate that an individual has T1DM or is at risk for developing it. Islet cell cytoplasmic antibodies, antibodies to glutamic acid decarboxylase, antibodies to insulin, antibodies to insulinoma-associated 2 or protein tyrosine phosphatase, and zinc transporter 8 are some of the pancreatic antibodies. The risk of developing T1DM increases with the number of detected antibodies and their titers.
Toxins present in the environment have also been proposed as a factor. According to the hygiene thesis, more significant sanitization is associated with an uptick in autoimmune-mediated illnesses. It is hypothesized that inadequate immune system development results from the loss of childhood exposure to infectious pathogens. According to a recent study, ingestion of cow’s milk proteins increases the likelihood of developing islet autoimmunity in those with low to moderate-risk HLA-DR genotypes but not significantly in people with high-risk genotypes.
High mortality and morbidity are linked to type 1 DM. About 50% of patients will experience a significant complication throughout their lifetime. The prognosis is favorable for individuals who survive over the first 20 years.
The condition is incurable; over time, the patient may experience vision loss, neuropathy, premature coronary artery disease, and foot ulcers. The quality of life is low for many type 1 diabetic patients due to maintaining euglycemia for the rest of life.
Subcutaneous injection:
Initial dose: 0.2-0.4 units/kg/day divided every 8 hours subcutaneous
Maintenance dose: 0.5-1 unit/kg/day divided every 8 hours subcutaneous
Insulin pump
Use the proper rapid-acting insulin formulation, which combines a patient-controlled premeal bolus dose and a basal continuous insulin infusion rate
Infusion IV over 30 minutes every day up to 14 consecutive days
Dosage regimen:
Day 1: 65 mcg/m2
Day 2: 125 mcg/m2
Day 3: 250 mcg/m2
Day 4: 500 mcg/m2
Days 5-14: 1,030 mcg/m2
0.2
unit/kg
Solution
Subcutaneous (SC)
once a day
increase the dose as required
insulin degludec/insulin aspart
Insulin-naive patients' starting dose
:
Subcutaneous (SC)
1/3 to 1/2 of the total daily insulin dose
The remaining daily insulin dosage should be distributed between each meal as a short- or rapid-acting insulin
0.2-0.4 units/kg
insulin isophane human/insulin regular human
0.5 - 0.7
unit/kg
Suspension
Subcutaneous (SC)
once a day
0.2 - 0.4
unit/kg
Solution
Subcutaneous (SC)
every 8 hrs
Start off with one-third to half of the total dose. The remaining of total insulin dose should be divided equally as short acting in between the meals
Initial dose ranges from 0.2-0.4 units/kg subcutaneously in the patients who were not on insulin therapy previously
For the patients who have not taken insulin therapy before
Start with one-third of the total dose of insulin, utilize the remaining of the two-third as a short acting
0.2-0.4 units/kg as an initial range
It may take 5 days to completely manifest the initial dose
The initial insulin dose may be incapable of covering the metabolic requirements in the prior 24 hours
An initial targeted dose of 0.4-0.5 units/kg is subcutaneously divided on the daily basis
0.2-0.4 units/kg subcutaneously, divided daily can be considered to bypass hypoglycemia
Maintenance Dose
0.4 to 1 unit/kg subcutaneously divided on the daily basis
Basal insulin- 40-50% of the targeted dose as a single or 2 divided doses
subcutaneously
Prandial insulin- the left out 50-60% dose of the targeted dose is divided daily around the meals
Dose Adjustments
Dose before any surgery, requires reduction
For an evening surgery- reduce the insulin detemir by 10-25% before the procedure
For morning surgery- administer half or two thirds of the morning dose (prandial+basal)
0.5-1 unit/kg/day subcutaneously divided into doses
Slim people may need 0.4-0.6 unit/kg/day
Whereas, obese may need 0.8-1.2 units/kg/day
Intermediate/Long-acting insulin- Around 1/3rd of the total day to day dose is injected subcutaneously
Rapid/Short-acting insulin- Insulin before the meal should satisfy the remnant of the day to day insulin
0.5-1 unit/kg subcutaneously, each day. It includes total dose (prandial+basal)
For intravenous dose- 0.05 to 1 unit/ml in NS. Closely monitor the serum potassium and blood glucose during administration
Beginning dose- 0.5-1 unit/kg/day subcutaneously in divided doses
Healthy individuals may require 0.4-0.6 unit/kg/day, and for healthy individuals, it is 0.8-1.2 units/kg/day
Subcutaneous injection:
Initial dose: 0.2-0.4 units/kg/day divided every 8 hours subcutaneous Maintenance dose: 0.5-1 unit/kg/day divided every 8 hours subcutaneous
Infusion IV over 30 minutes every day up to 14 consecutive days
Dosage regimen:
Day 1: 65 mcg/m2
Day 2: 125 mcg/m2
Day 3: 250 mcg/m2
Day 4: 500 mcg/m2
Days 5-14: 1,030 mcg/m2
0.2
unit/kg
Solution
Subcutaneous (SC)
once a day
increase the dose as required
insulin degludec/insulin aspart
Insulin-naive patients' starting dose
:
0.2 - 0.4
units/kg
Subcutaneous (SC)
daily once
≥1 year: Type 1 diabetes mellitus: 1/3 to 1/2 of the total daily insulin dose
The remaining daily insulin dosage should be distributed between each meal as a short- or rapid-acting insulin
insulin isophane human/insulin regular human
0.5 - 0.7
unit/kg
Suspension
Subcutaneous (SC)
once a day
0.1
unit/kg
Intravenous (IV)
The dose is meant for children and adolescents less than 17 years
For less than 1 year, safety and efficacy are not seen
Start off with one-third to half of the total dose. The remaining of total insulin dose should be divided equally as short acting in between the meals
The dose ranges from 0.2-0.4 units/kg subcutaneously
For more than 6 years- 1/3rd of the total insulin daily, utilize remaining 2/3rd as short acting or before the meals
Safety and efficacy not seen in children below 3 years
For more than 3 years- 0.4-1 unit/kg each day subcutaneously of the total insulin dose
If required use adult dosing of 0.5-1 unit/kg each day
For more than 2 years- 1/3rd of the total daily dose of insulin subcutaneously
Maintenance dose is less than 1.2 units/kg each day during the growth rush
For less than 12 years- Safety and efficacy are not seen
For more than 12 years- 0.5-1 unit/kg/day subcutaneously
Maintain the dose at less than 1.2 units/kg/day
https://www.ncbi.nlm.nih.gov/books/NBK507713/
Insulin-producing beta cells in the pancreas are destroyed by type 1 diabetes mellitus, an autoimmune condition. Insulin is a crucial anabolic hormone that influences the development and metabolism of carbohydrates, lipids, proteins, and minerals.
Importantly, insulin promotes the storage of glucose as glycogen and the synthesis of fatty acids in the liver, permits glucose to enter muscle and adipose cells, stimulates the uptake of amino acids, prevents the breakdown of fat in adipose tissue, and promotes the uptake of potassium into cells.
Insulin replacement therapy is necessary for life for those with T1DM. Without insulin, Diabetic ketoacidosis (DKA), a potentially fatal condition, develops.
Although it can begin at any age, T1DM is one of the most common chronic disorders in children. The incidence and prevalence of T1DM, which accounts for 5 to 10% of adults with diabetes, have steadily increased. T1DM currently affects an estimated 1.24 million Americans, and by 2050, that figure is projected to reach 5 million.
The most typical age of presentation is in the early stages of life, between the ages of 4 and 6. Additionally, there is a significant geographic difference in occurrence around the globe.
With rates around 400 times higher than those recorded in Venezuela and China, which have the lowest documented incidence, Finland and other Northern European countries have the highest reported incidences. The non-Hispanic white population in the United States has the most significant rate of T1DM, which affects both genders relatively equally.
T1DM progresses through three stages. Asymptomatic stage 1 is characterized by greater than or equivalent to 2 pancreatic autoantibodies, normal fasting glucose, and normal glucose tolerance. The presence of more than two pancreatic autoantibodies, dysglycemia, impaired glucose tolerance, or glucose tolerance with a 2-hour PG of 140 to 199 mg/dL, or a Hemoglobin A1c between 5.7% and 6.4%, are all required for stage 2 diagnosis. In stage 3, diabetes or hyperglycemia, two or more pancreatic autoantibodies, and clinical symptoms present.
T1DM manifests in children as hyperglycemic symptoms, with DKA occurring in one-third of cases. Symptoms may appear abruptly, especially in young adults. It can develop into a medical emergency if not assessed and treated immediately. Patients most frequently have polydipsia, polyuria, and polyphagia when hyperglycemic. Osmotic diuresis, which is brought on by hyperglycemia, is a secondary cause of polyuria. Infants and young children may exhibit nocturnal enuresis.
Regarding individuals with T1DM, the onset of symptoms can vary greatly. HbA1c and plasma glucose tests can be used to diagnose diabetes. The HbA1c level should not be used for diagnosis if the patient has just developed symptoms because the patient’s average glucose levels during the previous two to three months may be normal. T1DM can be identified in patients with the characteristic symptoms when their random plasma glucose level is greater than or equal to 200 mg/dl.
In T1DM, the pancreatic islets’ beta cells are gradually destroyed by the immune system over time, leading to an ultimate lack of insulin. Researchers consider there is a genetic predisposition for T1DM, with a solid relationship to HLA alleles, particularly DRB103-DQB10201 and DRB 10401. The exact cause of T1DM is yet unknown. Many additional genes influence heritability. An affected mother’s offspring have a risk of 1 to 4%, an affected father’s offspring has a chance of 3 to 8%, and an offspring of affected parents have a risk of up to 30% of having T1DM.
Pancreatic autoantibodies in the blood may indicate that an individual has T1DM or is at risk for developing it. Islet cell cytoplasmic antibodies, antibodies to glutamic acid decarboxylase, antibodies to insulin, antibodies to insulinoma-associated 2 or protein tyrosine phosphatase, and zinc transporter 8 are some of the pancreatic antibodies. The risk of developing T1DM increases with the number of detected antibodies and their titers.
Toxins present in the environment have also been proposed as a factor. According to the hygiene thesis, more significant sanitization is associated with an uptick in autoimmune-mediated illnesses. It is hypothesized that inadequate immune system development results from the loss of childhood exposure to infectious pathogens. According to a recent study, ingestion of cow’s milk proteins increases the likelihood of developing islet autoimmunity in those with low to moderate-risk HLA-DR genotypes but not significantly in people with high-risk genotypes.
High mortality and morbidity are linked to type 1 DM. About 50% of patients will experience a significant complication throughout their lifetime. The prognosis is favorable for individuals who survive over the first 20 years.
The condition is incurable; over time, the patient may experience vision loss, neuropathy, premature coronary artery disease, and foot ulcers. The quality of life is low for many type 1 diabetic patients due to maintaining euglycemia for the rest of life.
https://www.ncbi.nlm.nih.gov/books/NBK507713/
Founded in 2014, medtigo is committed to providing high-quality, friendly physicians, transparent pricing, and a focus on building relationships and a lifestyle brand for medical professionals nationwide.
USA – BOSTON
60 Roberts Drive, Suite 313
North Adams, MA 01247
INDIA – PUNE
7, Shree Krishna, 2nd Floor, Opp Kiosk Koffee, Shirole Lane, Off FC Road, Pune 411004, Maharashtra
Founded in 2014, medtigo is committed to providing high-quality, friendly physicians, transparent pricing, and a focus on building relationships and a lifestyle brand for medical professionals nationwide.
MASSACHUSETTS – USA
60 Roberts Drive, Suite 313,
North Adams, MA 01247
MAHARASHTRA – INDIA
7, Shree Krishna, 2nd Floor,
Opp Kiosk Koffee,
Shirole Lane, Off FC Road,
Pune 411004, Maharashtra
