Hyperglucagonemia means the presence of high glucagon concentrations in the bloodstream. In this event, if it is related to a glucagon-secreting tumor, it is called Glucagonoma Syndrome. This is a very rare disease which is caused by the malignant tumor of the alpha cell of the pancreas which is responsible for the production of glucagon.
Epidemiology
The occurrences of glucagonoma syndrome occurs at 1/20,000,000 population. Dominantly, the international frequency is 1/20,000,000 population. In patients with glucagonoma syndrome, presentation occurs in the median age of 55 years. Mortality regarding glucagonoma syndrome is frequent and primarily attributable to a complication of deep venous thrombosis.
Anatomy
Pathophysiology
Excess Glucagon Secretion: The hormone glucagon, which elevates the blood glucose levels by stimulating glycogenolysis, the breakdown of glycogen and gluconeogenesis and the synthesis of glucose in the liver is hyper secreted. It results to chronic hyperglycemia and makes the patient develop diabetes mellitus depending on the severity of the condition.
Gluconeogenesis and Glycogenolysis: More increases in the concentration of glucagon promote two processes, gluconeogenesis and glycogenolysis, and this creates excessive glucose. This leads to the increase in the blood sugar concentration and worsening in insulin sensitivity.
Hyperlipidemia and Ketogenesis: Glucagon has a potent lipolytic effect, that in turn, inhibits glucose uptake reducing blood glucose levels, and augments the blood free fatty acids. This serves to increase ketone bodies generation in the liver, thus potentially leading to ketosis in more severe conditions.
Catabolism of Proteins: Overproduction of glucagon, which causes hyperglycemia, encourages proteolysis, releasing amino acids for gluconeogenesis. This leads to the production of weight loss and muscle atrophy, which are manifestations of the glucagonoma syndrome.
Necrolytic Migratory Erythema (NME): This is a characteristics skin lesion associated with glucagonoma syndrome. Its mechanism is not well understood, but NME has been possibly associated with amino acid deficiencies resulting from hyperglucagonemia-mediated increased protein catabolism and metabolism.
Gastrointestinal Symptoms: The syndrome may even present with gastrointestinal disturbances, including diarrhea and malabsorption, possibly because of glucagon on gut motility and secretions.
Etiology
Glucagonoma (Pancreatic Tumor): The most common cause is a glucagonoma, usually arising from the pancreatic islets of Langerhans alpha cells. These tumors are often malignant.
Genetic Syndromes: Most of them are reported to relate to Multiple Endocrine Neoplasia Type 1 (MEN 1), an autosomal dominant trait that raises the propensity of tumors in several glands in the endocrine system including Glucagonomas.
Pancreatic Alpha Cell Hyperplasia: While rare although, the hyperglucagonemia related to excessive population of the alpha cells in the pancreas without the presence of tumor could occur.
Secondary Causes: On some occasions hyperglucagonemia is secondary to chronic diseases such as hepatic cirrhosis, renal failure or diabetes mellitus, however these conditions do not present the complete clinical manifestation of glucagonoma syndrome.
Genetics
Prognostic Factors
Stage of the Tumor at Diagnosis
Presence of Metastasis
Tumor Differentiation and Grading
Clinical History
Age Group:
Hyperglucagonemia also referred to as glucagonoma syndrome, is more often identified in middle age to elderly individuals, preferably the aged 40 and above.
Physical Examination
Fasting plasma glucagon levels.
Imaging studies to localize the tumor (e.g., CT scan, MRI).
Biopsy of the tumor, if indicated.
Age group
Associated comorbidity
Necrolytic Migratory Erythema (NME)
Diabetes Mellitus
Venous Thromboembolism
Mucositis or Stomatitis
Associated activity
Acuity of presentation
Necrolytic migratory erythema (NME): A red, blistering skin rash which is usually the first manifestation of the disease.
Hyperglycemia from excess glucagon may cause new-onset or worsening of diabetes mellitus.
Diabetes by increasing circulating blood glucose, its stimulation of gluconeogenesis and glycogenolysis which leads to weight loss and muscle wasting when glucagon is present in excessive amounts.
Diarrhea and gastrointestinal disturbances.
Thromboembolic events and other complications may also occur and are attributed to Chronic disease factors.
Primary Treatment: Surgery is the mainstay of the management of glucagonoma syndrome, with the primary aim being the resection of the tumor. If the tumor is localized and resectable, then surgical resection may be curative or at least palliative.
Debulking Surgery: If complete surgical removal of the tumor is not possible, debulking or the removal of as much of the mass, as is manageable, can help in controlling signs and symptoms and increase survival time.
Medical Management
Somatostatin Analogs: Octreotide or lanreotide can control the symptoms by controlling the secretion of glucagon and may reduce the diarrhea and other characteristics seen in glucagonoma.
Chemotherapy: Consequently, for the patient with unresectable tumor or metastatic disease, chemotherapy may be given. Schedules contain such preparations as streptozocin or doxorubicin.
Targeted Therapies: If, for example, there are signs of the advanced stage of the disease, everolimus or sunitinib can be used as modern therapy medication.
Insulin Therapy: Hyperglycemic conditions due to glucagonoma can be treated with insulin and or other anti-diabetic medications.
Supportive Care
Nutritional Support: The patients may require nutritional supplementation to overcome diarrheal manifestations or weight loss. A dietitian is therefore helpful in advising on how to cope with symptoms or consider in disease management without compromising on nutrition.
Symptomatic Treatment: Control of such complications as diarrhea, weight loss, and hyperglycemia is vital. Pharmacological intervention and mainly modification of behavior are possible interventions that may enhance quality of life.
Frequent Meals: Taking many small meals at long intervals of time proved helpful in controlling some of the symptoms as glucose fluctuations and hypoglycemia.
Low-Carbohydrate Diet: A low carbohydrate diet could be helpful in managing the hyperglycemia and hyperglucagonemia while a low carbohydrates diet should be made depending on the person’s condition.
Monitoring and Management:
Blood Glucose Monitoring: Monitoring of blood glucose levels is very vital to enable assessment of any changes and likely adjustments in therapies to be done.
Regular Medical Check-Ups: Regular follow up appointments with an appropriate healthcare provider to assess development of the syndrome and to modify the treatment strategies accordingly.
Supportive Care:
Pain Management: Addressing any pain or discomfort associated with the syndrome.
Nutritional Counselling: Nutrition consultation with a dietitian on how best to construct their meals to cater to their nutritional needs while at the same time reducing their symptoms
Effectiveness of Somatostatin Analogues in Treating Hyperglucagonemia
Octreotide: Given as a long-acting preparations such as octreotide LAR (long-acting release) which is administered monthly.
Lanreotide: Another somatostatin long-acting analog that is administered monthly by injection. Other long-acting somatostatin analogue that can be used in administration through monthly injection.
Surgical Resection: A localized and resectable glucagonoma should be excised surgically. Removing the whole tumor can be curative, relieve symptoms, and improve prognosis. Many patients receive a distal pancreatectomy, where the tail and sometimes the body of the pancreas are resected if it happens to be in the pancreas.
Debulking Surgery: If the tumor cannot be resected entirely, then the surgeon may opt for debulking surgery so that parts of the tumor are removed to lighten the burden and symptoms for that patient. This is essentially the removal of as much of the tumor as possible.
Diagnosis and Evaluation: Clinical Assessment: There can be presence of symptoms like necrolytic migratory erythema, diabetes mellitus, weight loss, and anemia. Lab Tests: Serum glucagon levels, glucose level, and for other abnormalities. Imaging: Computerized tomography scan and Magnetic resonance imaging to ascertain the location and spread of glucagonoma. This tumor usually occurs in the pancreas. Symptomatic Treatment: The symptoms of hyperglycemia and skin lesions should be addressed. An insulin therapy or oral hypoglycemic agent may be needed for the diabetic patient. Nutritional Care: Help the patient to avoid any weight loss and nutritional deficiencies through nutritional support.
Medical Management: Tumor Resection: Surgical resection of a localised, resectable glucagonoma is the primary treatment. In the case of this tumor, complete resolution can be obtained if the tumor is small in size and does not contain metastasis.
Medical Management: Somatostatin Analogs: The drugs like octreotide would relieve symptoms by preventing the release of glucagon Chemotherapy: If the tumor has advanced to metastatic stage or is inoperable, chemotherapy or targeted therapy might be initiated
Long Term Follow-up and Follow Up: Routine Assessments: Regularly observe glucagon levels, blood sugar, and status of the tumor to evaluate treatment efficacy and catch-up any recurrence or progression. Managing Complications: Treat complications arising due to the syndrome itself or its management.
»
Home » CAD » Hyperglucagonemia (Glucagonoma Syndrome)
Hyperglucagonemia (Glucagonoma Syndrome)
Updated :
September 20, 2024
Hyperglucagonemia means the presence of high glucagon concentrations in the bloodstream. In this event, if it is related to a glucagon-secreting tumor, it is called Glucagonoma Syndrome. This is a very rare disease which is caused by the malignant tumor of the alpha cell of the pancreas which is responsible for the production of glucagon.
The occurrences of glucagonoma syndrome occurs at 1/20,000,000 population. Dominantly, the international frequency is 1/20,000,000 population. In patients with glucagonoma syndrome, presentation occurs in the median age of 55 years. Mortality regarding glucagonoma syndrome is frequent and primarily attributable to a complication of deep venous thrombosis.
Excess Glucagon Secretion: The hormone glucagon, which elevates the blood glucose levels by stimulating glycogenolysis, the breakdown of glycogen and gluconeogenesis and the synthesis of glucose in the liver is hyper secreted. It results to chronic hyperglycemia and makes the patient develop diabetes mellitus depending on the severity of the condition.
Gluconeogenesis and Glycogenolysis: More increases in the concentration of glucagon promote two processes, gluconeogenesis and glycogenolysis, and this creates excessive glucose. This leads to the increase in the blood sugar concentration and worsening in insulin sensitivity.
Hyperlipidemia and Ketogenesis: Glucagon has a potent lipolytic effect, that in turn, inhibits glucose uptake reducing blood glucose levels, and augments the blood free fatty acids. This serves to increase ketone bodies generation in the liver, thus potentially leading to ketosis in more severe conditions.
Catabolism of Proteins: Overproduction of glucagon, which causes hyperglycemia, encourages proteolysis, releasing amino acids for gluconeogenesis. This leads to the production of weight loss and muscle atrophy, which are manifestations of the glucagonoma syndrome.
Necrolytic Migratory Erythema (NME): This is a characteristics skin lesion associated with glucagonoma syndrome. Its mechanism is not well understood, but NME has been possibly associated with amino acid deficiencies resulting from hyperglucagonemia-mediated increased protein catabolism and metabolism.
Gastrointestinal Symptoms: The syndrome may even present with gastrointestinal disturbances, including diarrhea and malabsorption, possibly because of glucagon on gut motility and secretions.
Glucagonoma (Pancreatic Tumor): The most common cause is a glucagonoma, usually arising from the pancreatic islets of Langerhans alpha cells. These tumors are often malignant.
Genetic Syndromes: Most of them are reported to relate to Multiple Endocrine Neoplasia Type 1 (MEN 1), an autosomal dominant trait that raises the propensity of tumors in several glands in the endocrine system including Glucagonomas.
Pancreatic Alpha Cell Hyperplasia: While rare although, the hyperglucagonemia related to excessive population of the alpha cells in the pancreas without the presence of tumor could occur.
Secondary Causes: On some occasions hyperglucagonemia is secondary to chronic diseases such as hepatic cirrhosis, renal failure or diabetes mellitus, however these conditions do not present the complete clinical manifestation of glucagonoma syndrome.
Stage of the Tumor at Diagnosis
Presence of Metastasis
Tumor Differentiation and Grading
Age Group:
Hyperglucagonemia also referred to as glucagonoma syndrome, is more often identified in middle age to elderly individuals, preferably the aged 40 and above.
Fasting plasma glucagon levels.
Imaging studies to localize the tumor (e.g., CT scan, MRI).
Biopsy of the tumor, if indicated.
Necrolytic Migratory Erythema (NME)
Diabetes Mellitus
Venous Thromboembolism
Mucositis or Stomatitis
Necrolytic migratory erythema (NME): A red, blistering skin rash which is usually the first manifestation of the disease.
Hyperglycemia from excess glucagon may cause new-onset or worsening of diabetes mellitus.
Diabetes by increasing circulating blood glucose, its stimulation of gluconeogenesis and glycogenolysis which leads to weight loss and muscle wasting when glucagon is present in excessive amounts.
Diarrhea and gastrointestinal disturbances.
Thromboembolic events and other complications may also occur and are attributed to Chronic disease factors.
Primary Treatment: Surgery is the mainstay of the management of glucagonoma syndrome, with the primary aim being the resection of the tumor. If the tumor is localized and resectable, then surgical resection may be curative or at least palliative.
Debulking Surgery: If complete surgical removal of the tumor is not possible, debulking or the removal of as much of the mass, as is manageable, can help in controlling signs and symptoms and increase survival time.
Medical Management
Somatostatin Analogs: Octreotide or lanreotide can control the symptoms by controlling the secretion of glucagon and may reduce the diarrhea and other characteristics seen in glucagonoma.
Chemotherapy: Consequently, for the patient with unresectable tumor or metastatic disease, chemotherapy may be given. Schedules contain such preparations as streptozocin or doxorubicin.
Targeted Therapies: If, for example, there are signs of the advanced stage of the disease, everolimus or sunitinib can be used as modern therapy medication.
Insulin Therapy: Hyperglycemic conditions due to glucagonoma can be treated with insulin and or other anti-diabetic medications.
Supportive Care
Nutritional Support: The patients may require nutritional supplementation to overcome diarrheal manifestations or weight loss. A dietitian is therefore helpful in advising on how to cope with symptoms or consider in disease management without compromising on nutrition.
Symptomatic Treatment: Control of such complications as diarrhea, weight loss, and hyperglycemia is vital. Pharmacological intervention and mainly modification of behavior are possible interventions that may enhance quality of life.
Endocrinology, Metabolism
Dietary Adjustments:
Frequent Meals: Taking many small meals at long intervals of time proved helpful in controlling some of the symptoms as glucose fluctuations and hypoglycemia.
Low-Carbohydrate Diet: A low carbohydrate diet could be helpful in managing the hyperglycemia and hyperglucagonemia while a low carbohydrates diet should be made depending on the person’s condition.
Monitoring and Management:
Blood Glucose Monitoring: Monitoring of blood glucose levels is very vital to enable assessment of any changes and likely adjustments in therapies to be done.
Regular Medical Check-Ups: Regular follow up appointments with an appropriate healthcare provider to assess development of the syndrome and to modify the treatment strategies accordingly.
Supportive Care:
Pain Management: Addressing any pain or discomfort associated with the syndrome.
Nutritional Counselling: Nutrition consultation with a dietitian on how best to construct their meals to cater to their nutritional needs while at the same time reducing their symptoms
Endocrinology, Metabolism
Octreotide: Given as a long-acting preparations such as octreotide LAR (long-acting release) which is administered monthly.
Lanreotide: Another somatostatin long-acting analog that is administered monthly by injection. Other long-acting somatostatin analogue that can be used in administration through monthly injection.
Endocrinology, Metabolism
Surgical Resection: A localized and resectable glucagonoma should be excised surgically. Removing the whole tumor can be curative, relieve symptoms, and improve prognosis. Many patients receive a distal pancreatectomy, where the tail and sometimes the body of the pancreas are resected if it happens to be in the pancreas.
Debulking Surgery: If the tumor cannot be resected entirely, then the surgeon may opt for debulking surgery so that parts of the tumor are removed to lighten the burden and symptoms for that patient. This is essentially the removal of as much of the tumor as possible.
Endocrinology, Metabolism
Diagnosis and Evaluation: Clinical Assessment: There can be presence of symptoms like necrolytic migratory erythema, diabetes mellitus, weight loss, and anemia. Lab Tests: Serum glucagon levels, glucose level, and for other abnormalities. Imaging: Computerized tomography scan and Magnetic resonance imaging to ascertain the location and spread of glucagonoma. This tumor usually occurs in the pancreas. Symptomatic Treatment: The symptoms of hyperglycemia and skin lesions should be addressed. An insulin therapy or oral hypoglycemic agent may be needed for the diabetic patient. Nutritional Care: Help the patient to avoid any weight loss and nutritional deficiencies through nutritional support.
Medical Management: Tumor Resection: Surgical resection of a localised, resectable glucagonoma is the primary treatment. In the case of this tumor, complete resolution can be obtained if the tumor is small in size and does not contain metastasis.
Medical Management: Somatostatin Analogs: The drugs like octreotide would relieve symptoms by preventing the release of glucagon Chemotherapy: If the tumor has advanced to metastatic stage or is inoperable, chemotherapy or targeted therapy might be initiated
Long Term Follow-up and Follow Up: Routine Assessments: Regularly observe glucagon levels, blood sugar, and status of the tumor to evaluate treatment efficacy and catch-up any recurrence or progression. Managing Complications: Treat complications arising due to the syndrome itself or its management.
Hyperglucagonemia means the presence of high glucagon concentrations in the bloodstream. In this event, if it is related to a glucagon-secreting tumor, it is called Glucagonoma Syndrome. This is a very rare disease which is caused by the malignant tumor of the alpha cell of the pancreas which is responsible for the production of glucagon.
The occurrences of glucagonoma syndrome occurs at 1/20,000,000 population. Dominantly, the international frequency is 1/20,000,000 population. In patients with glucagonoma syndrome, presentation occurs in the median age of 55 years. Mortality regarding glucagonoma syndrome is frequent and primarily attributable to a complication of deep venous thrombosis.
Excess Glucagon Secretion: The hormone glucagon, which elevates the blood glucose levels by stimulating glycogenolysis, the breakdown of glycogen and gluconeogenesis and the synthesis of glucose in the liver is hyper secreted. It results to chronic hyperglycemia and makes the patient develop diabetes mellitus depending on the severity of the condition.
Gluconeogenesis and Glycogenolysis: More increases in the concentration of glucagon promote two processes, gluconeogenesis and glycogenolysis, and this creates excessive glucose. This leads to the increase in the blood sugar concentration and worsening in insulin sensitivity.
Hyperlipidemia and Ketogenesis: Glucagon has a potent lipolytic effect, that in turn, inhibits glucose uptake reducing blood glucose levels, and augments the blood free fatty acids. This serves to increase ketone bodies generation in the liver, thus potentially leading to ketosis in more severe conditions.
Catabolism of Proteins: Overproduction of glucagon, which causes hyperglycemia, encourages proteolysis, releasing amino acids for gluconeogenesis. This leads to the production of weight loss and muscle atrophy, which are manifestations of the glucagonoma syndrome.
Necrolytic Migratory Erythema (NME): This is a characteristics skin lesion associated with glucagonoma syndrome. Its mechanism is not well understood, but NME has been possibly associated with amino acid deficiencies resulting from hyperglucagonemia-mediated increased protein catabolism and metabolism.
Gastrointestinal Symptoms: The syndrome may even present with gastrointestinal disturbances, including diarrhea and malabsorption, possibly because of glucagon on gut motility and secretions.
Glucagonoma (Pancreatic Tumor): The most common cause is a glucagonoma, usually arising from the pancreatic islets of Langerhans alpha cells. These tumors are often malignant.
Genetic Syndromes: Most of them are reported to relate to Multiple Endocrine Neoplasia Type 1 (MEN 1), an autosomal dominant trait that raises the propensity of tumors in several glands in the endocrine system including Glucagonomas.
Pancreatic Alpha Cell Hyperplasia: While rare although, the hyperglucagonemia related to excessive population of the alpha cells in the pancreas without the presence of tumor could occur.
Secondary Causes: On some occasions hyperglucagonemia is secondary to chronic diseases such as hepatic cirrhosis, renal failure or diabetes mellitus, however these conditions do not present the complete clinical manifestation of glucagonoma syndrome.
Stage of the Tumor at Diagnosis
Presence of Metastasis
Tumor Differentiation and Grading
Age Group:
Hyperglucagonemia also referred to as glucagonoma syndrome, is more often identified in middle age to elderly individuals, preferably the aged 40 and above.
Fasting plasma glucagon levels.
Imaging studies to localize the tumor (e.g., CT scan, MRI).
Biopsy of the tumor, if indicated.
Necrolytic Migratory Erythema (NME)
Diabetes Mellitus
Venous Thromboembolism
Mucositis or Stomatitis
Necrolytic migratory erythema (NME): A red, blistering skin rash which is usually the first manifestation of the disease.
Hyperglycemia from excess glucagon may cause new-onset or worsening of diabetes mellitus.
Diabetes by increasing circulating blood glucose, its stimulation of gluconeogenesis and glycogenolysis which leads to weight loss and muscle wasting when glucagon is present in excessive amounts.
Diarrhea and gastrointestinal disturbances.
Thromboembolic events and other complications may also occur and are attributed to Chronic disease factors.
Primary Treatment: Surgery is the mainstay of the management of glucagonoma syndrome, with the primary aim being the resection of the tumor. If the tumor is localized and resectable, then surgical resection may be curative or at least palliative.
Debulking Surgery: If complete surgical removal of the tumor is not possible, debulking or the removal of as much of the mass, as is manageable, can help in controlling signs and symptoms and increase survival time.
Medical Management
Somatostatin Analogs: Octreotide or lanreotide can control the symptoms by controlling the secretion of glucagon and may reduce the diarrhea and other characteristics seen in glucagonoma.
Chemotherapy: Consequently, for the patient with unresectable tumor or metastatic disease, chemotherapy may be given. Schedules contain such preparations as streptozocin or doxorubicin.
Targeted Therapies: If, for example, there are signs of the advanced stage of the disease, everolimus or sunitinib can be used as modern therapy medication.
Insulin Therapy: Hyperglycemic conditions due to glucagonoma can be treated with insulin and or other anti-diabetic medications.
Supportive Care
Nutritional Support: The patients may require nutritional supplementation to overcome diarrheal manifestations or weight loss. A dietitian is therefore helpful in advising on how to cope with symptoms or consider in disease management without compromising on nutrition.
Symptomatic Treatment: Control of such complications as diarrhea, weight loss, and hyperglycemia is vital. Pharmacological intervention and mainly modification of behavior are possible interventions that may enhance quality of life.
Endocrinology, Metabolism
Dietary Adjustments:
Frequent Meals: Taking many small meals at long intervals of time proved helpful in controlling some of the symptoms as glucose fluctuations and hypoglycemia.
Low-Carbohydrate Diet: A low carbohydrate diet could be helpful in managing the hyperglycemia and hyperglucagonemia while a low carbohydrates diet should be made depending on the person’s condition.
Monitoring and Management:
Blood Glucose Monitoring: Monitoring of blood glucose levels is very vital to enable assessment of any changes and likely adjustments in therapies to be done.
Regular Medical Check-Ups: Regular follow up appointments with an appropriate healthcare provider to assess development of the syndrome and to modify the treatment strategies accordingly.
Supportive Care:
Pain Management: Addressing any pain or discomfort associated with the syndrome.
Nutritional Counselling: Nutrition consultation with a dietitian on how best to construct their meals to cater to their nutritional needs while at the same time reducing their symptoms
Endocrinology, Metabolism
Octreotide: Given as a long-acting preparations such as octreotide LAR (long-acting release) which is administered monthly.
Lanreotide: Another somatostatin long-acting analog that is administered monthly by injection. Other long-acting somatostatin analogue that can be used in administration through monthly injection.
Endocrinology, Metabolism
Surgical Resection: A localized and resectable glucagonoma should be excised surgically. Removing the whole tumor can be curative, relieve symptoms, and improve prognosis. Many patients receive a distal pancreatectomy, where the tail and sometimes the body of the pancreas are resected if it happens to be in the pancreas.
Debulking Surgery: If the tumor cannot be resected entirely, then the surgeon may opt for debulking surgery so that parts of the tumor are removed to lighten the burden and symptoms for that patient. This is essentially the removal of as much of the tumor as possible.
Endocrinology, Metabolism
Diagnosis and Evaluation: Clinical Assessment: There can be presence of symptoms like necrolytic migratory erythema, diabetes mellitus, weight loss, and anemia. Lab Tests: Serum glucagon levels, glucose level, and for other abnormalities. Imaging: Computerized tomography scan and Magnetic resonance imaging to ascertain the location and spread of glucagonoma. This tumor usually occurs in the pancreas. Symptomatic Treatment: The symptoms of hyperglycemia and skin lesions should be addressed. An insulin therapy or oral hypoglycemic agent may be needed for the diabetic patient. Nutritional Care: Help the patient to avoid any weight loss and nutritional deficiencies through nutritional support.
Medical Management: Tumor Resection: Surgical resection of a localised, resectable glucagonoma is the primary treatment. In the case of this tumor, complete resolution can be obtained if the tumor is small in size and does not contain metastasis.
Medical Management: Somatostatin Analogs: The drugs like octreotide would relieve symptoms by preventing the release of glucagon Chemotherapy: If the tumor has advanced to metastatic stage or is inoperable, chemotherapy or targeted therapy might be initiated
Long Term Follow-up and Follow Up: Routine Assessments: Regularly observe glucagon levels, blood sugar, and status of the tumor to evaluate treatment efficacy and catch-up any recurrence or progression. Managing Complications: Treat complications arising due to the syndrome itself or its management.
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