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Acute Hypoglycemia
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The video associated with this article is no longer available on this site. Please view all of our videos on the MDedge YouTube channel
Thyroid Nodules
The video associated with this article is no longer available on this site. Please view all of our videos on the MDedge YouTube channel
To hear his lecture on “Investigating Thyroid Nodules,” and earn CE/CME credit, please attend the 2013 MEDS West in Irvine, CA, October 3-5. Click here for complete details.
The video associated with this article is no longer available on this site. Please view all of our videos on the MDedge YouTube channel
To hear his lecture on “Investigating Thyroid Nodules,” and earn CE/CME credit, please attend the 2013 MEDS West in Irvine, CA, October 3-5. Click here for complete details.
The video associated with this article is no longer available on this site. Please view all of our videos on the MDedge YouTube channel
To hear his lecture on “Investigating Thyroid Nodules,” and earn CE/CME credit, please attend the 2013 MEDS West in Irvine, CA, October 3-5. Click here for complete details.
Glucose Control and Avoidance of Hypoglycemia
Q: I am frustrated by the “always bring the blood sugars down slowly” philosophy, which I know is intended to avoid hypoglycemic symptoms. However, it often seems to be done at the expense of prolonged hyperglycemia, which is dangerous for patients’ long-term health and may cause more rapid beta-cell destruction. What’s the deal? There is evidence that rapid achievement of tight glucose control using intensive insulin therapy with multiple daily injections or insulin pumps in patients with newly diagnosed type 2 diabetes has favorable outcomes on recovery and maintenance of beta-cell function and prolonged glycemic remission, compared with treatment with oral hypoglycemic agents.1 However, this approach is time consuming and not practical in most primary care settings. Overcoming “clinical inertia” (the failure to initiate or intensify therapy when indicated) has been identified as a major barrier to achieving rapid glycemic control, to the detriment of the patient’s health. One recent study showed that more frequent follow-up with a multidisciplinary team and regular use of a computer-analyzed 7-point glucose profile resulted in more rapid and significantly better glycemic control with a lower A1C, compared to standard care.2 This approach is much more practical in a primary care setting. Additionally, we always treat our patients as individuals. There are very few maxims that are correct in all situations. Almost every answer to a clinical question begins with the qualifier “It depends….” The specifics of the individual case will clarify the appropriate answer. In regard to this particular question, the answer will vary by the clinical history of the patient. For example, for a pregnant patient with poor glycemic control, potential hospitalization and rapid titration of insulin would be the most judicious plan. In this case, quickly bringing glucose into tight control helps minimize risks to the developing fetus. However, if the patient is a frail 80-year-old with advanced cardiovascular disease, then slow and careful titration of medications would be the prudent course to meticulously avoid hypoglycemia. New guidelines from the American Diabetes Association and the European Association for the Study of Diabetes (ADA/EASD)3 are helpful in that they identify various clinical issues and give guidance on which medication regimens would be more appropriate for the specific clinical history. They categorize medications based on efficacy, weight gain, hypoglycemia, major side effects, and costs. Guidelines from the American Association of Clinical Endocrinologists/American College of Endocrinology (AACE/ACE)4 are also very useful, because they categorize treatment based on the A1C level, as well as potential for weight gain and hypoglycemia. For example, a patient with an A1C < 7.5% may be an appropriate candidate for monotherapy, while a symptomatic patient with an A1C > 9% would likely benefit from insulin therapy or triple oral agent therapy. First, it is helpful to set individual glycemic targets for your patient. The following factors can help you in determining A1C targets: • Psychosocial considerations (motivation, adherence to therapy, self-care capacity) • Resources or support systems (family support, community resources, living situation, etc) • Risk for hypoglycemia • Duration of diabetes • Life expectancy • Microvascular complications • Cardiovascular disease and coexisting conditions. For example, an older individual with poor motivation, lack of support systems, short life expectancy, and coexisting terminal cancer would have a less stringent A1C target of ≤ 8%, whereas a young, motivated individual with no complications or serious coexisting complications would have an A1C target of 6%. The new ADA/EASD guidelines list additional considerations for medication choices for various comorbidities, including coronary disease, heart failure, renal disease, liver dysfunction, and hypoglycemia. For each comorbidity listed, there are suggested medications that are preferred and those that should be avoided. If your goal is to avoid hypoglycemia, the ADA/EASD guidelines list medication choices that have low propensity to cause hypoglycemia (eg, metformin, pioglitazone, DPP-4 inhibitors, and GLP-1 receptor agonists). (Of note, special attention is given to medications that do not cause weight gain, such as GLP-1 receptor agonists, DPP-4 inhibitors, and metformin.) Finally, the consensus statement emphasizes the need for individualizing therapy. Many patients have multiple comorbidities and may have medication sensitivities, cost constraints, etc. All of these factors must be taken into consideration when making therapeutic choices. Keep in mind, “one size does not fit all” when it comes to diabetes therapy. The recent releases from both the ADA/EASD and AACE/ACE give us much more detailed guidance addressing medication choices in regard to efficacy, potential for hypoglycemia and weight gain, major side effects, and costs. As always, guidelines do not replace good clinical judgment, based on the patient sitting in front of you. REFERENCES 2. Pimazoni-Netto A, Rodbard D, Zanella MT; Diabetes Education and Control Group. Rapid improvement of glycemic control in type 2 diabetes using weekly intensive multifactorial interventions: structured glucose monitoring, patient education, and adjustment of therapy—a randomized controlled trial. Diabetes Technol Therapeutics. 2011;13(10):997-1004. 3. Inzucchi SE, Bergenstahl RM, Buse JB, et al. Management of hyperglycemia in type 2 diabetes: a patient centered approach. Diabetes Care. [Epub ahead of print; April 19, 2012]. 4. Rodbard HW, Jellinger PS, Davidson JA, et al. Statement by an American Association of Clinical Endocrinologists/American College of Endocrinology consensus panel on type 2 diabetes mellitus: an algorithm for glycemic control. Endocr Pract. 2009;15(6):540-559. |
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Q: I am frustrated by the “always bring the blood sugars down slowly” philosophy, which I know is intended to avoid hypoglycemic symptoms. However, it often seems to be done at the expense of prolonged hyperglycemia, which is dangerous for patients’ long-term health and may cause more rapid beta-cell destruction. What’s the deal? There is evidence that rapid achievement of tight glucose control using intensive insulin therapy with multiple daily injections or insulin pumps in patients with newly diagnosed type 2 diabetes has favorable outcomes on recovery and maintenance of beta-cell function and prolonged glycemic remission, compared with treatment with oral hypoglycemic agents.1 However, this approach is time consuming and not practical in most primary care settings. Overcoming “clinical inertia” (the failure to initiate or intensify therapy when indicated) has been identified as a major barrier to achieving rapid glycemic control, to the detriment of the patient’s health. One recent study showed that more frequent follow-up with a multidisciplinary team and regular use of a computer-analyzed 7-point glucose profile resulted in more rapid and significantly better glycemic control with a lower A1C, compared to standard care.2 This approach is much more practical in a primary care setting. Additionally, we always treat our patients as individuals. There are very few maxims that are correct in all situations. Almost every answer to a clinical question begins with the qualifier “It depends….” The specifics of the individual case will clarify the appropriate answer. In regard to this particular question, the answer will vary by the clinical history of the patient. For example, for a pregnant patient with poor glycemic control, potential hospitalization and rapid titration of insulin would be the most judicious plan. In this case, quickly bringing glucose into tight control helps minimize risks to the developing fetus. However, if the patient is a frail 80-year-old with advanced cardiovascular disease, then slow and careful titration of medications would be the prudent course to meticulously avoid hypoglycemia. New guidelines from the American Diabetes Association and the European Association for the Study of Diabetes (ADA/EASD)3 are helpful in that they identify various clinical issues and give guidance on which medication regimens would be more appropriate for the specific clinical history. They categorize medications based on efficacy, weight gain, hypoglycemia, major side effects, and costs. Guidelines from the American Association of Clinical Endocrinologists/American College of Endocrinology (AACE/ACE)4 are also very useful, because they categorize treatment based on the A1C level, as well as potential for weight gain and hypoglycemia. For example, a patient with an A1C < 7.5% may be an appropriate candidate for monotherapy, while a symptomatic patient with an A1C > 9% would likely benefit from insulin therapy or triple oral agent therapy. First, it is helpful to set individual glycemic targets for your patient. The following factors can help you in determining A1C targets: • Psychosocial considerations (motivation, adherence to therapy, self-care capacity) • Resources or support systems (family support, community resources, living situation, etc) • Risk for hypoglycemia • Duration of diabetes • Life expectancy • Microvascular complications • Cardiovascular disease and coexisting conditions. For example, an older individual with poor motivation, lack of support systems, short life expectancy, and coexisting terminal cancer would have a less stringent A1C target of ≤ 8%, whereas a young, motivated individual with no complications or serious coexisting complications would have an A1C target of 6%. The new ADA/EASD guidelines list additional considerations for medication choices for various comorbidities, including coronary disease, heart failure, renal disease, liver dysfunction, and hypoglycemia. For each comorbidity listed, there are suggested medications that are preferred and those that should be avoided. If your goal is to avoid hypoglycemia, the ADA/EASD guidelines list medication choices that have low propensity to cause hypoglycemia (eg, metformin, pioglitazone, DPP-4 inhibitors, and GLP-1 receptor agonists). (Of note, special attention is given to medications that do not cause weight gain, such as GLP-1 receptor agonists, DPP-4 inhibitors, and metformin.) Finally, the consensus statement emphasizes the need for individualizing therapy. Many patients have multiple comorbidities and may have medication sensitivities, cost constraints, etc. All of these factors must be taken into consideration when making therapeutic choices. Keep in mind, “one size does not fit all” when it comes to diabetes therapy. The recent releases from both the ADA/EASD and AACE/ACE give us much more detailed guidance addressing medication choices in regard to efficacy, potential for hypoglycemia and weight gain, major side effects, and costs. As always, guidelines do not replace good clinical judgment, based on the patient sitting in front of you. REFERENCES 2. Pimazoni-Netto A, Rodbard D, Zanella MT; Diabetes Education and Control Group. Rapid improvement of glycemic control in type 2 diabetes using weekly intensive multifactorial interventions: structured glucose monitoring, patient education, and adjustment of therapy—a randomized controlled trial. Diabetes Technol Therapeutics. 2011;13(10):997-1004. 3. Inzucchi SE, Bergenstahl RM, Buse JB, et al. Management of hyperglycemia in type 2 diabetes: a patient centered approach. Diabetes Care. [Epub ahead of print; April 19, 2012]. 4. Rodbard HW, Jellinger PS, Davidson JA, et al. Statement by an American Association of Clinical Endocrinologists/American College of Endocrinology consensus panel on type 2 diabetes mellitus: an algorithm for glycemic control. Endocr Pract. 2009;15(6):540-559. |
Q: I am frustrated by the “always bring the blood sugars down slowly” philosophy, which I know is intended to avoid hypoglycemic symptoms. However, it often seems to be done at the expense of prolonged hyperglycemia, which is dangerous for patients’ long-term health and may cause more rapid beta-cell destruction. What’s the deal? There is evidence that rapid achievement of tight glucose control using intensive insulin therapy with multiple daily injections or insulin pumps in patients with newly diagnosed type 2 diabetes has favorable outcomes on recovery and maintenance of beta-cell function and prolonged glycemic remission, compared with treatment with oral hypoglycemic agents.1 However, this approach is time consuming and not practical in most primary care settings. Overcoming “clinical inertia” (the failure to initiate or intensify therapy when indicated) has been identified as a major barrier to achieving rapid glycemic control, to the detriment of the patient’s health. One recent study showed that more frequent follow-up with a multidisciplinary team and regular use of a computer-analyzed 7-point glucose profile resulted in more rapid and significantly better glycemic control with a lower A1C, compared to standard care.2 This approach is much more practical in a primary care setting. Additionally, we always treat our patients as individuals. There are very few maxims that are correct in all situations. Almost every answer to a clinical question begins with the qualifier “It depends….” The specifics of the individual case will clarify the appropriate answer. In regard to this particular question, the answer will vary by the clinical history of the patient. For example, for a pregnant patient with poor glycemic control, potential hospitalization and rapid titration of insulin would be the most judicious plan. In this case, quickly bringing glucose into tight control helps minimize risks to the developing fetus. However, if the patient is a frail 80-year-old with advanced cardiovascular disease, then slow and careful titration of medications would be the prudent course to meticulously avoid hypoglycemia. New guidelines from the American Diabetes Association and the European Association for the Study of Diabetes (ADA/EASD)3 are helpful in that they identify various clinical issues and give guidance on which medication regimens would be more appropriate for the specific clinical history. They categorize medications based on efficacy, weight gain, hypoglycemia, major side effects, and costs. Guidelines from the American Association of Clinical Endocrinologists/American College of Endocrinology (AACE/ACE)4 are also very useful, because they categorize treatment based on the A1C level, as well as potential for weight gain and hypoglycemia. For example, a patient with an A1C < 7.5% may be an appropriate candidate for monotherapy, while a symptomatic patient with an A1C > 9% would likely benefit from insulin therapy or triple oral agent therapy. First, it is helpful to set individual glycemic targets for your patient. The following factors can help you in determining A1C targets: • Psychosocial considerations (motivation, adherence to therapy, self-care capacity) • Resources or support systems (family support, community resources, living situation, etc) • Risk for hypoglycemia • Duration of diabetes • Life expectancy • Microvascular complications • Cardiovascular disease and coexisting conditions. For example, an older individual with poor motivation, lack of support systems, short life expectancy, and coexisting terminal cancer would have a less stringent A1C target of ≤ 8%, whereas a young, motivated individual with no complications or serious coexisting complications would have an A1C target of 6%. The new ADA/EASD guidelines list additional considerations for medication choices for various comorbidities, including coronary disease, heart failure, renal disease, liver dysfunction, and hypoglycemia. For each comorbidity listed, there are suggested medications that are preferred and those that should be avoided. If your goal is to avoid hypoglycemia, the ADA/EASD guidelines list medication choices that have low propensity to cause hypoglycemia (eg, metformin, pioglitazone, DPP-4 inhibitors, and GLP-1 receptor agonists). (Of note, special attention is given to medications that do not cause weight gain, such as GLP-1 receptor agonists, DPP-4 inhibitors, and metformin.) Finally, the consensus statement emphasizes the need for individualizing therapy. Many patients have multiple comorbidities and may have medication sensitivities, cost constraints, etc. All of these factors must be taken into consideration when making therapeutic choices. Keep in mind, “one size does not fit all” when it comes to diabetes therapy. The recent releases from both the ADA/EASD and AACE/ACE give us much more detailed guidance addressing medication choices in regard to efficacy, potential for hypoglycemia and weight gain, major side effects, and costs. As always, guidelines do not replace good clinical judgment, based on the patient sitting in front of you. REFERENCES 2. Pimazoni-Netto A, Rodbard D, Zanella MT; Diabetes Education and Control Group. Rapid improvement of glycemic control in type 2 diabetes using weekly intensive multifactorial interventions: structured glucose monitoring, patient education, and adjustment of therapy—a randomized controlled trial. Diabetes Technol Therapeutics. 2011;13(10):997-1004. 3. Inzucchi SE, Bergenstahl RM, Buse JB, et al. Management of hyperglycemia in type 2 diabetes: a patient centered approach. Diabetes Care. [Epub ahead of print; April 19, 2012]. 4. Rodbard HW, Jellinger PS, Davidson JA, et al. Statement by an American Association of Clinical Endocrinologists/American College of Endocrinology consensus panel on type 2 diabetes mellitus: an algorithm for glycemic control. Endocr Pract. 2009;15(6):540-559. |
Thyroid Peroxidase Antibodies
Q: I have a patient with premature ovarian failure (diagnosed when she was 32) who is now in her late 40s. She is fatigued, and a blood test revealed a thyroid peroxidase antibodies level of 587 IU/mL. Would you supplement with thyroid replacement hormone, even though she has a TSH of 1.004?
The short answer is: No. Thyroid peroxidase (TPO) antibodies are a marker for the presence of autoimmune thyroid disease. Blood test results for TPO antibodies are positive in 95% of patients with chronic lymphocytic thyroiditis, also known as Hashimoto’s disease, and in 50% to 80% of patients with Graves’ disease.
Patients with high levels of TPO antibodies are at risk for future thyroid dysfunction. Not all patients with Hashimoto’s develop hypothyroidism, and if present, it may not persist. Patients with Hashimoto’s, although rarely, can experience a change from a hypothyroid to a euthyroid or even a hyperthyroid state, because of the development of coexisting TSH-receptor antibodies (TRAb), which include thyroid-stimulating immunoglobulin (TSI) and thyrotropin-binding inhibitory immunoglobulin (TBII), as seen in Graves’ disease.
Thyroid nodules are common with Hashimoto’s and are associated with a small risk (5% to 7%) for thyroid cancer. Sudden enlargement of the thyroid gland in a patient with Hashimoto’s should raise concern about thyroid lymphoma. Some endocrinologists will give supplemental thyroid hormone to a patient with Hashimoto’s, even if the TSH is normal, in an attempt to shrink the size of the gland. However, the closer the TSH is to < 1, the less room there is to further suppress it without making the patient overtly hyperthyroid, and the less likely it is that you will achieve much shrinkage of the gland.
Therefore, in the absence of a symptomatic goiter, there is no clinical reason to initiate any therapy. Even with mildly elevated TSH levels (5 to 10 mIU/L; ie, subclinical hypothyroidism) in an asymptomatic patient, there is considerable controversy about thyroid hormone initiation when the free T4 and T3 levels are normal. Most authorities agree that treatment should be initiated in most patients when the TSH rises above 10 mIU/L, regardless of symptoms. However, there are clearer indications to start thyroid hormone in women who want to become, or who are, pregnant, to maintain a TSH of < 2.5 mIU/L. Also, individuals with depression or hyperlipidemia warrant extra consideration for the use of thyroid hormone.
Since this particular patient had premature ovarian failure, which is often autoimmune in nature, she must be considered at risk for future development of hypothyroidism. This patient should be followed annually to ensure that her TSH does not rise. Should she develop symptoms suggestive of hypothyroidism and her TSH rises above 3, some endocrinologists would initiate a brief empiric trial of thyroid replacement to see if her symptoms respond when the TSH lowers again. If they do not, the thyroid hormone might be stopped, and the patient should continue to be followed.
Note: The definition of a “normal” TSH is evolving. Levels above 3.0 (suggested normal therapeutic range: 0.5 to 3.0) are considered possibly suspicious in symptomatic young people, while levels slightly above the normal reference range (5 to 7 mIU/L) may be deemed normal for the asymptomatic geriatric population.
The other point to remember is that when a clinician initiates any thyroid therapy, some patients fixate on the thyroid as the only source of their symptoms, such as fatigue, weight gain, and obesity, to the exclusion of any other etiologies. For example, sleep deprivation is a far more common cause of fatigue in our “open 24 hours” society, and lifestyle remains the major cause of obesity. Thus, there can be unintended consequences of a diagnosis of thyroid “disease.”
SUGGESTED READING
American Association of Clinical Endocrinologists medical guidelines for clinical practice for the evaluation and treatment of hyperthyroidism and hypothyroidism. www.aace.com/publications/guidelines. Accessed March 5, 2012.
Bremner AP, Feddema P, Leedman PJ, et al. Age-related changes in thyroid function: a longitudinal study of a community-based cohort. J Clin Endocrinol Metab. 2012 Feb 16; [Epub ahead of print].
Hutfless S, Matos P, Talor MV, et al. Significance of prediagnostic thyroid antibodies in women with autoimmune thyroid disease. J Clin Endocrinol Metab. 2011;96(9):E1466-E1471.
Kauffman RP, Castracane VD. Premature ovarian failure associated with autoimmune polyglandular syndrome: pathophysiological mechanisms and future fertility. J Womens Health (Larchmt). 2003;12(5):513-520.
| Clinician Reviews in partnership with |
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| Clinician Reviews in partnership with |
|
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| Clinician Reviews in partnership with |
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Q: I have a patient with premature ovarian failure (diagnosed when she was 32) who is now in her late 40s. She is fatigued, and a blood test revealed a thyroid peroxidase antibodies level of 587 IU/mL. Would you supplement with thyroid replacement hormone, even though she has a TSH of 1.004?
The short answer is: No. Thyroid peroxidase (TPO) antibodies are a marker for the presence of autoimmune thyroid disease. Blood test results for TPO antibodies are positive in 95% of patients with chronic lymphocytic thyroiditis, also known as Hashimoto’s disease, and in 50% to 80% of patients with Graves’ disease.
Patients with high levels of TPO antibodies are at risk for future thyroid dysfunction. Not all patients with Hashimoto’s develop hypothyroidism, and if present, it may not persist. Patients with Hashimoto’s, although rarely, can experience a change from a hypothyroid to a euthyroid or even a hyperthyroid state, because of the development of coexisting TSH-receptor antibodies (TRAb), which include thyroid-stimulating immunoglobulin (TSI) and thyrotropin-binding inhibitory immunoglobulin (TBII), as seen in Graves’ disease.
Thyroid nodules are common with Hashimoto’s and are associated with a small risk (5% to 7%) for thyroid cancer. Sudden enlargement of the thyroid gland in a patient with Hashimoto’s should raise concern about thyroid lymphoma. Some endocrinologists will give supplemental thyroid hormone to a patient with Hashimoto’s, even if the TSH is normal, in an attempt to shrink the size of the gland. However, the closer the TSH is to < 1, the less room there is to further suppress it without making the patient overtly hyperthyroid, and the less likely it is that you will achieve much shrinkage of the gland.
Therefore, in the absence of a symptomatic goiter, there is no clinical reason to initiate any therapy. Even with mildly elevated TSH levels (5 to 10 mIU/L; ie, subclinical hypothyroidism) in an asymptomatic patient, there is considerable controversy about thyroid hormone initiation when the free T4 and T3 levels are normal. Most authorities agree that treatment should be initiated in most patients when the TSH rises above 10 mIU/L, regardless of symptoms. However, there are clearer indications to start thyroid hormone in women who want to become, or who are, pregnant, to maintain a TSH of < 2.5 mIU/L. Also, individuals with depression or hyperlipidemia warrant extra consideration for the use of thyroid hormone.
Since this particular patient had premature ovarian failure, which is often autoimmune in nature, she must be considered at risk for future development of hypothyroidism. This patient should be followed annually to ensure that her TSH does not rise. Should she develop symptoms suggestive of hypothyroidism and her TSH rises above 3, some endocrinologists would initiate a brief empiric trial of thyroid replacement to see if her symptoms respond when the TSH lowers again. If they do not, the thyroid hormone might be stopped, and the patient should continue to be followed.
Note: The definition of a “normal” TSH is evolving. Levels above 3.0 (suggested normal therapeutic range: 0.5 to 3.0) are considered possibly suspicious in symptomatic young people, while levels slightly above the normal reference range (5 to 7 mIU/L) may be deemed normal for the asymptomatic geriatric population.
The other point to remember is that when a clinician initiates any thyroid therapy, some patients fixate on the thyroid as the only source of their symptoms, such as fatigue, weight gain, and obesity, to the exclusion of any other etiologies. For example, sleep deprivation is a far more common cause of fatigue in our “open 24 hours” society, and lifestyle remains the major cause of obesity. Thus, there can be unintended consequences of a diagnosis of thyroid “disease.”
SUGGESTED READING
American Association of Clinical Endocrinologists medical guidelines for clinical practice for the evaluation and treatment of hyperthyroidism and hypothyroidism. www.aace.com/publications/guidelines. Accessed March 5, 2012.
Bremner AP, Feddema P, Leedman PJ, et al. Age-related changes in thyroid function: a longitudinal study of a community-based cohort. J Clin Endocrinol Metab. 2012 Feb 16; [Epub ahead of print].
Hutfless S, Matos P, Talor MV, et al. Significance of prediagnostic thyroid antibodies in women with autoimmune thyroid disease. J Clin Endocrinol Metab. 2011;96(9):E1466-E1471.
Kauffman RP, Castracane VD. Premature ovarian failure associated with autoimmune polyglandular syndrome: pathophysiological mechanisms and future fertility. J Womens Health (Larchmt). 2003;12(5):513-520.
Q: I have a patient with premature ovarian failure (diagnosed when she was 32) who is now in her late 40s. She is fatigued, and a blood test revealed a thyroid peroxidase antibodies level of 587 IU/mL. Would you supplement with thyroid replacement hormone, even though she has a TSH of 1.004?
The short answer is: No. Thyroid peroxidase (TPO) antibodies are a marker for the presence of autoimmune thyroid disease. Blood test results for TPO antibodies are positive in 95% of patients with chronic lymphocytic thyroiditis, also known as Hashimoto’s disease, and in 50% to 80% of patients with Graves’ disease.
Patients with high levels of TPO antibodies are at risk for future thyroid dysfunction. Not all patients with Hashimoto’s develop hypothyroidism, and if present, it may not persist. Patients with Hashimoto’s, although rarely, can experience a change from a hypothyroid to a euthyroid or even a hyperthyroid state, because of the development of coexisting TSH-receptor antibodies (TRAb), which include thyroid-stimulating immunoglobulin (TSI) and thyrotropin-binding inhibitory immunoglobulin (TBII), as seen in Graves’ disease.
Thyroid nodules are common with Hashimoto’s and are associated with a small risk (5% to 7%) for thyroid cancer. Sudden enlargement of the thyroid gland in a patient with Hashimoto’s should raise concern about thyroid lymphoma. Some endocrinologists will give supplemental thyroid hormone to a patient with Hashimoto’s, even if the TSH is normal, in an attempt to shrink the size of the gland. However, the closer the TSH is to < 1, the less room there is to further suppress it without making the patient overtly hyperthyroid, and the less likely it is that you will achieve much shrinkage of the gland.
Therefore, in the absence of a symptomatic goiter, there is no clinical reason to initiate any therapy. Even with mildly elevated TSH levels (5 to 10 mIU/L; ie, subclinical hypothyroidism) in an asymptomatic patient, there is considerable controversy about thyroid hormone initiation when the free T4 and T3 levels are normal. Most authorities agree that treatment should be initiated in most patients when the TSH rises above 10 mIU/L, regardless of symptoms. However, there are clearer indications to start thyroid hormone in women who want to become, or who are, pregnant, to maintain a TSH of < 2.5 mIU/L. Also, individuals with depression or hyperlipidemia warrant extra consideration for the use of thyroid hormone.
Since this particular patient had premature ovarian failure, which is often autoimmune in nature, she must be considered at risk for future development of hypothyroidism. This patient should be followed annually to ensure that her TSH does not rise. Should she develop symptoms suggestive of hypothyroidism and her TSH rises above 3, some endocrinologists would initiate a brief empiric trial of thyroid replacement to see if her symptoms respond when the TSH lowers again. If they do not, the thyroid hormone might be stopped, and the patient should continue to be followed.
Note: The definition of a “normal” TSH is evolving. Levels above 3.0 (suggested normal therapeutic range: 0.5 to 3.0) are considered possibly suspicious in symptomatic young people, while levels slightly above the normal reference range (5 to 7 mIU/L) may be deemed normal for the asymptomatic geriatric population.
The other point to remember is that when a clinician initiates any thyroid therapy, some patients fixate on the thyroid as the only source of their symptoms, such as fatigue, weight gain, and obesity, to the exclusion of any other etiologies. For example, sleep deprivation is a far more common cause of fatigue in our “open 24 hours” society, and lifestyle remains the major cause of obesity. Thus, there can be unintended consequences of a diagnosis of thyroid “disease.”
SUGGESTED READING
American Association of Clinical Endocrinologists medical guidelines for clinical practice for the evaluation and treatment of hyperthyroidism and hypothyroidism. www.aace.com/publications/guidelines. Accessed March 5, 2012.
Bremner AP, Feddema P, Leedman PJ, et al. Age-related changes in thyroid function: a longitudinal study of a community-based cohort. J Clin Endocrinol Metab. 2012 Feb 16; [Epub ahead of print].
Hutfless S, Matos P, Talor MV, et al. Significance of prediagnostic thyroid antibodies in women with autoimmune thyroid disease. J Clin Endocrinol Metab. 2011;96(9):E1466-E1471.
Kauffman RP, Castracane VD. Premature ovarian failure associated with autoimmune polyglandular syndrome: pathophysiological mechanisms and future fertility. J Womens Health (Larchmt). 2003;12(5):513-520.