Hypothyroidism Clinical Presentation

  • Author: Shikha Bharaktiya, MD; Chief Editor: George T Griffing, MD   more...
 
Updated: Jul 22, 2011
 

History

Hypothyroidism commonly manifests as a slowing in physical and mental activity but may be asymptomatic. Symptoms and signs of this disease are often subtle and neither sensitive nor specific. Classic signs and symptoms, such as cold intolerance, puffiness, decreased sweating, and coarse skin, previously reported in 90-97% of patients, may actually occur in only 50-64% of younger patients. Many of the more common symptoms are nonspecific and difficult to attribute to a specific cause. Individuals can also present with obstructive sleep apnea (secondary to macroglossia) or carpal tunnel syndrome. Women can present with galactorrhea and menstrual disturbances. Consequently, the diagnosis of hypothyroidism is based on clinical suspicion and confirmed by laboratory testing.

Myxedema coma is a severe form of hypothyroidism that results in an altered mental status, hypothermia, bradycardia, hypercarbia, and hyponatremia. Cardiomegaly, pericardial effusion, cardiogenic shock, and ascites may be present. Myxedema coma most commonly occurs in individuals with undiagnosed or untreated hypothyroidism who are subjected to an external stress, such as low temperature, infection, or medical intervention (eg, surgery or hypnotic drugs).

The following are symptoms of hypothyroidism:

  • Fatigue, loss of energy, lethargy
  • Weight gain
  • Decreased appetite
  • Cold intolerance
  • Dry skin
  • Hair loss
  • Sleepiness
  • Muscle pain, joint pain, weakness in the extremities
  • Depression
  • Emotional lability, mental impairment
  • Forgetfulness, impaired memory, inability to concentrate
  • Constipation
  • Menstrual disturbances, impaired fertility
  • Decreased perspiration
  • Paresthesia and nerve entrapment syndromes
  • Blurred vision
  • Decreased hearing
  • Fullness in the throat, hoarseness

The following are symptoms more specific to Hashimoto thyroiditis:

  • Feeling of fullness in the throat
  • Painless thyroid enlargement
  • Exhaustion
  • Neck pain, sore throat, or both
  • Low-grade fever
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Physical

Signs found in hypothyroidism are usually subtle, and their detection requires a careful physical examination. Moreover, they are often dismissed as part of aging; however, clinicians should consider a diagnosis of hypothyroidism when such signs are present.

Physical signs of hypothyroidism include the following:

  • Hypothermia
  • Weight gain
  • Slowed speech and movements
  • Dry skin
  • Jaundice
  • Pallor
  • Coarse, brittle, strawlike hair
  • Loss of scalp hair, axillary hair, pubic hair, or a combination
  • Dull facial expression
  • Coarse facial features
  • Periorbital puffiness
  • Macroglossia
  • Goiter
  • Hoarseness
  • Decreased systolic blood pressure and increased diastolic blood pressure
  • Bradycardia
  • Pericardial effusion
  • Abdominal distension, ascites (uncommon)
  • Nonpitting edema (myxedema)
  • Pitting edema of lower extremities
  • Hyporeflexia with delayed relaxation, ataxia, or both

Additional signs specific to different causes of hypothyroidism, such as diffuse or nodular goiter or pituitary tumor, can occur.

Metabolic abnormalities associated with hypothyroidism include anemia, dilutional hyponatremia, hyperlipidemia, and reversible increase in creatinine.[5]

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Causes

Worldwide, iodine deficiency remains the foremost cause of hypothyroidism. In the United States and other areas of adequate iodine intake, autoimmune thyroid disease is most common. The prevalence of antibodies is higher in women, and increases with age.

Primary hypothyroidism

Note the following:

  • Autoimmune: The most frequent cause of acquired hypothyroidism is autoimmune thyroiditis (Hashimoto thyroiditis). The body recognizes the thyroid antigens as foreign, and a chronic immune reaction ensues, resulting in lymphocytic infiltration of the gland and progressive destruction of functional thyroid tissue. Up to 95% of affected individuals have circulating antibodies to thyroid tissue. Antimicrosomal or antithyroid peroxidase (anti-TPO) antibodies are found more commonly than antithyroglobulin antibodies (95% vs 60%). These antibodies may not be present early in the disease process and usually disappear over time.[6]
  • Postpartum thyroiditis: Up to 10% of postpartum women may develop lymphocytic thyroiditis in the 2-10 months after delivery. The frequency may be as high as 25% in women with type 1 diabetes mellitus. The condition is usually transient (2-4 mo) and can require a short course of treatment with levothyroxine (LT4), but postpartum patients with lymphocytic thyroiditis are at increased risk of permanent hypothyroidism. The hypothyroid state can be preceded by a short thyrotoxic state. High titers of anti-TPO antibodies during pregnancy have been reported to be 97% sensitive and 91% specific for postpartum autoimmune thyroid disease.
  • Subacute granulomatous thyroiditis: Inflammatory conditions or viral syndromes may be associated with transient hyperthyroidism followed by transient hypothyroidism (de Quervain or painful thyroiditis, subacute thyroiditis). These are often associated with fever, malaise, and a painful and tender gland.
  • Drugs: Medications such as amiodarone, interferon alpha, thalidomide, lithium, and stavudine have also been associated with primary hypothyroidism.
  • Iatrogenic: Use of radioactive iodine for treatment of Graves disease generally results in permanent hypothyroidism within 1 year after therapy. The frequency is much lower in patients with toxic nodular goiters and those with autonomously functioning thyroid nodules. Patients treated with radioiodine should be monitored for clinical and biochemical evidence of hypothyroidism. Thyroidectomy can be used. External neck irradiation (for head and neck neoplasms, breast cancer, or Hodgkin disease) may result in hypothyroidism; patients who have received these treatments require monitoring of thyroid function.
  • Rare: Rare causes include inborn errors of thyroid hormone synthesis.
  • Iodine deficiency or excess: Worldwide, iodine deficiency is the most common cause of hypothyroidism. Excess iodine, as in radiocontrast dyes, amiodarone, health tonics, and seaweed, inhibits iodide organification and thyroid hormone synthesis. Most healthy individuals have a physiologic escape from this effect; however those with abnormal thyroid glands may not. These include patients with autoimmune thyroiditis, surgically treated Graves hyperthyroidism (subtotal thyroidectomy) and prior radioiodine therapy.[7]

Central hypothyroidism

Central hypothyroidism (secondary or tertiary) results when the hypothalamic-pituitary axis is damaged. Various causes should be considered[8, 9] :

  • Pituitary adenoma
  • Tumors impinging on the hypothalamus
  • History of brain irradiation
  • Drugs (eg, dopamine, lithium)
  • Sheehan syndrome
  • Genetic disorders
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Contributor Information and Disclosures
Author

Shikha Bharaktiya, MD  Clinical Fellow, Department of Internal Medicine, Division of Endocrinology and Metabolism, University of Texas Medical School at Houston

Disclosure: Nothing to disclose.

Coauthor(s)

Philip R Orlander, MD  Assistant Dean for Educational Affairs, Vice-Chair of Medicine for Education, Director and Professor, Division of Endocrinology, University of Texas Health Science Center at Houston

Philip R Orlander, MD is a member of the following medical societies: American Association of Clinical Endocrinologists, American Diabetes Association, Endocrine Society, and Texas Medical Association

Disclosure: Nothing to disclose.

Walter R Woodhouse, MD, MSA  Associate Clinical Professor, Department of Family Practice, Medical College of Ohio

Walter R Woodhouse, MD, MSA is a member of the following medical societies: American Academy of Family Physicians, American Academy of Pain Medicine, and Society of Teachers of Family Medicine

Disclosure: Nothing to disclose.

Anu Bhalla Davis, MD  Assistant Professor, Department of Internal Medicine, Division of Diabetes, Endocrinology, and Metabolism, University of Texas Medical School at Houston

Disclosure: Nothing to disclose.

Specialty Editor Board

Frederick H Ziel, MD  Associate Professor of Medicine, University of California, Los Angeles, David Geffen School of Medicine; Physician-In-Charge, Endocrinology/Diabetes Center, Director of Medical Education, Kaiser Permanente Woodland Hills; Chair of Endocrinology, Co-Chair of Diabetes Complete Care Program, Southern California Permanente Medical Group

Frederick H Ziel, MD is a member of the following medical societies: American Association of Clinical Endocrinologists, American College of Endocrinology, American College of Physicians, American College of Physicians-American Society of Internal Medicine, American Diabetes Association, American Federation for Medical Research, American Medical Association, American Society for Bone and Mineral Research, California Medical Association, Endocrine Society, and International Society for Clinical Densitometry

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD  Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Arthur B Chausmer, MD, PhD, FACP, FACE, FACN, CNS  Professor of Medicine (Endocrinology, Adj), Johns Hopkins School of Medicine; Affiliate Research Professor, Bioinformatics and Computational Biology Program, School of Computational Sciences, George Mason University; Principal, C/A Informatics, LLC

Arthur B Chausmer, MD, PhD, FACP, FACE, FACN, CNS is a member of the following medical societies: American Association of Clinical Endocrinologists, American College of Endocrinology, American College of Nutrition, American College of Physicians, American College of Physicians-American Society of Internal Medicine, American Medical Informatics Association, American Society for Bone and Mineral Research, Endocrine Society, and International Society for Clinical Densitometry

Disclosure: Nothing to disclose.

Mark Cooper, MBBS, PhD, FRACP  Head, Diabetes & Metabolism Division, Baker Heart Research Institute, Professor of Medicine, Monash University

Disclosure: Nothing to disclose.

Chief Editor

George T Griffing, MD  Professor of Medicine, St Louis University School of Medicine

George T Griffing, MD is a member of the following medical societies: American Association for the Advancement of Science, American College of Medical Practice Executives, American College of Physician Executives, American College of Physicians, American Diabetes Association, American Federation for Medical Research, American Heart Association, Central Society for Clinical Research, Endocrine Society, International Society for Clinical Densitometry, and Southern Society for Clinical Investigation

Disclosure: Nothing to disclose.

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