Hypothyroidism Presenting as Tendinitis
William D. Knopp, MD; Matthew E. Bohm, MD; James C. McCoy, MDTHE PHYSICIAN AND SPORTSMEDICINE - VOL 25 - NO. 1 - JANUARY 97
In Brief: Hypothyroidism usually presents insidiously with symptoms such as fatigue, cold intolerance, and weight gain. Less common findings include myalgia, arthralgia, and joint effusion. In the patient described here, a triathlete, interpretation of early signs and symptoms as typical tendinitis led to months of treatment failure. Considering hypothyroidism in the differential diagnosis for patients who have overuse syndromes can expedite treatment. Definitive diagnosis rests on testing of serum thyroid hormone levels. Treatment, which is usually quickly effective, consists of gradually adjusted thyroid hormone replacement.
The symptoms of hypothyroidism, like those of other diseases with nonspecific, insidious onset, can be interpreted in many ways by both patient and physician. Particularly in active patients, for whom fatigue, aches, and "playing through pain" may be second nature, a high index of suspicion is needed to correctly interpret early signs and symptoms. Such was the case with the triathlete described here, whose symptoms were attributed to patellar tendinitis, shoulder impingement, lateral epicondylitis, and fibromyalgia before the correct diagnosis was made.
A 45-year-old man who had been competing in triathlons and marathons for 6 years gradually developed left knee pain. His usual training regimen consisted of running 20 miles, biking 75 miles, and swimming 4 miles each week. For 3 months he had iced the knee and decreased his training distances without relief.
Early course. On initial presentation, his physician gave a diagnosis of patellar tendinitis. He was treated with nonsteroidal anti-inflammatory drugs (NSAIDs), a further decrease in his training, and physical therapy. However, the patient's knee pain worsened, and his performance declined. To reduce the knee stress, he decreased his running mileage and increased his swimming distance to maintain the same training effect. One month later, left shoulder discomfort developed. He was again evaluated by his physician, who made a diagnosis of impingement syndrome. Conservative therapy consisting of icing, NSAIDs, decreased training, and physical therapy was initiated. Later, two subacromial corticosteroid injections were given and provided only brief relief.
Progressive illness. Over the next several months the shoulder and knee discomfort worsened. The athlete then began experiencing left elbow pain consistent with lateral epicondylitis, which further decreased his ability to train. Shortly thereafter he noticed a decrease in his endurance, and he was becoming increasingly fatigued during and after exercise. Eventually he had difficulty completing one lap in the pool because of pain and exhaustion. Ultimately, he was unable to continue training and found it difficult simply walking from room to room. Another physician was consulted, who made an initial diagnosis of fibromyalgia.
Physical examination. On physical examination in our office, the patient presented as a healthy-appearing male with good muscle tone. Examination of the knee revealed mild swelling and tenderness about the patellar tendon. No patellofemoral compression symptoms or crepitation was evident. Knee ligaments were normal and the patient exhibited no meniscal rotation signs. The shoulder examination was significant for impingement signs on the left. Rotator cuff strength was normal. Crossover and stability testing were normal, and the remainder of the shoulder exam was unremarkable. The elbow examination was positive for tenderness about the lateral epicondyle, particularly with resisted wrist extension. The heart, lung, abdomen, thyroid, skin, and neurologic exams, including deep tendon reflexes, were normal.
At this point, the differential diagnosis included patellar tendinitis, rotator cuff tendinitis, lateral epicondylitis, fibromyalgia, and, because of the patient's extreme fatigue, hypothyroidism.
Laboratory testing. Plain x-rays and magnetic resonance imaging (MRI) of the knee and shoulder were normal. Despite the absence of synovitis, a complete blood count, antinuclear antibody, rheumatoid factor, and erythrocyte sedimentation rate were ordered and were normal. However, the serum thyroid-stimulating hormone (TSH) was elevated at 20.4 microunits/mL (normal, 2 to 11 microunits/mL), and the serum thyroxine (T4) was low at 2.4 micrograms/dL (4 to 11 micrograms/dL).
Diagnosis. The final working diagnosis was patellar tendinitis, rotator cuff tendinitis, and lateral epicondylitis secondary to idiopathic hypothyroidism.
Treatment. The patient was started on thyroid hormone replacement with levothyroxine sodium. He noticed improvement in his symptoms 2 to 3 weeks after the initiation of treatment. His rehabilitation continued with gradual increases in activity level and improvement in athletic performance. He returned to competing in triathlons and marathons 3 1/2 months after initiation of levothyroxine. Previous musculoskeletal symptoms and fatigue did not recur. He has since attained personal best race times and has had his best triathlon season.
Hypothyroidism, a disorder commonly seen in primary care medicine, is a metabolic state caused by thyroid hormone deficiency. The overall prevalence in the adult population is 1%. The condition is more common in women, and the prevalence may reach 5% in the elderly (1). Once suspected, the diagnosis is easily established in all but rare cases by the history, physical examination, and laboratory findings.
Hypothyroidism can be primary or secondary. In primary hypothyroidism, the hormone deficiency results from a disease or process within the thyroid gland. Hashimoto's disease, an immune-mediated thyroiditis, is an example. In this condition, blockade of thyroid TSH-receptors results in decreased T4 production. The hypothalamus responds by increasing thyrotropin-releasing hormone (TRH) output, which results in TSH secretion, thus stimulating thyroid gland enlargement and goiter formation. In this and other forms of primary hypothyroidism, serum TSH is elevated and the free thyroxine (FT4) is low.
Secondary hypothyroidism, which is rare, is characterized by measurably decreased TSH secretion secondary to hypothalamic-pituitary axis impairment. Pituitary adenoma is the most common cause. The inadequate TSH results in a normal-to-small thyroid gland and decreased synthesis of triiodothyronine (T3) and T4.
The two most common causes of hypothyroidism (surgical thyroidectomy and radioactive iodine ablation for treatment of hyperthyroidism, followed by idiopathic atrophy of the thyroid) are both primary. Other causes include recent viral infection, side effects of other medications (lithium, para-aminosalicylic acid, excessive iodide), pituitary surgery or irradiation, and recent pregnancy (postpartum thyroiditis is seen in up to 5% of postpartum women (2,3)).
The onset of hypothyroidism is usually gradual. The decreases in thyroid hormone manifest as reduced metabolic rate and sensitivity to endogenous catecholamines. Common early signs and symptoms include fatigue (present in 91% of patients), cold intolerance (83%), weight gain (59%), dry skin (97%), constipation (61%), and menorrhagia (32% of women). As the disease progresses, depression, coarse hair (76%), hoarseness (52%), memory impairment (68%), muscle weakness (99%), myalgia, arthralgia, joint effusion, and hand paresthesia (such as carpal tunnel syndrome) may be present (4,5). In severe cases, myxedema may occur, presenting with doughy skin, edematous face, lethargy, slow speech, hearing loss, and an enlarged tongue, among other symptoms.
Physical examination may reveal an enlarged thyroid gland. A tender thyroid suggests subacute thyroiditis, while a nontender gland is more common in early Hashimoto's disease or postpartum thyroiditis. A rubbery, multinodular goiter suggests more advanced Hashimoto's. Deep tendon reflexes may be slowed. Symptoms of secondary hypothyroidism, such as the loss of axillary and pubic hair seen in ovarian and adrenal insufficiency, should also be noted, though they are much less common.
The first element of the laboratory evaluation should be a check of serum TSH concentration, since abnormalities mark and differentiate primary and secondary disease (6). Some authors suggest checking FT4 or the FT4 index. Obtaining total T3 levels is generally unnecessary, and a TRH study is not usually needed unless the TSH and T4 are low. If Hashimoto's disease is suspected, a positive antimicrosomal antibody test confirms the diagnosis. If the clinical exam strongly suggests hypothyroidism and the TSH is not elevated, testing for pituitary insufficiency is warranted. Further workup might include computed tomography or MRI, TRH stimulation testing, and luteinizing hormone, follicle-stimulating hormone, adrenocorticotropin, and prolactin levels. Also common in hypothyroidism, but of little diagnostic significance, are hypercholesterolemia (increased low-density lipoprotein and decreased high-density lipoprotein), anemia (usually normochromic, normocytic), and elevated serum concentrations of skeletal muscle enzymes (creatine kinase, alanine aminotransferase, aspartate aminotransferase, and lactate dehydrogenase).
Treatment for hypothyroidism regardless of cause requires thyroid hormone replacement with levothyroxine. The starting dose and rate of adjustment depend on factors such as age, height, weight, presence of heart disease, and symptom severity. A young, otherwise healthy person may be started on 0.05 mg to 0.10 mg of levothyroxine daily. Adjustments may be made at 0.025 mg to 0.05 mg increments every 4 to 6 weeks. Although T4 levels equilibrate in 2 to 3 weeks, TSH levels take at least 4 weeks to reach steady state. Feeling that overcautious therapy may needlessly prolong the hypothyroid state, some authors (7) suggest that an otherwise healthy patient with no medical problems or coronary artery disease may be started at the upper end of this spectrum. In a young, healthy patient, a full replacement dosage (1 to 2 micrograms/kg/day) can be started at the onset of therapy (7). Because patients older than 50 are at greater risk of heart disease, therapy should be initiated between 0.025 mg and 0.05 mg daily and adjusted in 0.025-mg increments. If angina or other cardiac symptoms present, the dose will need to be reduced (8). Other possible side effects of excessive replacement are palpitations, tremors, and anxiety. Excessive replacement may also increase the risk of osteoporosis (9-11). Long-term, most people need about 0.125 mg of levothyroxine per day. The elderly generally require about 20% less. TSH levels should be checked to monitor adjustments. Once stable, TSH levels may be checked once or twice yearly.
Participation in athletics commonly leads to some form of discomfort or injury, and symptoms associated with training may be the only presenting symptoms of hypothyroidism. Also, many athletes attempt to train through minor injuries. Thus, manifestations of hypothyroidism may be masked in active individuals, in whom musculoskeletal symptoms may be perceived as the normal strain of their training routine.
Our patient, as an endurance athlete, was vulnerable to overuse injuries and had symptoms relatively common for a triathlete. Although he developed tendinitis in three separate anatomic locations, the thought of an underlying medical disorder was initially overlooked. Only after many months of failed treatment, symptom progression, and onset of fatigue was hypothyroidism considered. Further clouding matters, the athlete had denied the classic symptoms of hypothyroidism, although he noted in retrospect that he might have experienced some of them. He described, for example, a mild dysphoria during the symptomatic period, which he had attributed to his inability to work out consistently. He had also decreased his food intake to avoid weight gain and had increased his fiber intake to avoid constipation, but had perceived these as sequelae of his decreased activity level.
The patient's symptoms improved rapidly after levothyroxine was started. Symptoms resolved within 4 months, despite his dramatically increasing his training program. Rapid improvement of rheumatologic symptoms of hypothyroidism, such as arthralgia, myalgia, and joint effusion, after initiation of levothyroxine is common (12,13). For example, patients presenting with generalized muscle and joint pain, stiffness, and cramps, many for more than a year, have been shown to improve significantly within 2 weeks of initiating thyroid replacement (14,15).
Rheumatologic and musculoskeletal symptoms of hypothyroidism as varied as those in adults have been reported in children. Like adults, children experience relief of their musculoskeletal complaints 2 to 8 weeks after beginning replacement therapy (16).
Hypothyroidism presenting, as in our patient, with symptoms of a specific primary musculoskeletal disorder is unusual. Studies of rheumatologic symptoms in hypothyroidism have not documented a specific diagnosis of tendinitis. This makes it impossible to determine whether any of the previously described symptoms, including myalgia, arthralgia, and joint effusion, could have represented a true case of tendinitis. The causal relationship between hypothyroidism and this patient's episodes of tendinitis cannot be proved by this case alone. However, the dramatic improvement and complete resolution of the symptoms with thyroid replacement therapy after failure with all other medical treatments suggest that normal tendon healing is impaired in hypothyroidism.
Widening the Differential
Our patient exhibited an atypical presentation of hypothyroidism, one that to our knowledge has not been previously described. In general, because of hypothyroidism's many vague and insidious symptoms, musculoskeletal pain or complaints of unknown etiology should raise the index of suspicion for this common and readily treatable disorder. Maintaining a broad differential diagnosis for each patient—even those who appear to have straightforward overuse syndromes—will help the alert physician corner this chameleon disease.
Dr Knopp is director of the primary care sports medicine fellowship program at MacNeal Hospital in Berwyn, Illinois. Dr Bohm, a family physician and past fellow at MacNeal Hospital, is now in private practice in Topeka, Kansas. Dr McCoy is vice president of medical affairs at St Francis Hospital in Evanston, Illinois, and is a member of the American Academy of Family Physicians. Address correspondence to William D. Knopp, MD, Family Practice Residency Program, MacNeal Hospital, 3231 S Euclid Ave, Berwyn, IL 60402.