This patient presented with severe muscle aches and objective findings of muscle swelling. Her muscle enzymes demonstrated severe hypothyroid myopathy, in association with rapid onset post-I-131 hypothyroidism. Her subsequent course was characterized by hair loss. The exam of her scalp revealed only mild hair thinning and no focal areas of alopecia, leading to a diagnosis of telogen effluvium.

Statistically, the symptoms of hypothyroidism are correlated to the severity of the hormonal deficiency [1]. However there is significant variability [2]. Some patients may report prominent fatigue with modest TSH elevations, while others may be surprisingly free of symptoms, even when profoundly hypothyroid. Unrecognized individual factors may play a role in this variability. The rate of thyroid hormone loss may also be important, with patients in whom hypothyroidism develops rapidly being more symptomatic. Patients with thyroid cancer and surgical hypothyroidism whose thyroxine replacement dose is suddenly held in preparation of radioiodine scanning become typically very symptomatic in a short period of time. Of course these patients are also profoundly hypothyroid, more so than the average patient with Hashimoto’s thyroiditis, whose milder hypothyroidism develops over a long period of time.

Mild muscle and joint aches are common in hypothyroidism. In a study from Canaris [1] muscle aches were among the most specific symptoms in identifying patients with hypothyroidism. Moderately to markedly elevated creatine phosphokinase (CPK) levels are observed in up to 60 % of patients with overt hypothyroidism [3]. These manifestations have been loosely referred to as “hypothyroid myopathy.” The etiology of hypothyroid myopathy remains unclear. A few pathology studies have shown selective loss of type-II fibers, increased nuclear counts and diffuse glycogen inclusions [4]. The range of clinical manifestations is wide, ranging from patients being completely asymptomatic with minimal CPK elevation, some others with significant but nonprogressive myalgias and a small minority developing severe myopathy, rhabdomyolisis, compartment syndrome, and renal failure [5]. The concurrent use of statins may be a risk factor for the development of hypothyroid myopathy. This is demonstrated in several case reports of patients who developed the condition after many years of statin treatment when the hypothyroidism occurred [6]. Thus so far one can draw the following clinical suggestions:

After restoration of euthyroidism, the patient reported concerning hair loss. Hair changes are common in hypothyroidism. In the era of sensitive TSH testing and frequent screening, most patients with hypothyroidism are diagnosed with early and mild forms. The classical finding of coarse, brittle, and sparse hair, which is typically seen only in profound and prolonged hypothyroidism, is nowadays rarely observed. Alopecia areata can be observed with increased frequency in patients with Hashimoto’s thyroiditis [7]. The association is independent of thyroid function status and reflects the common autoimmune background of the two conditions. Alopecia areata is characterized by patchy hair loss developing over a period of weeks or months. The condition is self-limited and remitting in a majority of cases, but it may result in partial or total permanent scalp hair loss (alopecia totalis) [8]. In our patient, the absence of patchy hair loss made alopecia areata unlikely. The history of sudden hair loss, without focal or regional baldness, in coincidence with recent rapid changes suggests the diagnosis of telogen effluvium. Human adult hair cycle is asynchronous, in that at any given moment there is a fraction of hair in the anagen, catagen, or telogen phase, respectively. As a consequence a small constant number of hairs is shed every day, as they end the telogen phase. In telogen effluvium, hair becomes synchronized and the majority of hair rapidly enters the telogen phase at the same time and is subsequently shed. This phenomenon is observed after pregnancy. During pregnancy hair is held in prolonged anagen as a consequence of the hormonal changes associated with pregnancy. This larger-than-normal proportion of hair in anagen then progresses to telogen synchronously after delivery. When the telogen phase is completed, some 3–4 months later, this hair is shed simultaneously, resulting in the distressing observation of large clumps of hair in the shower. However the intact follicles start producing new hair right away and over the next few months the hair is restored to its original thickness and quality. A similar phenomenon occurs after acute illnesses, except that the pathophysiology is sudden and synchronous exit from anagen [9]. This variety of telogen effluvium is particularly common after rapid changes in thyroid hormone levels. It is seen both after correction of hyperthyroidism or hypothyroidism, and after patients become suddenly hypothyroid, for example in preparation of whole body scanning. It is quite common to receive the distressed phone call from a patient who has noticed “clumps and clumps of hair coming off my scalp every day.” In spite of the frequency of this observation, the literature on this topic is surprisingly limited. A few months after stable normal levels of thyroid hormone are achieved, hair regrowth and restoration of previous hair quality are observed. Since there is no known treatment or prevention for this self-limited condition, patients need only be counseled on its reversible nature. Rare forms of chronic telogen effluvium occur, but can be only diagnosed when failure of remission is observed. Understanding of this phenomenon by the endocrinologist will spare unnecessary dermatological consultations.