Skeptical Hyperthyroid Cat

Radiation anxiety

Let's face it, there is a substantial societal anxiety associated with the term “nuclear.” In the United States this anxiety dates back to the threat of nuclear annihilation by the Soviet Union during the cold war (roughly 1947-1989) and has been further fueled by more recent nuclear reactor incidents including those at Three Mile Island (1979), Chernobyl (1986) and most recently Fukushima (2012). These incidents clearly demonstrate the significant potential for injury to people and animals when nuclear reactors are subjected to human error or nature disaster. The media hysteria that typically surrounds these incidents, and is at least partially driven by the desire of the media outlets to maximize monetization, further contributes to this societal anxiety.
Nuclear medicine is the branch of medicine that involves the use of radioactive materials in the diagnosis and treatment of disease. Unlike other routinely utilized anatomic imaging modalities including radiographs, CT, MRI and ultrasound, nuclear medicine is a physiologic imaging/therapeutic modality that involves the administration of radioactive pharmaceuticals that are selectively distributed and concentrated within the patient based on the patient’s physiology. In some individuals the societal anxiety that originated from concerns about nuclear annihilation and has been perpetuated by concerns about nuclear reactor malfunctions may extend to include the entire field of nuclear medicine. This anxiety may lead an individual to have a negative, occasionally irrational reaction to the idea of using radioactive isotopes to diagnose (e.g., Tc-99m) or treat (e.g., radioiodine or I-131) illness in their pets.
Like any medical procedure, radioiodine therapy needs to be administered to the appropriate patients by trained individuals using appropriate techniques. As I will describe below, what can go wrong for hyperthyroid cats being treated with radioactive iodine has very little to do with the fact that the therapy utilizes a radioactive material and everything to do with how and to whom it is administered.

What could go wrong?

Hyperthyroidism in cats is caused by a progressive, initially benign thyroid tumor called an adenoma. The cells that comprise these tumors produce thyroid hormone and reproduce autonomously essentially putting cats with this disease on an escalating trajectory of thyroid hormone levels and hence progressively accelerating metabolism. Progressive symptoms of weight loss, vomiting, diarrhea and ultimately heart failure will ensue unless control of these escalating thyroid hormone levels is accomplished. Radioiodine therapy with I-131 has a long history of successful resolution of hyperthyroidism for both human and feline patients (see sidebar). While the vast majority of hyperthyroid cats treated with radioiodine are cured of their thyroid disease and resolve all of the symptoms attributed to their thyrotoxicosis, there are exceptions to this rule. The following discussion enumerates the various forms of treatment failure that may occur following radioiodine therapy for hyperthyroidism in cats. Additionally you may also be interested in learning about the risks associated with radioiodine therapy for feline hyperthyroidism.

Persistent hyperthyroidism following radioiodine therapy

While success rates published for radioiodine therapy for the treatment of feline hyperthyroidism are routinely high, generally greater than 90%, not every hyperthyroid cat treated with radioiodine therapy is cured. In particular, cats with large or malignant tumors require higher doses of radioiodine for resolution of their disease. Unless these cats receive the higher doses they require, they are at a greater risk for persistent hyperthyroidism after treatment.[1],[2]

Despite the fact that radioiodine therapy is widely recognized as the treatment of choice for most cats with hyperthyroidism, various economic and logistical issues, as well as societal phobias, may impede its use in many cases. Therefore, long-term administration of an antithyroid drug (i.e., methimazole, carbimazole) is the most common means of treatment used in cats with hyperthyroidism. Successful medical management allows many hyperthyroid cats to live and do relatively well for many years, despite the fact that their thyroid adenomas will continue to grow progressively in size, sometimes developing into very large goiters. The standard fixed doses (i.e., 4 mCi) of I-131 used to treat cats with hyperthyroidism typically fail when administered to cats with large goiters.[1],[2] The failure to resolve the larger thyroid adenomas responsible for hyperthyroidism in cats with chronic disease leading to larger tumor size can be overcome by administering a larger dose of radioiodine. The need to administer these larger doses of radioiodine stems from the knowledge of the severity of their disease. Thyroid scintigraphy plays an integral role in ensuring that the total volume of adenomatous thyroid tissue in each individual patient is identified and should be performed in every hyperthyroid cat prior to radioiodine therapy to allow optimal, individualized radioiodine dosing. [2], [3] When thyroid scintigraphy is used to confirm the degree of disease present in individual cats, success rates for radioiodine therapy may improve to > 98%.

Hypothyroidism following radioiodine therapy

At the opposite extreme, hyperthyroid cats with small thyroid tumors that are treated with standard fixed doses of radioiodine may go on to become permanently hypothyroid, necessitating lifetime supplementation with thyroid hormone replacements and potentially worsening renal function, leading to shortened survival.
Radioiodine is an effective treatment for feline hyperthyroidism, but an optimal dosing technique to restore euthyroidism without inducing hypothyroidism remains elusive. Post-treatment hypothyroidism can lead to azotemia and reduced survival. A recent prospective, longitudinal study compared the frequency of persistent hyperthyroidism and iatrogenic hypothyroidism in cats with mild-to-moderate hyperthyroidism treated with either a low-dose or a standard-dose of I-131.[4] Most cats with mild-to-moderate hyperthyroidism were effectively treated with lower doses of I-131 and had a reduced risk of overt hypothyroidism compared to cats treated with standard doses of I-131. Multiple studies have shown that lower doses of radioiodine are effective in resolving thyrotoxicosis in cats with mild forms of the disease.[4],[5] The utility of administering these smaller doses of radioiodine is dependent on the knowledge of the degree of an individual cat’s thyroid disease. Thyroid scintigraphy plays an integral role in ensuring that the volume of adenomatous thyroid tissue in each individual patient is identified and should be performed in every hyperthyroid cat prior to radioiodine therapy to allow optimal, individualized radioiodine dosing.
In our practice approximately 5% of the cats referred for radioiodine therapy for hyperthyroidism prove not to be hyperthyroid at all. Transient, spurious elevations in thyroid hormone levels may occur in cats without thyroid disease. When radioiodine therapy is administered to cats that have been diagnosed as hyperthyroid based on laboratory evaluation alone, the risk of inappropriate therapy exists. Cats without thyroid adenomas causing hyperthyroidism will undergo potentially permanent damage to their normal thyroid gland as the result of radioiodine therapy, leading to permanent hypothyroidism. Once again, thyroid scintigraphy plays a key role in confirming the presence of the thyroid adenoma responsible for hyperthyroidism in cats and ensures that no cat will be treated with radioiodine inappropriately.[3]

Unmask renal failure

Even hyperthyroid cats that have the desired response following radioiodine therapy and return to persistent euthyroidism (i.e., have a persistently normal thyroid level) may demonstrate an apparent worsening of their kidney function following a resolution of their thyrotoxicosis.
While technically not a treatment failure, unmasking of a preexisting renal insufficiency is a regular occurrence that needs to be anticipated. Between 14% and 49% of cats with hyperthyroidism have pre-existing chronic kidney disease (CKD). [6-13] Recognizing CKD in cats with hyperthyroidism can be difficult. An early report suggested that GFR as estimated by renal scintigraphy was predictive in determining which cats with hyperthyroidism will become azotemic following radioiodine therapy. [6] Subsequent reports have been mixed, with some finding value in pretreatment GFR measurement [14-15] and other reports failing to confirm the value. [9],[12],[16] In response to the inability to accurately predict which hyperthyroid cats will become azotemic following a return to euthyroidism, the use of a trial course of medical therapy, usually referred to as the “methimazole trial”, has been advocated.[17-18] However, hyperthyroid cats that develop azotemia following a return to euthyroidism have a similar survival to hyperthyroid cats that do not develop post-treatment azotemia,[19],[20] and are unlikely to progress more than one International Renal Interest Society (IRIS) stage.[21] A recent consensus opinion of a panel of veterinary experts no longer recommends the routine use of a therapeutic trial in non-azotemic hyperthyroid cats to assess the effect of treatment on renal function.[22] Nevertheless, cats with pre-treatment laboratory evaluations that identify the presence of, or suggest the potential for, concurrent CKD will benefit from the initiation of standard supportive therapies based on IRIS staging. Some reports have shown limited value attempting to predict which hyperthyroid cats will become azotemic following a return to euthyroidism using more routinely available laboratory parameters, including serum creatinine, urine specific gravity, and thyroxine (T4) levels. [14-16] One report that evaluated pretreatment creatinine levels using a logistic regression model identified a pre-treatment creatinine concentration of greater than 1.4 mg/dL as predictive of the development of post-treatment azotemia with 77% sensitivity and 76% specificity.[15] While spontaneous hypothyroidism in the adult cat is uncommon,[23] iatrogenic hypothyroidism is a recognized complication that has been reported relatively commonly following treatment with antithyroid drugs,[15-18],[24] surgical thyroidectomy,[15],[24],and treatment with radioiodine.[25],[26],[27],[28],[29] Hypothyroidism has been associated with significant decreases in renal function in every species evaluated, including the rat, cat, dog, and human.[24],[30],[31],[32],[33],[34],[35],[36],[37],[38],[39],[40],[41],[42],[43] Systemic responses to hypothyroidism include reduced cardiac output, decreased renal blood flow, and ultimately a reduced GFR.
In the majority of cats with hyperthyroidism, the disease is caused by one or more benign, autonomously functioning thyroid adenomas, sometimes referred to as adenomatous thyroid hyperplasia. Only a small percentage of hyperthyroidism is caused by autonomously functional, differentiated thyroid carcinoma. Regardless of the exact histopathologic characterization of the thyroid tissue responsible for thyrotoxicosis, the one consistent clinical characteristic is autonomous function and growth. This autonomous thyroid hormone production causes a persistent and progressive thyrotoxicosis. Chronically elevated levels of circulating thyroid hormones lead to feedback suppression of the hypothalamus and the pituitary gland, resulting in chronically low TSH levels. Ultimately, chronically decreased TSH levels lead to atrophy of the normal thyroid tissue, which is dependent on TSH for its function and growth. Subclinical elevations in circulating thyroid hormone levels occurring at the earliest stages of hyperthyroidism will lead to feedback suppression of TSH release from the anterior pituitary long before clinical signs of thyrotoxicosis develop. As a result, cats with hyperthyroidism are typically diagnosed following months of suppression of normal thyroid tissue by persistently low TSH levels. This atrophy of normal thyroid tissue can lead to a period of transient hypothyroidism following curative radioiodine therapy.[2],[28],[44],[45],[46],[47] The declining levels of circulating thyroid hormones that follow radioiodine therapy lead to an increase in TSH release from the anterior pituitary. The reactivation and/or regeneration of the previously atrophied thyroid tissue that occurs in response to the increased TSH levels are not instantaneous; an interval of transient iatrogenic hypothyroidism is possible following radioiodine therapy. Ultimately, the elevated TSH levels that occur in response to declining levels of circulating thyroid hormones following radioiodine therapy lead to reactivation and/or regeneration of the previously atrophied thyroid tissue, returning the majority of these cats to persistent euthyroidism.
There is mounting evidence that iatrogenic hypothyroidism contributes to the progression of CKD, as well as shortened survival. The previous approach that focused on resolving thyrotoxicosis without consideration of the effects of iatrogenic hypothyroidism can no longer be supported. Current recommendations for the management of hyperthyroid cats must include a realization of the negative effects of both thyrotoxicosis and hypothyroidism on the kidney. When treating hyperthyroid cats with radioiodine, the use of individualized dosages that are determined with the goal of resolving adenomatous disease while avoiding iatrogenic hypothyroidism is recommended. [2] A key concept when treating cats with hyperthyroidism is the potential value of the standard supportive therapies traditionally utilized in cats with CKD. The reduction in GFR that accompanies a resolution of thyrotoxicosis should be anticipated and standard supportive therapies for pre-existing renal disease should be initiated to ensure tolerance for the incremental change in renal function that accompanies the return to euthyroidism. Most cats with concurrent CKD and hyperthyroidism will benefit from the administration of subcutaneous fluids following the initiation of antithyroid therapy. Many cats will benefit from the initiation of other standard therapies, including possible dietary phosphorus restriction, phosphate binders, histamine (H2) blockers, potassium supplementation, antihypertensive therapy when indicated, treatment of proteinuria when indicated, and supplemental B vitamin administration.

Persistent symptoms following resolution of elevated thyroid levels

The vast majority of hyperthyroid cats undergo a complete resolution of their clinical signs following successful radioiodine therapy. These cats regain the weight they lost while their thyroid hormone levels were elevated and similarly resolve their bouts of vomiting and/or diarrhea. Their coat quality improves, their inappropriate vocalization resolves and their agitation frequently bordering on aggression is replaced by a more tolerant and relaxed personality. A small percentage of cats continue to demonstrate clinical signs following the resolution of their elevated thyroid levels. To understand why some cats continue to demonstrate some of the symptoms that were attributed to hyperthyroidism even after successful radioiodine therapy has resulted in a return to persistently normal thyroid hormone levels we need to further explore the circumstances surrounding the diagnosis of hyperthyroidism.
The most common symptoms demonstrated by hyperthyroid cats include weight loss, vomiting and diarrhea. There are a large number of illnesses that occur in geriatric cats that share these symptoms with hyperthyroidism. Weight loss is common in a large number of diseases that affect older cats including, but not limited to cancer. Vomiting and diarrhea frequently accompany infiltrative bowel diseases like inflammatory bowel disease and alimentary lymphosarcoma. Compared to hyperthyroidism, most of these non-thyroid diseases are less easily diagnosed, many of them requiring advanced imaging techniques and invasive procedures like biopsy. By comparison, hyperthyroidism is a relatively more common disease in elderly cats. Hyperthyroidism is also a relatively straightforward disease to diagnose in the majority of cats with the illness. A single blood test allows the diagnosis in the large majority of cats with the disease. Once a diagnosis of hyperthyroidism is made the diagnostic investigation is often terminated in favor of focusing on the treatment for the elevated thyroid levels. For these reasons, some cats presented for radioiodine therapy for hyperthyroidism will have other, undiagnosed concurrent illnesses.
The majority of illnesses that cause weight loss in cats are accompanied by a decreased appetite. Alternatively, cats with hyperthyroidism typically demonstrate weight loss in the face of an increased appetite. Radioiodine treatment of hyperthyroid cats that have symptoms that include an increased appetite is generally a very high success rate procedure. When cats demonstrating a clinically decreased appetite are diagnosed with hyperthyroidism, the potential for concurrent disease is increased and additional diagnostic evaluation should ensue. This evaluation may take the form of additional imaging procedures including chest radiographs and abdominal ultrasound, or further laboratory screening for evidence of infiltrative gastrointestinal disease.
A relatively uncommon cause for a poor appetite in a hyperthyroid cat is a condition called apathetic hyperthyroidism. Apathetic hyperthyroidism is a relatively rare form of hyperthyroidism in which the cat becomes lethargic due to the effects of chronic, usually severe thyrotoxicosis, progressive muscle wasting and emaciation. Cat’s with apathetic hyperthyroidism demonstrate a reduced appetite that should improve with medical therapy for hyperthyroidism using antithyroid medication (e.g., methimazole). While apathetic hyperthyroidism has been reported to occur in as many as 10% of hyperthyroid cats, more recent reports support the presence of other concurrent illness contributing to the symptoms of inappetence, lethargy and weakness.[18] An additional diagnostic evaluation that can prove useful in hyperthyroid cats with a reduced appetite and no evidence of concurrent disease is referred to as the “methimazole trial”. Initially advocated as a means of predicting the renal response to the control of elevated thyroid hormone levels, the use of the methimazole trial has a more valuable function as a means of confirming the resolution of symptoms attributed to thyrotoxicosis with the return of normal circulating thyroid hormone levels. In addition to aiding in the diagnosis of apathetic hyperthyroidism, cats suffering from the severe weight loss and reduced appetite that accompany this condition will benefit from normalization of their thyroid hormone levels allowing them to regain weight and improve body condition. A hyperthyroid cat with a poor appetite that does not improve while on methimazole should be strongly suspected of having another concurrent illness that is responsible for the reduced appetite.
Ultimately cats with undiagnosed concurrent illnesses may continue to demonstrate symptoms of ongoing weight loss, declining body condition and potentially progressive gastrointestinal symptoms even after the resolution of their thyroid disease following otherwise successful radioiodine therapy.[2],[3]

Patient death

The persistently elevated thyroid hormone levels that accompany chronic hyperthyroidism routinely induce an increase in blood pressure and heart rate, both of which place an added strain on the patient’s cardiovascular system. If inadequately treated, hyperthyroidism is ultimately a life limiting disease. The cardiovascular stress that accompanies chronic hyperthyroidism can lead to an acute clinical deterioration secondary to the development of congestive heart failure and/or cerebrovascular accident (i.e., stroke), either potentially leading to the death of the patient. Radioiodine therapy is inherently a very low risk procedure. It does not involve the use of anesthetics or sedatives and is a minimally invasive procedure requiring only a single subcutaneous injection. However, the federal and state regulations surrounding radioiodine therapy require hospitalization of the cat until the large majority of the radioactive iodine has been excreted. The duration of this hospitalization is variable but largely determined by the dose of radioiodine administered. Cats with severe or chronic hyperthyroidism generally have large thyroid tumors, requiring larger radioiodine doses that lead to longer periods of mandatory hospitalization. While the experience of being away from home is generally well tolerated, it can be variably stressful to cats depending on their individual personalities. This stress can contribute to the risk of cardiovascular decompensation in cats with severe disease.
Cats with chronic, poorly managed hyperthyroidism eventually become emaciated secondary to the effects of chronic secondary malnutrition. These cats may develop what is called apathetic hyperthyroidism at which point their appetite declines and their continued deterioration progresses rapidly. At this stage of their disease these cats will frequently die from the effects of various organ system failures including but not limited to congestive heart failure. Emaciated cat’s (BCS = 1/5, typically weighing less than 5 pounds) are at risk for developing apathetic hyperthyroidism at which point their recovery becomes dependent on additional supportive therapies and is much more challenging to achieve.
Even well fleshed cats suffering from chronic, poorly controlled hyperthyroidism may have severe underlying cardiovascular disease that makes them potential candidates for acute decompensation when medical control of their elevated thyroid levels is withdrawn. To reduce the risk of possibly life threatening cardiovascular decompensation, cats managed with methimazole or iodine deficient diets (e.g., Hills y/d in excess of 1 year, or cats with previously measured T4 levels in excess of 20 μg/dl should discontinue methimazole or Hills y/d administration no more than 1 day prior to their appointment for radioiodine therapy.


Over 35 years of experience has demonstrated that treatment with appropriate doses of radioiodine will result in the resolution of the majority of the thyroid adenomas responsible for hyperthyroidism in cats leading to the normalization of their previously elevated thyroid hormone levels and the resolution of their clinical symptoms.

A small percentage of hyperthyroid cats treated with radioiodine however, will have a less than optimal outcome that may include the possibility of persistent hyperthyroidism, post radioiodine therapy hypothyroidism, complications associated with unmasked renal disease, the persistence of clinical symptoms despite resolution of thyrotoxicosis and even in the rare patient, death secondary to acute cardiovascular decompensation.

The potential for persistent hyperthyroidism or post radioiodine therapy hypothyroidism can be minimized by careful attention to optimal radioiodine dosing criteria that include the use of thyroid scintigraphy. Complications associated with the unmasking of pre-existing renal disease can be minimized by proactive therapy that includes optimal hydration and occasionally proactive thyroxine supplementation. The risk of persistent clinical signs following successful radioiodine therapy can be reduced by additional screening of cats with reduced appetite’s to enable diagnosis of other concurrent illness. Finally, acute patient death can be reduced by the avoidance of cardiovascular stress secondary to the extreme thyrotoxicosis that can accompany discontinuation of antithyroid medications in cats with large thyroid tumors secondary to chronic thyroid disease.


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40. Montenegro, J., et al., Changes in renal function in primary hypothyroidism. American journal of kidney diseases : the official journal of the National Kidney Foundation, 1996. 27(2): p. 195-8.
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History of Radioiodine There are a total of 37 isotopes of iodine, all of which except for stable I-127, undergo radioactive decay. The isotope I-131 was discovered by Glenn Seaborg and John Livingood in 1938 at the University of California, Berkeley. Since then, the therapeutic use of radioactive iodine (I-131) for the treatment of thyroid disease in man and other species has been widely reported. In particular, the use of radioactive iodine for the treatment of hyperthyroidism in people caused by the autoimmune disease named Graves’ disease (after the Irish physician Robert Graves) was first reported by Saul Hertz in 1941. Shortly thereafter the use of radioactive iodine for the therapy of hyperthyroidism in people caused by small benign tumors (e.g., adenomas) in the thyroid named Plummer’s disease (after the American physician Henry Stanley Plummer) was reported. Several decades later, Mark Peterson was the first to describe spontaneous hyperthyroidism in the cat in 1979. And shortly after that radioactive iodine therapy in cats with hyperthyroidism was reported by Jane Turrel in 1984. Radioiodine therapy for thyroid carcinoma causing hyperthyroidism in cats was subsequently reported, again by Jane Turrel in 1988. For over 35 years, radioiodine therapy has been the gold standard treatment for hyperthyroidism in cats.


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