Web Chapter 14 Complications and Concurrent Conditions Associated with Hypothyroidism in Dogs David L. Panciera, Blacksburg, Virginia Hypothyroidism can lead to many different clinical abnormalities because of the widespread influence that thyroid hormones have on cellular metabolism. Typical clinical signs of hypothyroidism include lethargy, weight gain, seborrhea, and alopecia; however, many other complications can develop. Recognition of the varied complications and conditions associated with hypothyroidism leads to appropriate diagnosis and treatment. Neurologic Complications A variety of neurologic abnormalities are associated with hypothyroidism. Peripheral neuropathies are recognized with increasing frequency in hypothyroid dogs. Generalized neuropathy may result from impaired axonal transport secondary to decreased activity of acetylcholinesterase, Mg-ATPase, and Na/K-ATPase; from demyelination; or from other factors. Dogs with generalized peripheral neuropathies may present with generalized weakness, exercise intolerance, inappetence, or unilateral forelimb lameness. Physical examination findings include depression, proprioceptive deficits and ataxia predominately in the hind limbs, hyporeflexia, and pain in the shoulder of dogs with forelimb lameness. Electromyographic abnormalities consistent with denervation are present in affected dogs. Dogs with hypothyroidism and generalized peripheral neuropathy generally respond rapidly and completely to thyroid hormone supplementation, with an increase in strength noted within the first week and complete resolution within 3 to 8 weeks of initiating treatment. Localized peripheral neuropathies involving the vestibular and facial nerves, often occurring concurrently, are also frequently recognized in hypothyroidism. Since most affected dogs do not show signs of generalized neuropathy, hypothyroidism must be differentiated from otitis media or otitis interna, idiopathic peripheral vestibular disease, and other causes of neuropathy. Localized neuropathy may result from metabolic neuropathy or compression of the vestibular and facial nerves as they pass through the internal acoustic meatus. Dogs typically present with an acute (occasionally more gradual) onset of head tilt, nystagmus, ataxia, and circling. Proprioception and segmental spinal reflexes are normal. Otic examination and radiographs of the tympanic bulla should be normal. Vestibular abnormalities respond more slowly to thyroid hormone supplementation than do other neuropathies; noticeable improvement may require 8 weeks. A residual head tilt may be present in some dogs. Generalized myopathy is consistently found in dogs with experimental hypothyroidism. Clinical signs of myopathy are subtle and difficult to detect, but resolution of this complication of hypothyroidism is likely in part responsible for the improvement in activity and exercise tolerance noted following levothyroxine supplementation. Serum markers of myopathy including creatine kinase and alanine aminotransferase activities are frequently increased to 2 to 3 times the reference range. The myopathy is characterized by a decrease in type II muscle fibers, nemaline rod inclusions, and myofiber degeneration. Megaesophagus can occur in hypothyroid dogs, but the pathogenesis of the disorder is unclear. Because the megaesophagus only occasionally resolves following treatment, the role of hypothyroidism is unknown. Hypothyroidism could cause megaesophagus by inducing either a neuropathy or a myopathy. Alternatively, megaesophagus has been described in hypothyroid dogs with myasthenia gravis. In this case, the myasthenia gravis and hypothyroidism could have a common immune-mediated pathogenesis similar to that reported in humans. Regardless of the relationship between hypothyroidism and megaesophagus, the prognosis for recovery of normal esophageal function is guarded to poor. However, a small number of hypothyroid dogs had complete resolution of megaesophagus with levothyroxine treatment. Another localized neuropathy attributed to hypothyroidism is laryngeal paralysis. Although some dogs with laryngeal paralysis are hypothyroid, the vast majority are not, and a clear causal relationship remains to be established. Central nervous system (CNS) disease can occur in hypothyroidism subsequent to cerebral hypoxia resulting from atherosclerosis or infarction, disruption of the blood-brain barrier, or metabolic neuropathy similar to that found in peripheral nerves. Central vestibular and cerebellar involvement is common and results in head tilt, vertical nystagmus, hypermetria, postural deficits, and upper motor neuron paresis. Seizures have not been documented to occur in hypothyroid dogs in the absence of other signs of CNS disease. Although these signs resolve more slowly than most other manifestations of hypothyroidism in some dogs and residual neurologic deficits may remain, improvement is generally noted within 1 week, with resolution occurring within 4 weeks of initiating levothyroxine treatment. Among the behavioral abnormalities that have been attributed to hypothyroidism, aggressive behavior has been reported to partially or completely resolve following thyroid hormone supplementation in the small number of dogs that were probably hypothyroid. Because of the paucity of documented cases, the relationship between behavioral problems and hypothyroidism remains speculative. Thyroid function tests should be interpreted cautiously in dogs with neurologic abnormalities, since euthyroid dogs with neuropathies and those with megaesophagus may have significantly lower basal serum thyroxine (T4) concentrations than do normal dogs. In addition, effects of any treatments the dog may have received, including corticosteroids, nonsteroidal antiinflammatory drugs, or sulfonamides, on thyroid function must be taken into account when interpreting thyroid function test results. Reproductive Complications A variety of reproductive abnormalities, including prolonged anestrus, irregular cycle length, decreased libido, and abortion, have been suggested to occur in hypothyroid bitches. Recently, short-term hypothyroidism was shown to not affect fertility or interestrus interval, but did cause increased periparturient mortality and low birth weight. When hypothyroidism had been present for approximately 1 year, increased periparturient mortality and low birth weight persisted, and the pregnancy rate decreased by 50%. These abnormalities were reversed by levothyroxine administration. Galactorrhea occasionally occurs in intact females with hypothyroidism secondary to increased prolactin secretion. Hypothyroid bitches may have severe galactorrhea during pseudopregnancy or galactorrhea that continues beyond the time expected for a normal pseudopregnancy. Prolactin secretion from the pituitary gland is stimulated by thyrotropin-releasing hormone, which is elevated in hypothyroid dogs. Ocular Complications Ocular complications of hypothyroidism are rare. Corneal lipidosis, corneal ulceration, lipid aqueous flare, uveitis, retinal detachment and hemorrhage, optic disc swelling, and keratoconjunctivitis sicca have been suggested to occur in hypothyroid dogs. Most of these abnormalities have not been definitively linked with hypothyroidism. Hyperlipidemia secondary to hypothyroidism can in rare cases result in corneal lipidosis, lipid aqueous flare, and chronic uveitis. Keratoconjunctivitis sicca has been reported in hypothyroid dogs, although a clear connection has not been established. Retrospective studies of hypothyroidism have not identified a significant number of dogs with concurrent keratoconjunctivitis sicca, and experimental hypothyroidism of 6 months’ duration failed to alter tear production or other ocular parameters. A common immune-mediated pathogenesis has been proposed for intercurrent hypothyroidism and keratoconjunctivitis sicca but has not been proved. It is recommended that dogs with ocular changes secondary to hyperlipidemia be evaluated for hypothyroidism by a thorough search for other evidence of hypothyroidism and evaluation of thyroid function tests. Dogs with keratoconjunctivitis sicca should have thyroid function tests performed if other evidence of hypothyroidism is found in the history and physical examination or hypercholesterolemia is documented. Renal Complications Hypothyroidism results in a decrease in the glomerular filtration rate (GFR), although serum creatinine concentration is not increased as a result of decreased production rate of creatinine, offsetting the effect of reduced GFR. Decreased renal blood flow secondary to reduced cardiac output and increased systemic peripheral resistance are likely responsible for the impaired renal function. The GFR increases after levothyroxine supplementation in hypothyroid dogs and there is no evidence that renal dysfunction persists.< div class='tao-gold-member'> Only gold members can continue reading. 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Web Chapter 14 Complications and Concurrent Conditions Associated with Hypothyroidism in Dogs David L. Panciera, Blacksburg, Virginia Hypothyroidism can lead to many different clinical abnormalities because of the widespread influence that thyroid hormones have on cellular metabolism. Typical clinical signs of hypothyroidism include lethargy, weight gain, seborrhea, and alopecia; however, many other complications can develop. Recognition of the varied complications and conditions associated with hypothyroidism leads to appropriate diagnosis and treatment. Neurologic Complications A variety of neurologic abnormalities are associated with hypothyroidism. Peripheral neuropathies are recognized with increasing frequency in hypothyroid dogs. Generalized neuropathy may result from impaired axonal transport secondary to decreased activity of acetylcholinesterase, Mg-ATPase, and Na/K-ATPase; from demyelination; or from other factors. Dogs with generalized peripheral neuropathies may present with generalized weakness, exercise intolerance, inappetence, or unilateral forelimb lameness. Physical examination findings include depression, proprioceptive deficits and ataxia predominately in the hind limbs, hyporeflexia, and pain in the shoulder of dogs with forelimb lameness. Electromyographic abnormalities consistent with denervation are present in affected dogs. Dogs with hypothyroidism and generalized peripheral neuropathy generally respond rapidly and completely to thyroid hormone supplementation, with an increase in strength noted within the first week and complete resolution within 3 to 8 weeks of initiating treatment. Localized peripheral neuropathies involving the vestibular and facial nerves, often occurring concurrently, are also frequently recognized in hypothyroidism. Since most affected dogs do not show signs of generalized neuropathy, hypothyroidism must be differentiated from otitis media or otitis interna, idiopathic peripheral vestibular disease, and other causes of neuropathy. Localized neuropathy may result from metabolic neuropathy or compression of the vestibular and facial nerves as they pass through the internal acoustic meatus. Dogs typically present with an acute (occasionally more gradual) onset of head tilt, nystagmus, ataxia, and circling. Proprioception and segmental spinal reflexes are normal. Otic examination and radiographs of the tympanic bulla should be normal. Vestibular abnormalities respond more slowly to thyroid hormone supplementation than do other neuropathies; noticeable improvement may require 8 weeks. A residual head tilt may be present in some dogs. Generalized myopathy is consistently found in dogs with experimental hypothyroidism. Clinical signs of myopathy are subtle and difficult to detect, but resolution of this complication of hypothyroidism is likely in part responsible for the improvement in activity and exercise tolerance noted following levothyroxine supplementation. Serum markers of myopathy including creatine kinase and alanine aminotransferase activities are frequently increased to 2 to 3 times the reference range. The myopathy is characterized by a decrease in type II muscle fibers, nemaline rod inclusions, and myofiber degeneration. Megaesophagus can occur in hypothyroid dogs, but the pathogenesis of the disorder is unclear. Because the megaesophagus only occasionally resolves following treatment, the role of hypothyroidism is unknown. Hypothyroidism could cause megaesophagus by inducing either a neuropathy or a myopathy. Alternatively, megaesophagus has been described in hypothyroid dogs with myasthenia gravis. In this case, the myasthenia gravis and hypothyroidism could have a common immune-mediated pathogenesis similar to that reported in humans. Regardless of the relationship between hypothyroidism and megaesophagus, the prognosis for recovery of normal esophageal function is guarded to poor. However, a small number of hypothyroid dogs had complete resolution of megaesophagus with levothyroxine treatment. Another localized neuropathy attributed to hypothyroidism is laryngeal paralysis. Although some dogs with laryngeal paralysis are hypothyroid, the vast majority are not, and a clear causal relationship remains to be established. Central nervous system (CNS) disease can occur in hypothyroidism subsequent to cerebral hypoxia resulting from atherosclerosis or infarction, disruption of the blood-brain barrier, or metabolic neuropathy similar to that found in peripheral nerves. Central vestibular and cerebellar involvement is common and results in head tilt, vertical nystagmus, hypermetria, postural deficits, and upper motor neuron paresis. Seizures have not been documented to occur in hypothyroid dogs in the absence of other signs of CNS disease. Although these signs resolve more slowly than most other manifestations of hypothyroidism in some dogs and residual neurologic deficits may remain, improvement is generally noted within 1 week, with resolution occurring within 4 weeks of initiating levothyroxine treatment. Among the behavioral abnormalities that have been attributed to hypothyroidism, aggressive behavior has been reported to partially or completely resolve following thyroid hormone supplementation in the small number of dogs that were probably hypothyroid. Because of the paucity of documented cases, the relationship between behavioral problems and hypothyroidism remains speculative. Thyroid function tests should be interpreted cautiously in dogs with neurologic abnormalities, since euthyroid dogs with neuropathies and those with megaesophagus may have significantly lower basal serum thyroxine (T4) concentrations than do normal dogs. In addition, effects of any treatments the dog may have received, including corticosteroids, nonsteroidal antiinflammatory drugs, or sulfonamides, on thyroid function must be taken into account when interpreting thyroid function test results. Reproductive Complications A variety of reproductive abnormalities, including prolonged anestrus, irregular cycle length, decreased libido, and abortion, have been suggested to occur in hypothyroid bitches. Recently, short-term hypothyroidism was shown to not affect fertility or interestrus interval, but did cause increased periparturient mortality and low birth weight. When hypothyroidism had been present for approximately 1 year, increased periparturient mortality and low birth weight persisted, and the pregnancy rate decreased by 50%. These abnormalities were reversed by levothyroxine administration. Galactorrhea occasionally occurs in intact females with hypothyroidism secondary to increased prolactin secretion. Hypothyroid bitches may have severe galactorrhea during pseudopregnancy or galactorrhea that continues beyond the time expected for a normal pseudopregnancy. Prolactin secretion from the pituitary gland is stimulated by thyrotropin-releasing hormone, which is elevated in hypothyroid dogs. Ocular Complications Ocular complications of hypothyroidism are rare. Corneal lipidosis, corneal ulceration, lipid aqueous flare, uveitis, retinal detachment and hemorrhage, optic disc swelling, and keratoconjunctivitis sicca have been suggested to occur in hypothyroid dogs. Most of these abnormalities have not been definitively linked with hypothyroidism. Hyperlipidemia secondary to hypothyroidism can in rare cases result in corneal lipidosis, lipid aqueous flare, and chronic uveitis. Keratoconjunctivitis sicca has been reported in hypothyroid dogs, although a clear connection has not been established. Retrospective studies of hypothyroidism have not identified a significant number of dogs with concurrent keratoconjunctivitis sicca, and experimental hypothyroidism of 6 months’ duration failed to alter tear production or other ocular parameters. A common immune-mediated pathogenesis has been proposed for intercurrent hypothyroidism and keratoconjunctivitis sicca but has not been proved. It is recommended that dogs with ocular changes secondary to hyperlipidemia be evaluated for hypothyroidism by a thorough search for other evidence of hypothyroidism and evaluation of thyroid function tests. Dogs with keratoconjunctivitis sicca should have thyroid function tests performed if other evidence of hypothyroidism is found in the history and physical examination or hypercholesterolemia is documented. Renal Complications Hypothyroidism results in a decrease in the glomerular filtration rate (GFR), although serum creatinine concentration is not increased as a result of decreased production rate of creatinine, offsetting the effect of reduced GFR. Decreased renal blood flow secondary to reduced cardiac output and increased systemic peripheral resistance are likely responsible for the impaired renal function. The GFR increases after levothyroxine supplementation in hypothyroid dogs and there is no evidence that renal dysfunction persists.< div class='tao-gold-member'> Only gold members can continue reading. Log In or Register to continue
