Hypothyroid Myopathy Research Articles

12511 Rhabdomyolysis Related Acute Kidney Injury Presenting as First Manifestation of Autoimmune Hypothyroidism: A Case Report

Abstract Disclosure: A. Tiwari: None. S. Mantravadi: None. N. Doshi: None. A. Dabaja: None. C. Saad: None. Introduction: Autoimmune thyroiditis is the predominant cause of primary hypothyroidism, with an incidence of estimated 0.3-1.5 cases per 1000 people, with female to male predominance of 7-10[1]. Hypothyroid myopathy affects 79 % of the affected population. Its common presentation is fatigue and cramp but in rare instances rhabdomyolysis can occur with trivial triggers like alcohol, exercise2, Case Presentation: A 32-year-old male with no significant medical history, presented with generalized weakness, myalgia, and facial puffiness for last three months. The patient engaged in regular-intensity workouts and reported consuming 12 beers several times a week for past 5 years. Physical examination revealed facial puffiness and proximal muscle weakness. Initial Laboratory findings showed elevated creatinine (1.68 mg/dL, baseline 1.0 mg/dL in April 2020), CK (8113 U/L), AST (260 U/L), ALT (129 U/L). Urinalysis revealed hematuria and mild proteinuria. Serum electrolytes were unremarkable. Abdominal ultrasound showed diffuse hepatic steatosis with normal kidney appearance. This could not explain the reason for the Acute Kidney Injury and further workup showed TSH (>150 mIU/L) and TPO antibodies (197.9 U/mL). Autoimmune panel was unremarkable. Thyroid ultrasound done subsequently revealed a markedly heterogeneous gland. Treatment included parenteral crystalloids, low-dose prednisone which was empirically added for suspected autoimmune myositis and was later discontinued once the autoimmune panel was negative, and Levothyroxine at the recommended dose. At the time of discharge, his creatinine was reduced to 1.33 mg/dL and CK to 2,298 U/L. Discussion: Severe rhabdomyolysis is a rare but significant complication of autoimmune thyroiditis, potentially leading to acute kidney injury (AKI) if not promptly diagnosed and treated. Resident physicians often attribute symptoms like myalgia and generalized weakness in males to clear evident rhabdomyolysis if they find a cause like alcohol consumption and exercise, potentially overlooking the actual etiology. We recommend thyroid workup in such patients to promptly detect and manage underlying etiology predisposing to muscle damage and subsequent kidney injury. Our patient never had any Physician encounter as his prior medical history was unremarkable, however we suggest thorough family history and thyroid profile should be a part of outpatient workup as well for patients who show other risk factors for rhabdomyolysis like daily alcohol consumption, vigorous workout, consume medications like HMG CoA inhibitors, antipsychotics etc. Presentation: 6/3/2024

High levels of creatine kinase in hypothyroid myopathy

High levels of creatine kinase in hypothyroid myopathy

Hoffmann’s syndrome in the differential work-up of myopathic complaints: a case report

BackgroundHoffmann’s syndrome is a rare form of hypothyroid myopathy in adults, which is mainly characterized by muscular weakness and muscular pseudohypertrophy.Case presentationWe report about a 61-year-old Western European man with myalgia, myxedema and pseudohypertrophy of the calf muscles. Laboratory tests revealed significantly elevated thyroid stimulating hormone (TSH) and creatine kinase (CK). Muscle MRI showed muscular hypertrophy of the lower limbs, but no signs of myositis or myopathy (no gadolinium enhancement, no edema, no fatty degeneration). In addition, electromyography (EMG) detected spontaneous activity. After the beginning of thyroxin-therapy it took six months until the muscle weakness improved and the myalgia regressed.ConclusionsHere, we focus on diagnostic routines and typical findings to differentiate Hoffmann’s syndrome from other myopathies. Clinical hallmarks of Hoffmann’s syndrome are pseudohypertrophy and weakness of the calf muscles in combination with elevated CK and elevated TSH. EMG is well suited to detect the involvement of the muscles and muscle MRI helps to differentiate it from other myopathies. Hoffmann’s syndrome is a rare myopathy due to hypothyroidism and plays a role in the differential diagnosis of myopathic complaints even if hypothyroidism has not been detected before.

THU658 My Giant Calves Gave Up My Diagnosis: An Extreme Manifestation Of A Very Rare Syndrome With A Severe Elevation Of Tsh Levels

Abstract Disclosure: E.E. Castro Feliu: None. A. Ludena De Freitas: None. A. Torres Rodríguez: None. G. Irizarry: None. Hoffmann’s Syndrome is a rare type of hypothyroidism myopathy in adults that classically presents with muscle cramps, weakness, muscle stiffness, hyporeflexia, delay deep tendon reflexes and pseudohypertrophy. This is the case of a 55-year-old male with history of poorly controlled hypothyroidism and medication non-compliance who was admitted to our institution for non-purulent cellulitis. Vital signs were within normal limits and Body Mass Index was 41.1. Upon physical examination flat affect, periorbital edema, moon facies features and macroglossia were distinguished. Skin had a doughy texture with areas of ichthyosis at upper and lower extremities. Goiter was absent. The most remarkable finding was bilateral calf hypertrophy, with measurements of 56 cm and 55.5 cm in diameter of right and left calves respectively. There was no tenderness to calf palpation and Homan’s sign was absent. Laboratories revealed dyslipidemia with a cholesterol of 308 mg/dL, triglycerides of 782 mg/dL, HDL of 26 mg/dL and LDL of 216 mg/dL with elevated inflammatory markers including sedimentation rate of 77 mm/hr and C-reactive protein of 6.45 mg/dL. Hypothyroidism was suspected therefore thyroid studies were ordered, which was compatible with severe hypothyroidism demonstrated by a record level TSH of 523 lU/ml. Other reported levels were Free T3 0.94pg/ml, total T3 0.5 ng/ml, free thyroxine <0.07 ng/dL, thyroid peroxidase <4, and thyroglobulin AB 19 IU/ml. Hoffmann’s Panel was confirmatory for this diagnosis reporting elevated levels of CPK 1509 U/L, LDH serum of 383 U/L and aldolase of 9.2 u/L. Ultrasound of the neck was non-contributory. Patient received antibiotic therapy for his skin infection and was also treated with IV Levothyroxine, which was prescribed orally upon discharge. Myopathy may be present in patients with longstanding untreated hypothyroidism in which pseudohypertrophy may occur, sometimes involving calf muscles (gastrocnemius). Hoffmann’s Syndrome is associated with changes in muscle fiber type from fast twitch type II to slow twitch type I and alteration of oxidative muscle enzyme activity with deceased calcium ATPase activity of fast twitch type II fibers leading to delayed relaxation. Biopsy of the affected muscle may reveal fiber necrosis, atrophy, hypertrophy with increased number of nuclei and increased connective tissue. Most cases of Hoffmann’s Syndrome improve after treatment with Levothyroxine, therefore, implementing this management on time can be curative. This case highlights the importance of considering this diagnosis when muscle dystrophies are studied and myopathic disorders are suspected, even in the absence of overt manifestations of hypothyroidism. Presentation: Thursday, June 15, 2023

A Case Report of Bilateral Foot Drop in a Young Girl

Acute unilateral foot drop is a well-known entity, but bilateral foot drop in progressive fashion is rare. In particular, slow-progressing bilateral foot drop occurs with various metabolic causes, as in anorexia nervosa, hypothyroid myopathy, Crohn’s disease, and post-electroconvulsive therapy. Parasagittal intracranial and spinal pathologies and cauda equine may also cause progressive bilateral foot drop. This case is presented with bilateral foot drop due to common peroneal nerve entrapment.

DAMAGE TO THE AUTONOMIC NERVOUS SYSTEM IN PATIENTS WITH HYPOTHYROIDISM

The most studied in hypothyroidism (HT) in this regard are neuromuscular disorders (hypothyroid myopathy and myotonic phenomenon) and damage to peripheral nerves, the prevalence of which is highly variable. Among the signs of organic brain damage, vestibulocerebellar disorders and, less frequently, extrapyramidal disorders are mentioned. In the structure of chronic encephalopathy in hypothyroidism, psycho-emotional and intellectual disorders are most often described (2,3,4,5).

Hypothyroid Myopathy: A Commonly Missed Complication of Hypothyroidism

Muscle disease is a known complication of hyperthyroidism as well as hypothyroidism. The muscle disease is associated with elevated creatine kinase and pain. This the case of a 63-year-old female who presented to the ED from her cancer therapy with elevated creatine kinase of 2,000 IU/L (International units/Liter). She reports muscle pain in her shoulders and hips for the past 3 days. Patient was recently diagnosed with hypothyroidism and has started on levothyroxine 75 mcg. Her Thyroid Stimulating Hormone (TSH) stays elevated at 65 IU (international units). Other autoimmune causes of elevated creatine kinase were excluded via testing, leaving hypothyroid myopathy as the only possible probable cause of this patient elevated creatine kinase. Muscle pain and creatine kinase should resolve with proper levothyroxine dose and compliance to therapy when patient becomes euthyroid. Unfortunately, the patient passed away from complications related to fall.

Abstract #1405039: Melting Muscle: Rhabdomyolysis as a Rare Initial Presentation of Hashimoto’s Thyroiditis

Rhabdomyolysis is characterized by muscular necrosis and the release of intracellular muscle contents into circulation. The most common cause of primary hypothyroidism is Hashimoto’s thyroiditis (HT) in iodine-adequate areas. Although hypothyroid myopathy is commonly seen, rhabdomyolysis is a rare reported but serious complication in patients with HT. This case report aims to highlight this rare complication, so that diagnosticians will consider this in their differential diagnosis. A 44-year-old African American male with a history of asthma and hypertension presented to the emergency room due to mild generalized muscle cramps started several weeks ago. It worsened recently after he started a new job that required him to work in the yard for 3-6 hours daily. He denied any new medications, recent trauma, drug use, insect bites, sick contacts, recent travel, or strenuous exercise. His vital signs were stable. Initial laboratory workups were significant for elevated creatinine kinase at 4299 unit/L and creatinine of 1.57 mg/dl. Notably, his thyroid stimulating hormone was 42.94 uIU/mL, free thyroxine (T4) was 0.48 ng/mL, and his anti-microsomal antibody was >1300 units/mL. He was admitted to hospital for rhabdomyolysis secondary to Hashimoto’s thyroiditis. Levothyroxine therapy and intravenous fluid were given. His condition improved and was ultimately discharged with close primary and endocrinology follow-up. Hypothyroidism is well-associated with musculoskeletal problems, and it is estimated that around one-third of patients are accompanied with myopathy symptoms. Mechanism of hypothyroidism-induced myopathy is not fully understood. It is thought, however, to be linked to thyroxine’s role in glycogenolysis and mitochondrial oxidative processes. Thus, insufficiency of thyroxine may damage myocytes due to oxidative stress and may eventually lead to rhabdomyolysis. Although Hashimoto’s thyroiditis is recognized as one of the most common causes of hypothyroidism, as per our knowledge, this is the first case that a patient initially presenting with rhabdomyolysis was found out to have Hashimoto’s thyroiditis. Thus, hypothyroidism should be kept on the differential in patients with suspicion of rhabdomyolysis, and a thyroid panel should be considered as one of the initial workups.

Abstract #1408127: A Case of Rhabdomyolysis Resulting in Fulminant Acute Kidney Injury in a Patient with Severe Hypothyroidism

Rhabdomyolysis is characterized by muscle necrosis and the release of intracellular muscle contents into circulation. Hypothyroidism is known to be associated with musculoskeletal problems, rarely rhabdomyolysis. We report a case of severe hypothyroidism due to a prior thyroidectomy with poor medication adherence, who presented with rhabdomyolysis resulting in severe acute kidney injury requiring urgent dialysis. A 65-year-old male with a past medical history of papillary thyroid cancer status post total thyroidectomy presented with lethargy, confusion, decreased oral intake and decreased urination. He recently ran out of levothyroxine. Notably, the patient had also been taking rosuvastatin. On examination, the patient was afebrile, with a pulse of 70 bpm and blood pressure of 111/70 mmHg. He was oriented to self and place but not to time. He demonstrated slow deep voice along with macroglossia and trace non-pitting lower extremity edema. There were no signs of proximal myopathy or neurological deficits. Workup was remarkable for TSH >90.00 mcU/mL, free T4 < 0.1 ng/dl, CPK 22,030 mcg/L, AST 233 U/L, ALT 205 U/L, creatinine 31.6 mg/dl, and BUN 124 mg/dl. The last known TSH was 4.5, free T4 was 1 ng/dL, and creatinine was 0.9 in January 2021. The urine specimen was positive for loaded red blood cells. Renal ultrasound showed no obstruction. Diagnosis of rhabdomyolysis with acute renal failure was made and he was promptly started on dialysis. Endocrinology was consulted and he was started on intravenous levothyroxine. A renal biopsy confirmed acute tubular necrosis due to rhabdomyolysis. After several days, his symptoms improved, and he was transitioned to oral levothyroxine however he remained on dialysis on discharge. Hypothyroid myopathy is most often limited to myalgia, cramps, and sometimes mildly elevated levels of muscle enzymes. Rhabdomyolysis can rarely develop due to severe hypothyroidism. Muscle breakdown in hypothyroidism is caused by poor contractility, low myosin ATPase activity, and low ATP turnover in the skeletal muscles. These metabolic abnormalities may sensitize patients with hypothyroidism to develop rhabdomyolysis. Acute renal failure, as a result of an accumulation of myoglobin in renal tubules, is the most life-threatening complication of rhabdomyolysis and can develop in up to 33% of patients. There have been very few case reports of hypothyroidism causing rhabdomyolysis, with a precipitating factor such as exercise, trauma, or drugs such as statin. Our patient presented with severe hypothyroidism complicated by rhabdomyolysis resulting in acute renal failure requiring dialysis. The patient was also on a statin which may cause statin-induced rhabdomyolysis due to hypothyroidism. This case emphasizes the importance of adherence to levothyroxine in hypothyroid patients as well as the importance of considering rhabdomyolysis in patients with severe hypothyroidism as a cause of acute renal failure. It also shows the importance of reviewing the patient's medication list and discontinuing all those medications which can escalate the process of rhabdomyolysis in a patient with hypothyroidism.

Hoffman’s syndrome-a rare neurological presentation of hypothyroid myopathy

Hoffman's syndrome is a rare form of hypothyroid myopathy, which causes proximal muscle weakness and pseudohypertrophy of muscles. It is a complication of untreated or uncontrolled Hypothyroidism.The neurological manifestations of hypothyroidism usually occur late in the course of disease. It is quite rare to present with neurological manifestations in the earlier stage of disease. Very few cases of Hoffman’s syndrome were reported from India. Here we report a case of 27-year-old male who presented to the medicine OPD with initial symptoms of proximal muscle weakness, fatigue and calf muscle hypertrophy. On further evaluation patient was found to have hypothyroid myopathy in the form of Hoffman’s syndrome.

A Rare Case Of Hoffman Syndrome Presented As Hypothyroid Myopathy

Hypothyroidism's neurological manifestations are uncommon as first symptoms, and they usually appear later in the disease's course.Muscle hypertrophy is a very uncommon occurrence in hypothyroid people 1. Hoffmann's syndrome is a kind of hypothyroidism thatmanifests as muscle stiffness and pseudohypertrophy in adults. In most cases of hypothyroid myopathy, laboratory tests reveal elevatedlevels of muscle enzyme. The electro physiological investigation may reveal signs that indicate myopathy, neuropathy, or a combinedpattern of myopathy and neuropathy. Hormone replacement therapy 7 restores symptoms and normalises enzyme levels in the blood.Now, presenting a case of young age male presenting with hypothyroidism having features of calf muscle hypertrtrophy

ODP513 Rhabdomyolysis: A Rare Presentation Of Central hypothyroidism

Abstract Background Hypothyroidism is one of the most common endocrine disorders affecting approximately 5 percent of Americans aged 12 and older. The most common cause of hypothyroidism globally is iodine deficiency whereas in the United States, Hashimoto's thyroiditis is the most prevalent. Less frequently, hypothyroidism can be caused by central hypothyroidism. In uncontrolled states, this entity can lead to an array of complications with rhabdomyolysis being among the latest manifestations. We present a case when the patient was admitted to the hospital for significant rhabdomyolysis, and after workup, was found to be related to new onset central hypothyroidism. Clinical Case A 34-year-old African American male presented to our facility with proximal muscle weakness and pain in the bilateral hips and right shoulder for three days. During the interview, the patient was acutely debilitated demonstrating slow body movements and grimaces on passive and active range of motion. Motor strength and sensation was preserved in bilateral extremities. The patient denied any recent injury, compression, extensive exercise, seizure, or durg use. The patient, however, reported a family history of rheumatological and endocrine conditions. Labs were obtained and revealed a creatinine kinase level of 10,5000 U/L; creatinine kinase- MB 53.5 ng/mL; creatinine 1. 0 mg/dL; AST 146 U/L; ALT 72 U/L; CRP 8.6 mg/L. The patient was stabilized with appropriate fluid and steroid therapy. On further investigation, TSH and T4 levels were 0.30 µlU/mL and 0.55 ng/dL, respectively. MRI with and without contrast did not show any intracranial pituitary abnormality or mass. The patient was started on levothyroxine and instructed to remain on the drug as an outpatient to prevent future occurrences. He was subsequently discharged after CK levels normalized and proximal muscle weakness improved. The patient was instructed to have a repeat thyroid function test and T4 levels in 6 weeks with appropriate follow up. Conclusion Idiopathic central hypothyroidism is a rare cause of hypothyroidism estimated to occur in 1: 20,000-80,000 in the general public. The lack of a pituitary mass lesion on MRI added to the rarity of this presentation. Hypothyroid myopathy causing rhabdomyolysis is a known but rare consequence of untreated hypothyroidism, which may present with muscle weakness, pain, and elevated serum muscle enzyme. Prompt workup to rule out a multitude of other causes is required, and the patient should be closely monitored for electrolyte and kidney function changes. Levothyroxine remains the treatment of choice for correction of central hypothyroidism with dose adjustments based on patient symptoms and serum free T4 values. Presentation: No date and time listed

Study of undiagnosed clinical hypothyroidism in patients with obstructive sleep apnea

Abstract Introduction Symptoms of hypothyroidism and obstructive sleep apnea (OSA) overlap. Previous research studies have found a clear association between both disorders. Different mechanisms could explain this association such as airway narrowing owing precipitation of mucoproteins in the upper airways, hypothyroid myopathy, and decreased ventilatory drive. The research aimed to study the occurrence of undiagnosed clinical hypothyroidism among patients with OSA. Patients and method Retrospective study was conducted in Chest department, Kasr Al Ainy hospital, Cairo University; it included 140 patients diagnosed as obstructive sleep apnea. History taking, clinical examination, blood tests including thyroid profile, Body measurements, the Epworth Sleepiness scale (ESS), Polysomnography (PSG) and Neck ultrasound were performed to all. Results It included 48 females (34.3%) and 92 males (65.7%), with a mean age of 53.09 ± 12.84 years. Patients were classified into two groups: OSA with euthyroid state (108 patients=77.1%) and OSA with hypothyroidism (32 patients=22.9%). Significant differences were found between both groups regarding neck ultrasound abnormalities, with P value less than 0.001. Regarding comorbidities, anthropometric measurements, Epworth sleepiness score, and apnea-hypopnea index, no significant difference was found. Although desaturation index and SpO2 less than 90% were higher in hypothyroid group (26.08 ± 25.42 and 47.16 ± 43.61, respectively), the difference did not reach statistical significance. Conclusion The percent of clinical hypothyroidism in patients with OSA was 22.9% among our studied patients.

Hypothyroid myopathy in a patient with MCTD with Hashimoto’s disease.

Hypothyroid myopathy in a patient with MCTD with Hashimoto’s disease.

Особливості ураження нервової системи при первинному гіпотиреозі (огляд літератури)

В огляді наведені дані про патогенетичні механізми розвитку патології центральної та периферичної нервової системи при первинному гіпотиреозі. Нестача тиреоїдних гормонів призводить до змін в організації центральної нервової системи, зниження енергетичного забезпечення нейронів, зміни синтезу деяких специфічних білків нервової системи, що зумовлює розвиток кретинізму в дітей. Доведена роль гіпотиреозу у виникненні когнітивних порушень у дорослих, таких як зниження пізнавальної функції, пам’яті й уваги. Погіршення логічного мислення виявляється вже у хворих на субклінічний гіпотиреоз. Порушення медіаторного обміну призводить до формування депресії. Найбільш вивченими при гіпотиреозі є нервово-м’язові порушення (гіпотиреоїдна міопатія й міотонічний феномен) та ураження периферичних нервів. Приховувати первинний гіпотиреоз можуть тунельні нейропатії, полінейропатія й атактичний синдром. Попри численні дослідження, що стосуються гіпотиреозу та його неврологічних ускладнень, деякі питання патогенезу, діагностики, перебігу й лікування неврологічної патології при первинному гіпотиреозі потребують подальшого дослідження.

Hoffmann syndrome; a rare form of hypothyroid myopathy

Hoffman syndrome is a rare clinical presentation characterized by the presence of proximal weakness and muscle pseudo-hypertrophy in a hypothyroid patient. 50-year-old male presented with gradual onset muscle stiffness and weakness involving both bilateral upper and lower limbs for 3-months duration. Examination revealed generalized hypertrophy of the muscles, mainly involving the Gastrocnemius with proximal muscle weakness and slow relaxing deep tendon reflexes. His Thyroid Stimulating Hormone and creatinine kinase were elevated. Anti-Thyroid peroxidase antibodies were positive. Electromyogram (EMG) and muscle biopsy was suggestive of a myopathic disorder and a diagnosis of Hoffmann syndrome was made. Complete resolution of weakness was observed following thyroxine therapy. Hoffmann syndrome is a rare, myopathic disorder seen in long standing, untreated hypothyroidism and it has a favourable response to thyroid hormone replacement in majority of patients.

A Complex Case of Polymyositis Overlapping With Hypothyroid Myopathy Without Underlying Autoimmune Thyroid Disorder

A 78-year-old woman with a past medical history of hypothyroidism and Sjogren's syndrome presented with a two-month history of gradually progressive bilateral lower extremity weakness. Significant elevation in thyroid-stimulating hormone (TSH) and muscle enzyme, such as creatine kinase, was noticed on presentation. Due to concerns of hypothyroid myopathy, the patient was started on thyroxine and triiodothyronine supplementation. The patient reported no significant improvement in her weakness in the one-month follow-up. Laboratory workup revealed improving TSH levels but worsening creatine kinase levels. Electromyography study showed primarily myopathic features, such as abnormal insertional activity concerning for mild inflammatory myopathy. Muscle biopsy showed mild inflammatory exudate and features of myopathy with ongoing denervation. The patient was diagnosed with polymyositis and started on prednisone 0.5 mg/kg daily with a taper course and methotrexate. The patient reported significant improvement in her weakness when seen in six weeks with normalizing creatine kinase levels. The hallmark difference between hypothyroid myopathy (including polymyositis-like syndrome) and conventional polymyositis is the complete clinical recovery and resolution of laboratory abnormalities after treatment with thyroid hormone replacement in hypothyroid myopathy. There was no evidence of underlying autoimmune thyroid disorder which makes this case unique. This case highlights the complex case of polymyositis overlapping with hypothyroid myopathy with no underlying autoimmune disorder.

Anti-Ku Antibody-Related Scleroderma-Polymyositis Overlap Syndrome Associated With Hypothyroid Myopathy.

Anti-Ku Antibody-Related Scleroderma-Polymyositis Overlap Syndrome Associated With Hypothyroid Myopathy.

Hoffmann\u2019s syndrome necessitating forearm fasciotomy: a case report

BackgroundHoffmann’s syndrome is a rare form of hypothyroid myopathy. Only a few cases of fasciotomy in this setting have previously been reported.Case presentationA 41-year-old Caucasian man under treatment for hypothyroidism presented with acute-onset severe pain in his forearm for no obvious reason and was admitted to our emergency room. He eventually developed compartment syndrome which necessitated surgical decompression. Soon after surgery he complained of similar symptoms in his calves. By the time his hypothyroid status was confirmed, conservative treatment and orally administered levothyroxine gradually made the pain from his calves disappear, without further surgical treatment.ConclusionHoffmann’s syndrome may precipitate a compartment syndrome in the absence of trauma.

76-Year-Old Woman With Generalized Weakness

76-Year-Old Woman With Generalized Weakness