Hashimoto's Encephalitis Research Articles

Hashimoto's encephalitis - A case report

A 50 year-old woman with a background of focal epilepsy presented to Emergency Department (ED) in convulsive status epilepticus.After 1 year seizure-free on levetiracetam,she initially presented with headache, tremor, fatigue and general malaise. She was discharged, then re-presented to ED several days later in status epilepticus. Two doses of diazepam administered pre-hospital failed to terminate the seizure. She was loaded with phenytoin,intubated and ventilated and commenced on a midazolam infusion. She spent 7 days in neuro-intensive care and was discharged home on levetiracetam 1.5 g twice daily and phyentoin 250 mg twice daily.One month later, she re-presented to ED with 4 days of worsening tremors and reduced mobility. Physical examination revealed multifocal myoclonus. She had experienced significant cognitive decline and neuropsychiatric symptoms including severe anxiety, delusions and paranoia.InvestigationsImagingInitial MRI head with gadolinium showed marked symmetric abnormality within the white matter of both hemispheres extending into subcorticol regions, most predominant at the vertex and involving U fibres. The neuro-radiologist commented that the differential for these changes was broad, including an encephalitis, PML, meningitis or a leukoencephalopathy.Repeat MRI head 1 month later showed complete resolution of the white matter changes leaving no sequelae.Blood testsHer past medical history included subclinical hypothyroidism. Thyroid function tests showed an elevated TSH of 21.33 and thyroid peroxidase(TPO) antibody level of 188.0 IU/mL, with FT4 levels within normal range.Extensive relevant blood screen, including the following was all negative• NMDA, glycine receptor and anti-cardiolipin antibody• Connective tissue screen, anti-MPO and anti-PR3• Serum electrophoresis• Paraneoplastic antibody screen including Cerebellum IIF, MA2, MA1, amphiphysin, CV2(CRMP5), Anti-Ri (ANNA 2) Ab, Anti Yo Ab and Anti Hu Ab• HIV and syphilis serology• JC virus• Plasma amino acid, urine organic acid and ammoniaLumbar punctureCSF WCC 1/mm3CSF protein- 816 mg/LCSF viral PCR (including JC virus) and oligoclonal bands negativeEEG- normal background activity with no clear focal or diagnostic epileptiform abnormalities.Treatment and follow-upThe clinical picture, elevated TPO antibodies and absence of other relevant investigation abnormality raised Hashimoto's encephalitis as a potential unifying diagnosis. She had a good response to inpatient treatment with steroids, her neuropsychiatric features resolved and she has remained seizure-free since discharge. She remains under neurology outpatient follow-up.Discussion:It can be challenging to make a diagnosis of Hashimoto encephalitis, and other potential causes such as infection, metabolic or paraneoplastic processes must be rigorously ruled out (1). In this case, high titres of TPO alongside the clinical presentation with recurrent seizures and cognitive decline were key in making the diagnosis (2,3). Due to an overlap of features, including myoclonus and rapid cognitive decline, it was important to consider Creutzfeldt-Jakob disease (CJD) in the differential. We ruled out CJD due to the rapid response to steroid therapy and lack of typical EEG and MRI findings (4). Overall, due to low prevalence and non-specific MRI and EEG features, this diagnosis can be difficult to make and requires thorough systemic clinical assessment.

È intelligente ma non si applica: quando è solo una questione di anticorpi

A diagnosis of steroid responsive encephalitis associated to autoimmune thyroiditis (Hashimoto encephalitis) was eventually made in a child with complex tics and decline of school performance.

Abstract #1377584: Brain on Fire: A Case of Hashimoto's Encephalitis in a 29-Year-Old Female

A 29-year-old female presents to the hospital for insomnia, hallucination, and bizarre behavior. The patient had been feeling well until approximately three days early when she became psychotic after fasting from food for three days. She began having auditory and visual hallucinations and then started having seizures. Initially, the patient was admitted to a hospital in another city where she was diagnosed with Autoimmune Encephalitis for which she received IVIg. Brain MRI showed questionable T2 changes around the fourth ventricle on the left during hospital admission. The patient was discharged home after her symptoms improved. However, she was brought to our hospital for psychiatric consultation as her condition deteriorated. Upon arrival at Larkin Community Hospital, the patient was hemodynamically stable, breathing room air, and continued to complain of having delusions and hallucinations. Initial Vital Signs: BP: 122/74 mmHg, HR: 70 bpm, RR: 18, T: 98°F. weight 56.2 kg, BMI 24.21. She was in nonacute distress, although anxious with pressured speech. She was cooperative and able to follow commands and track the examiner. Her NIH Stroke Scale/Score (NIHSS) was 0 and Glasgow Coma Scale (GCS) was 15. She denied using illicit drugs, smoking, and alcohol. Neurology decided to repeat LP CSF r/o NMDA Antibody encephalitis and started empirically a 5-day course of azithromycin to cover for streptococcal infections while awaiting further results. Thyroglobulin antibodies were ordered to rule out Steroids Responsive Encephalopathy and it came back elevated (91.2). She was started on Solu-Medrol 500mg IV daily for 3 days which was increased to 1000mg IV daily to complete 5 days. Even though, she developed tachycardia in the 120s; she started feeling much better as well as improved her symptoms. “Steroid-responsive encephalopathy associated with autoimmune thyroiditis” (SREAT) is an uncommon condition that is associated with Hashimoto thyroiditis. It is also called Hashimoto encephalopathy (HE). This condition was originally described in 1966 by Brain et al1. HE is a rare disorder with an approximate prevalence of 2/100,0002. It affects women more often than men. This diagnosis is typically made when a patient has encephalopathy associated with antithyroid (anti-thyroid peroxidase [TPO]) and/or anti-thyroglobulin (TG) antibodies, when other causes have been excluded. The symptoms typically seen include subacute onset of confusion with altered level of consciousness, seizures, and myoclonus. Based on the literature review of 251 cases of SREAT by Laurent et al3, SREAT has various presentations including coma to isolated psychiatric disorder. This disorder is thought to be immune mediated as opposed to being the result of an altered thyroid state on the nervous system. In most of the reported cases of SREAT, the patients are euthyroid during the presentation of symptoms. However, the exact mechanism of SREAT is still unknown. The diagnosis is made after excluding other toxic, infectious, and metabolic causes of encephalopathy with examination of cerebrospinal fluid and neuroimaging.

Clinical characteristics and short-term outcomes of autoimmune encephalitis in adults

To characterize clinical, paraclinical features and short-term outcomes in different types of autoimmune encephalitis (AE) in a one-center cohort of Russian patients, as well as to evaluate the frequency and significance of the joint expression of antineuronal and anti-glial antibodies (Abs) in AE. Forty-one patients were diagnosed with AE at the Research Center of Neurology from November 2020 to December 2022. Demographic, clinical characteristics, results of laboratory tests, MRI of brain, treatment and outcomes of disease were analyzed. The analysis of Abs to glial antigens (myelin-oligodendrocyte glycoprotein - MOG, glial fibrillar acidic protein - GFAP, aquaporin 4 - AQP-4) was performed by indirect immunofluorescence assay (Euroimmun, Germany). In 24 (58.5%) patients was established definite AE, confirmed by specific Abs detection; in 2 (4.9%) - definite limbic encephalitis, in 15 (36.6%) - seronegative probable AE (including 3 cases of Hashimoto's encephalitis). GFAP-Abs in cerebrospinal fluid (CSF) were detected only in two patients - with clinical and MRI-picture of autoimmune GFAP-astrocytopathy (A-GFAP-A). GFAP- and MOG-Abs in the blood were detected in 25.7% and 6%, respectively, AQP-4-Abs were not detected. There were no correlations between co-expression with glial Abs and clinical characteristics. Systemic and antithyroid Abs were present in 15% and 31%, respectively. Paraneoplastic AE accounted for 22%. For the first time in the Russian population, 2 cases of A-GFAP-A, 6 cases of AE associated with COVID-19 were described. The most common first syndrome were epileptic seizure (34%), psychiatric (29%) and cognitive (14%) disorders. Relapses of AE was observed in 22%. Inflammatory changes in CSF were detected in 41%, focal changes on MRI in 68%. First-line immune therapy was performed in all patients, 85% of cases received pulse therapy with methylprednisolone. Second-line immune therapy (rituximab or cyclophosphamide intravenously) was performed in 19.5%, 78% of patients achieved significant improvement during treatment (scores ≤2 on the modified Rankin scale). The results allow us to consider COVID-19 as a trigger of AE. The absence of detection of GFAP-Abs in CSF in patients with other types of AE contributes to the confirmation of the specificity of GFAP-seropositivity of CSF for the diagnosis of A-GFAP-A. The expression of GFAP- and MOG-Abs in AE can serve as confirmation of the immuno-mediated etiology of the disease, which is especially important for the AE diagnosis in the absence of antineuronal Abs.

LBSAT313 Hashimoto Encephalitis Presenting With Stroke-like Symptoms In An Adult Male

Abstract Hashimoto encephalopathy (HE) is a term used to describe an encephalopathy of presumed autoimmune origin characterized by high titers of antithyroid peroxidase antibodies, an essential feature of this disorder. Pertinent laboratory findings include an elevated serum level of antithyroid peroxidase antibody (TPOAb) and/or antithyroglobulin antibody (TgAb) and negative autoimmune markers of encephalitis in cerebrospinal fluid (CSF). The analysis of CSF may show increased cellularity due to lymphocytic pleocytosis. However, there is no clear relationship between the severity of neurologic symptoms and the type or serum concentration of antibodies. Approximately two-thirds of patients of HE will experience seizures. Patients can present with a recurrence/remission or a diffuse, progressive pattern characterized by slowly progressive cognitive impairment with dementia, confusion, or hallucinations. We present a rare case of Hashimoto's encephalopathy associated with hyperthyroidism in a 61-year-old man evaluated for left facial droop and right upper extremity weakness, successfully treated with corticosteroids and methimazole. We conclude that the diagnosis of HE should be suspected early and be on the differential in patients who present with encephalopathy, which workup shows positive anti-thyroid antibodies and CSF with lymphocytosis. Treatment for meningitis or other life-threatening conditions should never be postponed, as HE is a diagnosis of exclusion that usually requires an extensive laboratory and diagnostic workup. Early diagnosis has an excellent outcome once treatment is started as it is a steroid-responsive encephalopathy associated with autoimmune thyroiditis. Presentation: Saturday, June 11, 2022 1:00 p.m. - 3:00 p.m.

Inpatient Management of Encephalopathy.

Unexplained encephalopathy is a common occurrence in tertiary care centers and neurologic disorders should be considered after ruling out the infectious, toxic and metabolic etiologies. Neuroimaging combined with a thorough history and examination is often helpful in ruling out stroke and fulminant demyelinating encephalopathies. Autoimmune encephalopathy should be suspected in any patient with unexplained acute or subacute onset encephalopathy or rapidly progressing dementia. Anti-N-methyl-D-aspartate receptor (NMDA-R) encephalitis is the most studied form and Hashimoto encephalitis is the most controversial form of autoimmune encephalopathies. Obtaining a combined serum and Cerebrospinal fluid (CSF) autoantibody testing will increase the diagnostic yield of autoimmune and paraneoplastic encephalitis. When diagnosing NMDA receptor antibodies CSF is always more sensitive than serum and in contrast, voltage-gated potassium channel (VGKC) complex antibodies are more readily detectable in serum than in CSF. Neural-specific antibody tests frequently result after several weeks and treatment should be administered without a significant delay to prevent brain damage. Autoimmune encephalitis is often treatment responsive when immunotherapy (glucocorticoids, intravenous immune globulin, plasma exchange) is used in various combinations. The absence of inflammatory markers and autoantibodies in the serum or CSF may not rule out the possibility of paraneoplastic encephalopathies.

Steroid-Responsive Encephalopathy Associated with Thyroiditis

steroid responsive encephalopathy associated with autoimmune thyroiditis (SREAT) is an autoimmune entity with a strong association with elevated antithyroid antibodies. It is a rare cause of encephalopathy and is usually a diagnosis of exclusion. Responsive to corticosteroids is required to make the diagnosis. Herein, we report a male patient presented with recurrent convulsive episodes not controlled well by anticonvulsant drugs and had drops in Glasgow coma scale (GCS). After unremarkable of extensive investigations, Hashimoto's encephalitis was suspected and antithyroid peroxidase antibodies test turned out to be positive, while thyroid function tests were normal and the diagnosis of steroid-responsive encephalopathy associated with autoimmune thyroiditis (SREAT) was made. He received a course of intravenous methylprednisolone for 5 days and responded very well to therapy, with an improvement of his GCS to 15/15.

Catatonia Secondary to Hashimoto's Encephalitis: A Case Report

Introduction: Catatonia is a neuropsychiatric syndrome with motor and behavioral symptoms. In addition to psychiatric illnesses, this syndrome can also be associated with general medical conditions. Few cases of catatonia associated with autoimmune disorders have been reported. Case report: We report the case of a 56-year-old female patient diagnosed with Hashimoto's encephalitis, who presented firstly with mystical delusions and tachypsychia. Despite the proper treatment for psychosis, the symptoms worsened and she developed catatonia. Complementary investigations showed high titers of anti-thyroperoxidase antibodies. Hashimoto encephalitis was suspected and intravenous prednisolone was started. As there was an only partial improvement in psychiatric symptoms, plasmapheresis was chosen. The patient evolved with a drastic improvement in symptoms after the third session of plasmapheresis. Conclusion: An organic etiology should always be considered in cases of catatonia, especially in those with no previous psychiatric history. Doctors should always think about measuring thyroid function when faced with a case of catatonia.

Cerebellar Syndrome Associated with Thyroid Disorders.

Thyroid disorders, including hypothyroidism, hyperthyroidism and Hashimoto encephalopathy, are considered the most common cause of cerebellar dysfunction due to hormonal imbalance. Typically, cerebellar impairment occurs in the course of hypothyroidism and Hashimoto encephalopathy. Information about demographic, clinical and laboratory features of cerebellar disease associated with thyroid disorders is poor. Our review of the literature (1965 to 2018) identified 28 cases associated with hypothyroidism and 37 cases associated with Hashimoto encephalitis. Both patients with hypothyroidism and Hashimoto encephalopathy presented with signs of ataxia that were similarly distributed in the two groups and were mostly predictive of vermis involvement and frequent impairment of cerebellar hemispheres. Additional neurological signs, like dystonia, psychiatric symptoms, ocular disturbances and myoclonus, could be found in the Hashimoto encephalopathy group alone. When present, atrophy of vermis and often of both cerebellar hemispheres was the main imaging abnormality in both hypothyroidism and Hashimoto encephalopathy. Anti-thyroid antibodies could be detected in three quarters of patients with hypothyroidism and in all patients with Hashimoto encephalopathy. In the patients with hypothyroidism, thyroid replacement therapy yielded complete or partial remission of ataxia. In the Hashimoto encephalopathy group, immunosuppressive treatment provided complete remission of ataxia in about 60% of patients, partial remission in the remaining cases. Owing to the treatable nature of the condition and the high prevalence of thyroid disease among general population, cerebellar syndrome associated with thyroid disorders should be considered an important clinical entity. Information from this review will hopefully stimulate and strengthen awareness of thyroid-associated ataxia among clinicians.

Autoantibody-associated schizophreniform psychoses: clinical symptomatology

According to present concepts, primary psychotic disorders in the schizophrenia spectrum are probably caused by acomplex interaction between multigenetic vulnerability and causally relevant environmental factors. In contrast, secondary psychotic disorders are the result of likely identifiable organic factors either in terms of afirst causation (etiology) or asecondary cause (pathogenesis). In this context, autoantibody(ab)-associated autoimmune encephalitis (AE) plays an increasingly important role. Within the group of ab-associated AE with neuropsychiatric symptoms, anti-N-methyl-D-aspartate receptor encephalitis is the most prevalent one. Psychopathologically, polymorphic psychotic symptoms are often observed at onset of AE; however, over the course of this condition or even initially other neuropsychiatric phenomena are also common. The ill-defined entity of a steroid-responsive encephalopathy with thyroid antibodies (Hashimoto's encephalitis) is aheterogeneous syndrome that may also comprise isolated psychotic disorders presenting as classical schizophrenia.

Management of Autoimmune Encephalitis: An Observational Monocentric Study of 38 Patients.

Over the last years the clinical picture of autoimmune encephalitis has gained importance in neurology. The broad field of symptoms and syndromes poses a great challenge in diagnosis for clinicians. Early diagnosis and the initiation of the appropriate treatment is the most relevant step in the management of the patients. Over the last years advances in neuroimmunology have elucidated pathophysiological basis and improved treatment concepts. In this monocentric study we compare demographics, diagnostics, treatment options and outcomes with knowledge from literature. We present 38 patients suffering from autoimmune encephalitis. Antibodies were detected against NMDAR and LGI1 in seven patients, against GAD in 6 patients) one patient had coexisting antibodies against GABAA and GABAB), against CASPR2, IGLON5, YO, Glycine in 3 patients, against Ma-2 in 2 patients, against CV2 and AMPAR in 1 patient; two patients were diagnosed with hashimoto encephalitis with antibodies against TPO/TG. First, we compare baseline data of patients who were consecutively diagnosed with autoimmune encephalitis from a retrospective view. Further, we discuss when to stop immunosuppressive therapy since how long treatment should be performed after clinical stabilization or an acute relapse is still a matter of debate. Our experiences are comparable with data from literature. However, in contrary to other experts in the field we stop treatment and monitor patients very closely after tumor removal and after rehabilitation from first attack.

Hashimoto Encephalopathy: Encephalitis versus Vasculopathy and the Impact of Concussion

Patients with Hashimoto encephalitis may present with seizures, stroke-like episodes, transient focal and global neurological deficits, and a variety of neuropsychiatric disturbances. The encephalopathy evolves with elevated anti-thyroid peroxidase antibodies, independent of hormonal thyroid function. A vasculitic basis is considered in cases that show inflammatory vasculopathy in brain biopsy and postmortem tissues. A relation to autoimmune encephalitis is supported by etiologic localization of the disturbance to vulnerable areas of the mesial temporal lobe and the association of potentially pathogenic antibodies. Both mechanisms presume disruption of the blood-brain barrier. We report a patient with Hashimoto encephalopathy in whom repeated concussions antedated onset of the disorder with overlapping areas of altered brain metabolism and vascular perfusion in the hippocampus, deemed to be most vulnerable in autoimmune encephalopathy and concussive brain injury.

Hashimoto Encephalopathy: Impact of Concussion

Patients with Hashimoto encephalitis may present with seizures, stroke-like episodes, transient focal and global neurological deficits, and a variety of neuropsychiatric disturbances. The encephalopathy evolves with elevated anti-thyroid peroxidase antibodies, independent of hormonal thyroid function. A teenager experienced repeated concussions antedating onset of Hashimoto encephalopathy. Neuroradiological studies showed overlapping areas of altered brain metabolism and vascular perfusion in the hippocampus, deemed most vulnerable in autoimmune encephalopathy. Concussive brain injury may be a contributing factor in the development of encephalopathy due to its capacity to alter the blood-brain barrier.

Chapter 20 - Immune-mediated disorders

Paraneoplastic and autoimmune encephalitis comprise a group of immune-mediated disorders that are associated with different immune effector mechanisms. Classic paraneoplastic neurologic syndromes are triggered by an antitumor immune response. The disease is considered to result from a T-cell response; in addition, patients harbour high titers of autoantibodies against intracellular antigens that are considered as epiphenomenon but are useful diagnostic markers. Neuropathology consists of T-cell-dominated inflammation, marked neuronal loss, and microglial activation with upregulation of HLA-DR. In the last decade, an increasing number of diseases associated with autoantibodies against neuronal surface antigens have been described. There is strong evidence that these autoantibodies are pathogenic and the associated syndromes are generally termed as antineuronal autoimmune encephalitis. Patients typically present with limbic, multifocal, or diffuse encephalitis and respond to immunotherapy. Neuropathologic descriptions are restricted to few biopsy and autopsy specimens and show mild inflammatory infiltrates and microglial activation, together with reduced expression of the respective target antigens, immunoglobulin deposits, and a variable degree of complement activation. Other putative autoimmune disorders of the central nervous system include, among others, Rasmussen encephalitis, chronic lymphocytic inflammation with pontine perivascular enhancement responsive to steroids (CLIPPERS), acute cerebellitis, Susac syndrome, and Hashimoto encephalitis. While pathologic studies suggest an immune-mediated disease for Rasmussen encephalitis, CLIPPERS, acute cerebellitis, and Susac syndrome, neuropathologic descriptions of Hashimoto encephalitis are rare and the pathogenesis deserves further study.

Hashimoto encephalitis as a rare cause of non tumoral opso-myoclonic ataxia

Hashimoto encephalitis as a rare cause of non tumoral opso-myoclonic ataxia

Hashimoto Encephalitis Presented With Clinical Manifestations of Pseudotumor Cerebri: A Case Report

Hashimoto Encephalitis Presented With Clinical Manifestations of Pseudotumor Cerebri: A Case Report

Antithyroperoxidase Antibodies in Encephalopathy: Diagnostic Marker or Incidental Finding?

Patients with acute encephalopathy who are thoroughly examined for an underlying diagnosis and in whom infectious, metabolic, and malignant causes are excluded can form a true diagnostic dilemma. If antithyroperoxidase antibodies (anti-TPO abs) are present, the diagnosis “steroid responsive encephalopathy, associated with autoimmune thyroiditis” (SREAT), better known as Hashimoto encephalitis, will often be considered. The precise pathophysiology of SREAT, including the possible role of the anti-TPO abs and the possible relationship between the encephalopathy and thyroid function, remains to be elucidated. Here we present three young patients with SREAT. Our patients illustrate that in unexplained encephalopathy, after exclusion of other causes (diagnosis of exclusion), determination of the anti-TPO abs may contribute to the diagnosis of SREAT. They also illustrate that thyroid function or the concentration of the anti-TPO abs does not seem to be associated with the severity of the clinical presentation of SREAT. We hypothesize that SREAT has an immunologic etiology. The presence of anti-TPO abs, however, should be considered to be a marker for autoimmunity and not a causative. It probably reflects the presence of predisposition of autoimmunity in these patients. Therefore, this condition should not be called Hashimoto encephalitis any longer.

The growing spectrum of antibody-associated inflammatory brain diseases in children.

Objective:To describe the clinical spectrum, diagnostic evaluation, current management, and neurologic outcome of pediatric antibody-associated inflammatory brain diseases (AB-associated IBrainD).Methods:We performed a single-center retrospective cohort study of consecutive patients aged ≤18 years diagnosed with an AB-associated IBrainD at The Hospital for Sick Children, Toronto, Ontario, Canada, between January 2005 and June 2013. Standardized clinical data, laboratory test results, neuroimaging features, and treatment regimens were captured.Results:Of 169 children (93 female, 55%) diagnosed with an IBrainD, 16 (10%) had an AB-associated IBrainD. Median age at presentation was 13.3 years (range 3.1–17.9); 11 (69%) were female. Nine patients (56%) had anti–NMDA receptor encephalitis, 4 (25%) had aquaporin-4 autoimmunity, 2 (13%) had Hashimoto encephalitis, and 1 (6%) had anti–glutamic acid decarboxylase 65 (GAD65) encephalitis. The key presenting features in children with anti–NMDA receptor encephalitis, Hashimoto encephalopathy, and anti-GAD65 encephalitis included encephalopathy, behavioral symptoms, and seizures; patients with aquaporin-4 autoimmunity showed characteristic focal neurologic deficits. Six patients (38%) required intensive care unit admission at presentation. Median time from symptom onset to diagnosis was 55 days (range 6–358). All but 1 patient received immunosuppressive therapy. One child with anti–NMDA receptor encephalitis died due to multiorgan failure. At last follow-up, after a median follow-up time of 1.7 years (range 0.8–3.7), 27% of the children had function-limiting neurologic sequelae.Conclusions:Children with AB-associated IBrainD represent an increasing subgroup among IBrainD; 1 in 4 children has function-limiting residual neurologic deficits. Awareness of the different clinical patterns is important in order to facilitate timely diagnosis and initiate immunosuppressive treatment.

Iatrogenic thyrotoxicosis secondary to compounded liothyronine.

A 71-year-old woman presented with ST segment elevation myocardial infarction (STEMI) associated with hypotension (100/70 mm Hg) and dizziness. Her husband stated that she appeared confused and was experiencing visual hallucinations. Her medical history was significant for hypertension, pulmonary embolism, hypothyroidism, and gastroesophageal reflux disease. Preadmission medications were reported as amlodipine 2.5 mg daily and pantoprazole 40 mg daily. She denied any recreational drug use or history of mental illness (including hallucinations). She was living independently at home with her husband. The patient’s atypical cardiac symptoms prompted referral to the neurology service. However, neurogenic causes such as Hashimoto encephalitis and cerebrovascular accident were ruled out by negative results on thyroid antibody testing and computed tomography of the head. Incidentally, the laboratory panel for Hashimoto encephalitis included measurement of thyroid hormones, which showed that the level of free tri-iodothyronine was greater than 50 pmol/L (normal range 3–6.8 pmol/L). Thyroidstimulating hormone was 0.03 mIU/L (normal range 0.34–5.6 mIU/L) and free thyroxine was 15 pmol/L (normal range 10–23 pmol/L). The thyroid was not examined, and Grave disease was ruled out on the basis of the normal thyroxine level. In light of the laboratory results, a more detailed investigation for an exogenous iatrogenic cause was initiated. The only discrepancy between the patient’s in-hospital medications and her preadmission medications was a compounded product that she had been taking before the admission, specifically compounded liothyronine capsules (25 μg of liothyronine in hydroxypropyl methylcellulose [hypromellose] for once-daily dosing). The diagnosis was iatrogenic thyrotoxicosis secondary to a compounding error involving liothyronine. The patient’s symptoms, her history related to the current illness, and the supratherapeutic level of tri-iodothyronine were consistent with acute toxicity. She was given supportive care until her mental status and hemo dynamics returned to normal and was then discharged to home. The consequences of the poisoning included STEMI, acute renal injury secondary to hypotension (with serum creatinine twice her baseline value), and a 13-day hospital stay for delirium. Hospital staff contacted the patient’s outpatient pharmacy and alerted them to these findings.

A case of Hashimoto encephalitis in a patient with severe autoimmune hypothyroidism

A case of Hashimoto encephalitis in a patient with severe autoimmune hypothyroidism