High titers of anti-TPO-Ab are found in nearly all reported cases [5, 6, 12, 23] and it is considered to be a hallmark of the disease
High titers of anti-TPO-Ab are found in nearly all reported cases [5, 6, 12, 23] and it is considered to be a hallmark of the disease. changes. A diagnosis of SREAT was made and she was treated with intravenous methylprednisolone followed by oral prednisolone. Her condition improved dramatically within 48 hours of starting steroids. SREAT is a diagnosis of exclusion in patients with a central nervous system disorder. There are no specific clinical features or investigative findings. Elevated anti-TPO antibodies are considered a hallmark of SREAT and steroid responsiveness supports the diagnosis. Prompt diagnosis and treatment reverses the neurological dysfunction in most cases. 1. Background Steroid-Responsive Encephalopathy Associated with Autoimmune Thyroiditis (SREAT) also known as Hashimoto’s Encephalopathy is a rare association with autoimmune thyroid disease [1]. Although classified as an autoimmune encephalitis, the pathogenesis of SREAT is still uncertain [1, 2]. SREAT has an estimated prevalence of 2.1 per population of 100,000 [3]. There is a female preponderance with cases being reported in patients aged 14 to 70 years (average age of onset 40 to 55 years) [4C6]. Clinical manifestations of SREAT are varied and nonspecific [2, 5C7]. Therefore, it is often misdiagnosed or underdiagnosed. Due to the lack of any specific diagnostic investigations, SREAT is mainly SAR125844 a diagnosis of exclusion, to be considered in the setting of encephalopathy with high anti-TPO-Ab titers and responsiveness to glucocorticoid therapy. We report a case of SREAT diagnosed in a 65-year-old female, who was SPRY1 clinically euthyroid, presenting with behavior changes and neuropsychiatric manifestations with an acute febrile illness. 2. Case History A 65-year-old female with diabetes, hypertension and on treatment for hypothyroidism presented to the National Hospital of Sri Lanka with a history of fever and headache for three days and progressively worsening confusion. She also gave a history of on and off giddiness and lightheadedness particularly during standing from supine or seated positions. The family members had noted that she had become increasingly withdrawn and has had episodic confusion. She did not have any respiratory or gastrointestinal symptoms. She has been on treatment for type 2 diabetes mellitus and hypertension for ten years and for hypothyroidism for 3 years. She also had stable chronic kidney disease (stage III). She was on metformin, gliclazide, losartan, and levothyroxine with good compliance to therapy with a regular medical clinic follow-up. There was no prior history of any psychiatric illnesses or substance abuse. There was no family history of similar illnesses either. During the hospital stay, she had intermittent fever spikes with temperature varying between 37C and 39C. Her blood pressure was 170/90?mmHg on admission and there was no postural drop in blood pressure. Mental state examination revealed a depressed mood, loose associations, and tangential thoughts. However, she did not have any hallucination or delusions. Mini-Mental State Examination Score was 25. There was no suicidal or homicidal ideation. Her Glasgow SAR125844 Coma Score (GCS) was 14/15. There was no neck stiffness or focal neurological deficits. The rest of the system examination was unremarkable. Funduscopic examination revealed grade 2 hypertensive retinopathy. Her initial laboratory investigations revealed a total white blood count of 15 103 with 85% neutrophils. ESR was 65?mm in the 1st hour and CRP was 25.5?mg/l. With the presence of confusion and neuropsychiatric manifestations in the setting of an acute febrile illness, intravenous ceftriaxone and acyclovir were commenced suspecting meningoencephalitis. However, her cerebrospinal fluid (CSF) analysis revealed only two lymphocytes per mm3 with normal protein and sugar levels. The electroencephalogram (EEG) showed diffused background attenuation and SAR125844 right sided frontal intermittent rhythmic delta activity (FIRDA). The MRI brain showed prominent sulci and gyri with age related atrophy and periventricular white matter ischemic changes. Her free T4 was 1.24?ng/dL (0.89C1.76) and thyroid stimulating hormone (TSH) level was 0.57?mIU/L (0.55C4.78). She had a substantially high titer of anti-TPO (over 1000?IU/ml) and anti-thyroglobulin (2471.9?IU/ml) antibodies. The thyroid ultrasound scan did not show any inflammation of the gland. Serum creatinine was stable at approximately 140 to 160? mmol/l and serum electrolytes including sodium, potassium, ionized calcium, and phosphate were normal throughout the hospital stay. Aspartate aminotransferase (AST) was 148?U/L and alanine aminotransferase (ALT) was 132?U/L. Her ultrasound abdomen showed loss of corticomedullary demarcation in normal sized kidneys and a normal liver. The other liver function tests were normal. All other blood investigations including antinuclear antibody titer and serological tests for herpes simplex virus (HSV), cytomegalovirus, human immunodeficiency virus (HIV), viral hepatitis B, viral hepatitis C, and syphilis were negative. Her.