ABSTRACT Thyroid disorders in children represent a common and usually treatable endocrine disorder. Anemia in children is another prevalent illness that can present in a variety of ways, ranging from mild and asymptomatic to more severe types with obvious symptoms. Moreover, anemia is a frequent, although often underestimated, clinical problem accompanying thyroid diseases and constitutes an important clinical issue. Anemia has been documented in 20%–60% of hypothyroid children and 33% of cases of Graves’ disease (GD). On the other hand, iron deficiency anemia (IDA) and thalassemia major can be associated with impaired thyroid function, particularly hypothyroidism. The causative relationship between both disorders appears to be complex and occasionally unclear. This article offers a thorough summary of the relationship and reciprocal impact of anemia and thyroid problems in children. It is important for the clinician to evaluate thyroid status in children with anemia and vice versa, considering the possible connection between thyroid problems and anemia. Adequate correction of the anemia and early identification and treatment of thyroid dysfunction are essential to significantly improve clinical outcomes of these children.
ABSTRACT Thyroid storm (TS) or thyrotoxic crisis is a rare medical emergency that may initially present with various clinical manifestations including nausea, palpitations, and fever. Although quite unusual, TS may also clinically present with neurological manifestations of agitation, delirium and anxiety as well as ophthalmological manifestations, including proptosis and eyelid lag. A detailed literature review of case reports and various studies has reported nystagmus to be an extremely rare initial clinical manifestation of TS. We report a case of a young female, newly diagnosed with hyperthyroidism, who primarily presented with complaints of isolated nystagmus. She was diagnosed with TS and immediately started on medications. Her nystagmus improved once she was treated for TS. In conclusion, nystagmus as a manifestation of TS is an unusual phenomenon but can be reversible with appropriate treatment of the underlying cause.
ABSTRACT Subclinical hypothyroidism (SCH), defined by elevated thyroid-stimulating hormone with normal free thyroxine, is traditionally regarded as a clinically silent and benign endocrine state. This assumption, however, is increasingly challenged in psychiatric populations, where even subtle neuroendocrine disturbances may exert significant effects on mood regulation, cognition, stress responsivity, and suicidal behavior. Individuals with mental illness represent a biologically vulnerable group characterized by hypothalamic–pituitary–adrenal axis dysregulation, systemic inflammation, circadian disruption, autoimmune activation, and exposure to psychotropic medications, factors that may amplify the neuropsychiatric impact of mild thyroid dysfunction. Emerging epidemiological and clinical evidence links SCH and autoimmune thyroid disease with depression severity, treatment resistance, and increased suicidal behavior, particularly among adolescents and young adults. In India, where thyroid disorders are highly prevalent and suicide remains a major public health concern, thyroid reference intervals are largely derived from Western populations and are not validated against psychiatric outcomes. This viewpoint argues that SCH is not clinically silent in psychiatric illness and proposes a shift from population-based laboratory cutoffs toward outcome-anchored, context-specific thyroid interpretation. Recalibrating thyroid assessment using suicidality and psychiatric severity as meaningful endpoints may enhance early biological risk detection, support precision psychiatry, and contribute to suicide prevention strategies in resource-constrained settings.
Introduction: Liver dysfunction in Graves’ disease is usually attributed to thyrotoxicosis or antithyroid drug-induced liver injury. Methimazole-induced liver injury is a known cause of cholestatic liver injury pattern in patients treated for Graves’ disease. Persistent or progressive cholestatic liver dysfunction despite drug withdrawal indicates an underlying autoimmune hepatobiliary disorder. Differentiating Drug-induced liver injury from autoimmune liver disease is challenging, when autoimmune serology and radiological investigations are unremarkable. Case Report and Results: A 49-year-old gentleman presented with 2-months history suggestive of thyrotoxicosis. Diagnosis of Graves’ disease was confirmed with biochemical investigations(tsh-0.05miu/ml, total t4-21.5mcg/dl, totalt3349ng/dl and echnetium-99m thyroid scintigraphy. Baseline liver enzymes were normal. Methimazole and propranolol were initiated, with subsequent dose reduction according to thyroid function test. Nine weeks after treatment initiation, patient presented with jaundice and pruritis and liver function was suggestive of cholestatic pattern. Despite drug withdrawal, liver function worsened, (AST/ALT 61/76 U/L, ALP 235 U/L, total bilirubin 5.27 mg/dL). Viral hepatitis screening, autoimmune serology (ANA, AMA, ASMA, LKM-1), serum IgG, and Magnetic Resonance Cholangiopancreatography (MRCP) were within normal range. Liver biopsy was suggestive of interface hepatitis, intrahepatic cholestasis, onion-skin periductal fibrosis with bile duct obliteration, granulomas, and portal fibrosis (Ishak 1/6), consistent with primary sclerosing cholangitis with autoimmune hepatitis overlap. Prednisolone (40 mg/day) was initiated, methimazole was replaced with lithium, and definitive treatment with radioiodine I131 (10 mCi) was done. Liver function progressively normalized with corticosteroid therapy, which was successfully tapered over 20 weeks. Patient after 20 weeks of radioiodine ablation became hypothyroid and is currently euthyroid on levothyroxine replacement. Conclusion: This case highlights that cholestatic liver injury after methimazole treatment should not only attributed to drug induced liver injury. Seronegative PSC-AIH overlap may present with a normal MRCP and negative autoimmune markers. It was uncertain whether the observed liver pathology was primarily related to or precipitated by methimazole exposure or coincidental autoimmune hepatobiliary disorder.
