Background:Type 2 diabetes mellitus (T2DM) has been associated with impairment of cognitive function. Studies show a strong negative correlation between the levels of glycosylated hemoglobin and cognitive function in adult patients above the mean age of 60 years. In healthy adults, age-related cognitive impairment is mostly reported after the age of 60 years, hence the decline in cognitive function can be a part of normal aging without diabetes. Since the majority of patients with diabetes are between the ages of 40 and 59 years, it is crucial to ascertain whether the levels of glycosylated hemoglobin negatively correlate with the levels of cognitive function scores in adult patients of age 60 years or younger, similar to the way it correlates in patients older than 60 years of age, or not.Aims:We observed the relationship between the levels of glycosylated hemoglobin and the levels of cognitive function in patients of age 60 years or younger with T2DM.Materials and Methods:Eighty-two patients with T2DM underwent cognitive assessment testing by using a Modified Mini-Mental State Examination (3MS), and their cognitive function scores were correlated with their glycosylated hemoglobin levels, durations of diabetes, and levels of education.Results:Cognitive impairment was observed in 19.5% of the studied patients. We found a weakly negative relationship between the glycosylated hemoglobin level and cognitive function score (r = -0.292), a moderately negative relationship between the duration of diabetes and cognitive function score (r = -0.303), and a weakly positive relationship between the level of education and cognitive function score (r = 0.277).Conclusion:Cognitive impairment affects one-fifth of the patients of age 60 years or younger with T2DM. It is weakly negatively related to the glycosylated hemoglobin level, moderately negatively related to the duration of diabetes, and weakly positively related to the level of education.

Objective: We present a patient with long standing hypothyroidism that developed hyperthyroidism secondary to Graves’ disease. Recognition of this disease phenomenon is crucial to ensure prompt diagnosis and close follow-up. Methods: The patient was evaluated with thyroid function testing and thyroid antibody testing. Further evaluation included ophthalmologic examination and radioactive iodine uptake imaging. Results: A 56-year-old female with past medical history of human immunodeficiency virus (HIV), hepatitis C infection, and hypothyroidism presented for evaluation of thyroid disease. She had been off of levothyroxine for the last 8 months due to biochemical findings of thyrotoxicosis. Family history was significant for hyperthyroidism and hypothyroidism. Labs were consistent with hypothyroidism so levothyroxine was restarted. Exam showed lid lag and proptosis. Ophthalmologic evaluation found bilateral 23 mm proptosis. Additional lab testing was positive for thyroid peroxidase antibody and thyroid stimulating immunoglobulin. Following levothyroxine use, the patient developed subclinical hyperthyroidism and thyroid replacement was stopped. The patient remained euthyroid for one year off of levothyroxine. Following one year, she developed mild hyperthyroidism with increased radioactive iodine uptake. She was placed on propranolol for symptomatic relief. Months later, thyroid function testing normalized. Conclusion: In Graves’ disease, hypothyroidism and conversion of hypothyroidism to hyperthyroidism are rare, yet important to recognize, clinical phenomenon. The stimulatory and inhibitory properties of thyroid-stimulating hormone receptor antibodies are speculated to play a role in individuals with alternating hypothyroidism and hyperthyroidism. These individuals can present a diagnostic and therapeutic challenge. Clinicians must maintain a high clinical suspicion for this disease entity.

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