ABSTRACT
Refractory hypothyroidism has been increasingly identified worldwide. Primary hypothyroidism is considered refractory when there is a persistent elevation of thyroid-stimulating hormone (TSH) above the upper limit of normal despite escalating doses of levothyroxine with or without the persistence of hypothyroid symptoms. Further escalation of levothyroxine to supratherapeutic doses could be associated with potential complications such as iatrogenic hyperthyroidism, cardiac failure, and other conditions. Therefore, physicians should rule out non-compliance and pursue a further evaluation to identify etiologies for increased requirements or decreased absorption of levothyroxine in patients not achieving therapeutic doses. Here, we present a 40-year-old Indian male with worsening refractory hypothyroidism that resolved following eradication of his Helicobacter pylori (H. pylori) infection. Herein, we highlight a unique and reversible cause of refractory hypothyroidism. With this case report, we hope to encourage physicians to include H. pylori testing in the evaluation of primary hypothyroidism refractory to treatment.
ABSTRACT
BACKGROUND: We have described the clinical stages of the brain aging and Alzheimer's disease (AD) continuum. In terms of the pre-dementia stages of AD, we introduced the terminology "mild cognitive impairment" (MCI) for the first pre-dementia stage and "subjective cognitive decline" (SCD) for the pre-MCI stage. We now report the characteristics of a pre-SCD condition eventuating in likely AD. OBJECTIVE: The aim of this study was to characterize a pre-SCD condition eventuating in AD. METHOD: Sixty healthy persons with "no cognitive decline" (NCD) were recruited and 47 were followed (mean baseline age, 64.1 ± 8.9 years; mean follow-up time, 6.7 ± 3.1 years). Outcome was determined at the final assessment prior to 2002 as "decliner," if SCD or worse, or "nondecliner" if NCD. RESULTS: After controlling for age, gender, years of education, and follow-up time, there was a between-group difference in the decline rate (p < 0.001). Also, after controlling for demographic variables and follow-up time, the combinatorial psychometric score was lower at baseline in the future decliners (p = 0.035). Of the 9 psychometric variables, after controlling for demographic variables and follow-up time, 3 were significantly lower at baseline in future decliners. Since AD is known to be age related and all subjects in this study were otherwise healthy, we also did an analysis without controlling for age. The combinatorial psychometric score was highly significantly better at baseline in the future nondecliners than in the future decliners (p = 0.008). CONCLUSION: This is ostensibly the first study to link psychometric cognitive decline to the subsequent SCD stage of eventual AD.
