AbstractContextIt is well recognized that some hypothyroid patients on levothyroxine (LT4) remain symptomatic, but why patients are susceptible to this condition, why symptoms persist and what is the role of combination therapy with LT4 and liothyronine (LT3), are questions that remain unclear. Here we explore evidence of abnormal thyroid hormone (TH) metabolism in LT4-treated patients, and offer a rationale for why some patients perceive LT4 therapy as a failure.Evidence AcquisitionThe review is based on a collection of primary and review literature gathered from a PubMed search of hypothyroidism, levothyroxine, liothyronine, and desiccated thyroid extract, among other keywords. PubMed searches were supplemented by Google Scholar and the authors’ prior knowledge of the subject.Evidence SynthesisIn most LT4-treated patients, normalization of serum TSH levels results in decreased serum T3/T4 ratio, with relatively lower serum T3 levels; in at least 15% of the cases, serum T3 levels are below normal. These changes can lead to a reduction in TH action, which would explain the slower rate of metabolism and elevated serum cholesterol levels. A small percentage of patients might also experience persistent symptoms of hypothyroidism, with impaired cognition and tiredness. We propose that such patients carry a key clinical factor, e.g. specific genetic and/or immunologic makeup, that is well compensated while the thyroid function is normal but might become apparent when compounded with relatively lower serum T3 levels.ConclusionsAfter excluding other explanations, physicians should openly discuss and consider therapy with LT4 and LT3 with those hypothyroid patients that have persistent symptoms or metabolic abnormalities despite normalization of serum TSH level. New clinical trials focused on symptomatic patients, genetic makeup and comorbidities, with the statistical power to identify differences between monotherapy and combination therapy, are needed.
Mantle cell lymphoma is a mature B-cell non-Hodgkin lymphoma characterized by the hallmark (11;14) chromosomal translocation, which often presents with lymphadenopathy and extra-nodal involvement. Young, fit patients are generally treated with chemotherapy approaches that incorporate high-dose cytarabine (e.g. the Nordic regimen) followed by autologous hematopoietic cell transplantation. Because of the significant activity of cytarabine in mantle cell lymphoma, increasingly, high- and intermediate-dose cytarabine are being used in the treatment of elderly mantle cell lymphoma patients. In practice, many patients present with significant organ dysfunction and there is limited data on the use of high- to intermediate-dose cytarabine and bendamustine in this setting. Here, we report a case of a critically ill, elderly patient with mantle cell lymphoma and concomitant acute kidney injury and oliguria who was successfully treated with a cycle of cytarabine (Ara-C) and bendamustine accompanied by intermittent hemodialysis.
In patients treated with TH, the TH had no independent effect on BG levels. Mortality was associated with increased BG levels after cardiac arrest but before initiation of TH or an insulin drip. Likely, it is the severity of stress from the cardiac arrest that causes the hyperglycemia in these patients.
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