Graves’ disease combined with acute myocarditis and thyrotoxic periodic paralysis in a male:a case report and review of the literature

Graves’ disease is the most common reason for hyperthyroidism which manifest as multi-system changes.Among these clinical manifestations acute myocarditis and thyrotoxic periodic paralysis are very rare and patients who are combined with both two haven’t been reported yet.The etiology may attribute to autoimmunity.

The role of action potential changes in depolarization-induced failure of excitation contraction coupling in mouse skeletal muscle

Excitation-contraction coupling (ECC) is the process by which electrical excitation of muscle is converted into force generation. Depolarization of skeletal muscle resting potential contributes to failure of ECC in diseases such as periodic paralysis, intensive care unit acquired weakness and possibly fatigue of muscle during vigorous exercise. When extracellular K+ is raised to depolarize the resting potential, failure of ECC occurs suddenly, over a narrow range of resting potentials. Simultaneous imaging of Ca2+ transients and recording of action potentials (APs) demonstrated failure to generate Ca2+ transients when APs peaked at potentials more negative than –30mV. An AP property that closely correlated with failure of the Ca2+ transient was the integral of AP voltage with respect to time. Simultaneous recording of Ca2+ transients and APs with electrodes separated by 1.6mm revealed AP conduction fails when APs peak below –21mV. We hypothesize propagation of APs and generation of Ca2+ transients are governed by distinct AP properties: AP conduction is governed by AP peak, whereas Ca2+ release from the sarcoplasmic reticulum is governed by AP integral. The reason distinct AP properties may govern distinct steps of ECC is the kinetics of the ion channels involved. Na channels, which govern propagation, have rapid kinetics and are insensitive to AP width (and thus AP integral) whereas Ca2+ release is governed by gating charge movement of Cav1.1 channels, which have slower kinetics such that Ca2+ release is sensitive to AP integral. The quantitative relationships established between resting potential, AP properties, AP conduction and Ca2+ transients provide the foundation for future studies of failure of ECC induced by depolarization of the resting potential.

DECREMENTAL RESPONSE ON PROLONGED EXERCISE TEST IN A PATIENT WITH THYROTOXIC PERIODIC PARALYSIS

Paralysis of acute onset often presents a diagnostic challenge for the assessing physician because of a large number of differential diagnosis and overlap of clinical features among them. Thyrotoxic periodic paralysis is an uncommon cause of acute weakness. In addition to serological tests, electromyography findings during prolonged exercise test are very helpful in confirming the diagnosis. Only a few case reports of thyrotoxic periodic paralysis have been published from Middle East and none of them have described this specific electrophysiological data. A man in his 20s presented to us with acute onset weakness in both legs which was evaluated further and found to have hypokalemia. The work up for the etiology revealed thyrotoxic status and a final diagnosis of thyrotoxic periodic paralysis was established. The prolonged exercise test performed in this patient showed typical progressive decremental respsonse with nadir at 40 minutes after the exercise.

Glucocorticoid-Induced Hypokalemic Periodic Paralysis after Short-Term Use of Tenofovir with Hypophosphatemia: A Case Report

Hypokalemic periodic paralysis (HPP) is a neuromuscular disorder associated with muscular dysfunction caused by hypokalemia. There are various causes of HPPs and rarely, HPP appears to be relevant to tenofovir or glucocorticoid treatment. There have been several case reports of tenofovir-related nephrotoxicity or tenofovir-induced HPP. However, a case report of glucocorticoid-induced HPP in a patient using tenofovir temporarily has not been reported. Herein, we report a case of glucocorticoid-induced HPP with short-term use of tenofovir. A 28-year-old man visited the emergency room with decreased muscle power in all extremities (2/5 grade). In their past medical history, the patient was treated with tenofovir for two months for a hepatitis B virus infection. At the time of the visit, the drug had been discontinued for four months. The day before visiting the emergency room, betamethasone was administered at a local clinic for herpes on the lips. Laboratory tests showed hypokalemia, hypophosphatemia, and mild metabolic acidosis. However, urinalysis revealed no abnormal findings. Consequently, it can be postulated that this patient developed HPP by glucocorticoids after taking tenofovir temporarily. This is the first case report of glucocorticoid-induced HPP in a patient using tenofovir. Clinicians who prescribe tenofovir should be aware of HPP occurring when glucocorticoids are used.