Publications

Addison’s disease which is due to dysfunction of the adrenal gland, with abnormal secretion of glucocorticoids and mineralocorticoids, is rare. By inducing inflammation and disorders of water and electrolyte metabolism, Addison’s disease may accelerate progression of co-existed cardiovascular diseases. Addison’s disease combined with cardiovascular disease is infrequent, only 10 cases in the literature. In this case a 51-year-old male patient with unstable angina pectoris and hypotension is reported. Changes on coronary angiography within 2 years suggest rapid progression of coronary artery disease in a patient with low cardiovascular risk. An additional clue of skin hyperpigmentation, fatigue and further examination confirm the diagnosis of Addison’s disease caused by adrenal tuberculosis. After hormone replacement treatment, the frequency and severity of the angina pectoris are alleviated significantly, as were hypotension, hyperpigmentation and fatigue. The combination of Addison’s disease and coronary artery disease in one patient is rare. Addison’s disease can induce inflammation and disorders of water and electrolyte metabolism, which may further accelerate the course of coronary artery disease. Meanwhile, the hypotension in Addison’s disease may affect the coronary blood flow, which may result in an increased susceptibility to unstable angina in the presence of coronary stenosis. Read the full article here.

Thrombotic thrombocytopenic purpura (TTP) is considered to be a rare cause of ischemic stroke (IS). A case of a newly diagnosed patient with acquired immune-mediated TTP (iTTP) is reported, in whom two IS events developed during 48 h. A 59-year-old diabetic male is presented to the hospital 24 h after symptoms onset, including left hemiparesis, dysarthria, and decreased consciousness. A brain CT scan is performed with the suspicion of acute IS, indicating infarct lesions in the right middle cerebral artery (MCA) territory. The patient is not eligible for thrombolytic therapy due to admission delay. Over the next 24 h, the patient’s neurological condition deteriorates, and the second brain CT scan shows new ischemic lesions. Initial laboratory evaluation indicates thrombocytopenia without evidence of anemia. However, in the following days, thrombocytopenia progresses, microangiopathic hemolytic anemia (MAHA) develops and the diagnosis of iTTP is confirmed. The patient undergoes plasma exchange, pulse IV methylprednisolone and Rituximab is also added due to the refractory course of the disease. After a prolonged hospital course, he has considerable neurologic recovery and is discharged. Thrombotic thrombocytopenic purpura should be considered in any patient presenting with IS and having thrombocytopenia or anemia without other symptoms of TTP. Read the full article here.