Ahmad Kamal Aslam

Atrial fibrillation associated with systemic lupus erythematosus and use of methylprednisolone.

Systemic lupus erythematosus is known to have cardiac manifestations consisting of pericarditis, myocarditis, endocarditis, and coronary vasculitis. Pericarditis is the most common cardiac manifestation of systemic lupus erythematosus. Myocarditis may be suspected in patients presenting with unexplained tachycardia, conduction disturbances, unexplained systolic dysfunction with or without heart failure, or arrhythmias. The development of arrhythmias in systemic lupus erythematosus could be secondary to pericarditis, myocarditis, or ischemia caused by coronary vasculitis. The development of atrial fibrillation in systemic lupus erythematosus is not commonly reported. There have been few reports on the patients developing atrial fibrillation after being started on methylprednisolone therapy. Described here is a case of the development of atrial fibrillation in a newly diagnosed 37-year-old patient with systemic lupus erythematosus who was started on intravenous methylprednisolone therapy.

Cardiac troponin I in sickle cell crisis

Gross and microscopic findings consistent with acute and healed myocardial injury without coronary artery disease have been described in autopsy studies of patients with sickle cell crisis. The present study was designed to determine whether serum levels of cardiac troponin I are elevated in sickle cell crisis. Cardiac troponin I levels were measured in 32 patients age>18 years with the admission diagnosis of sickle cell crisis. All patients had cardiac troponin I level drawn >24 h after the onset of symptoms. The clinical profile and electrocardiograms were analyzed. Out of 32 patients, 2 patients had serum cardiac troponin I elevated, both had presented with acute chest syndrome. Serum cardiac troponin I may be elevated during sickle cell crisis, possibly by myocardial ischemia resulting from microvascular coronary obstruction during sickle cell crisis.

Aplastic anemia associated with interferon beta-1a.

Subcutaneous interferon beta-1a is a recognized treatment of relapsing multiple sclerosis, and it may delay the onset of definite multiple sclerosis in patients with a first clinical demyelinating episode. Interferon beta-1a exerts beneficial effects on cognitive functioning via both short-term and long-term mechanisms. The beneficial effect is thought to be a result of immune modulation, with inhibition of leukocyte proliferation and antigen presentation and an increased amount of interleukins. The systemic side effects of interferon beta-1a are flu-like syndrome and development of neutralizing antibodies, the clinical significance of which is not known. There have been concerns about the rare development of an acute demyelinating disease after interferon beta-1a therapy as a result of upregulation of inflammatory mediators. In the clinical trials, there is evidence of development of mild anemia with a hemoglobin level below 10 g/dL only in 3% of the patients. There has been no reported case of development of aplastic anemia in patients being treated with interferon beta-1a. Described here is a case of development of aplastic anemia with interferon beta-1a in a patient with multiple sclerosis. Our patient underwent a complete hematologic evaluation to rule out other causes of aplastic anemia. Association with interferon beta-1a was highly suspected.

Fatal splenic sequestration crisis with multiorgan failure in an adult woman with sickle cell-beta+ thalassemia

Acute splenic sequestration crisis is a potentially fatal condition mostly seen in children with sickle cell anemia (HbSS) up to 6 years of age. Sickle cell-beta thalassemia has been associated with development of splenic sequestration crisis in rare reports. There have also been rare reports of the development of fatal acute splenic sequestration crisis together with severe multiorgan failure in adult patients with sickle cell-beta thalassemia. We describe a case of fatal splenic sequestration crisis together with multiorgan failure in a 34-year-old African-American woman with sickle cell-beta thalassemia syndrome.

Thrombotic Microangiopathic Syndrome as Presenting Manifestation of HIV

Abstract: Thrombotic thrombocytopenic purpura-hemolytic uremic syndrome (TTP-HUS) is a rare but well-described complication of advanced human immunodeficiency virus (HIV) infection. However, TTP-HUS had been rarely described as the presenting manifestation of HIV infection. We describe a case of a 45-year-old female who presented with classic manifestations of TTP-HUS and was subsequently found to have HIV. Patient responded to conventional treatment with plasma exchange. We conclude that clinicians need to have a high index of suspicion for retroviral infection when evaluating patients with TTP-HUS even when risk behaviors are not readily apparent.