Background. Blackwater fever (BWF) is a severe clinical syndrome occurring as a complication of malarial infection characterized by intravascular hemolysis, hemoglobinuria, and acute renal failure in people exposed to Plasmodium falciparum and, to some extent, in people who were exposed to medications like quinine and mefloquine. The exact pathogenesis of classic BWF remains unclear. The mechanism leading to damage to the red blood cells (RBCs) can be immunologic nonimmunologic, leading to massive intravascular hemolysis. Case Presentation. We present a case of classic blackwater fever in a 24-year-old otherwise previously healthy male without any history of antimalarial prophylaxis use, returning from recent travel to Sierra Leone. He was detected to have P. falciparum malaria in the peripheral smear test. He was treated with artemether/lumefantrine combination therapy. Unfortunately, his presentation was complicated by renal failure and was managed with plasmapheresis and renal replacement therapy. Conclusion. Malaria continues to be a parasitic disease that can have devastating effects and continues to be a challenge globally. Although cases of malaria in the United States are rare and cases of severe malaria, mainly attributed to P. falciparum, are even more uncommon. Care should be taken to retain a high level of suspicion to consider the diagnosis, especially in returning travelers from endemic areas.
Iron overload disorders can present as non-specific symptoms and develop gradually but, if untreated, can be very fatal. The common causes include multiple blood transfusions for chronic anemia and increased iron absorption, including hereditary hemochromatosis (HH). HH is one of the common causes of iron overload disorders and usually presents with liver cirrhosis in a setting of significantly elevated ferritin and elevated transferrin saturation. Alcoholic hepatitis is a clinical syndrome of progressive inflammatory liver injury associated with long-term heavy intake of ethanol. However, in patients with alcohol abuse, excessive alcohol consumption can disrupt iron metabolism releasing large amounts of iron into circulation. This can cause severely elevated ferritin due to disruption of iron metabolism, simulating iron overload disorders such as HH, especially if the patient also has liver cirrhosis. Even though a high transferrin saturation of greater than 45% is recommended as a cutoff transferrin value as high sensitivity for detecting iron overload disorders, it has a low specificity and positive predictive value and often identifies people with other causes of acutely elevated ferritin levels such as alcohol liver disease and hepatitis. Recognizing this feature and timely management can spare the patient from unnecessary phlebotomies and prompt treatment for alcoholic hepatitis. We present an interesting case of severe alcoholic hepatitis mimicking HH with severely elevated ferritin levels and transferrin saturation with underlying liver cirrhosis.
Hashimoto's thyroiditis, a chronic autoimmune inflammation of the thyroid glands, is the most common cause of hypothyroidism in iodine-sufficient areas, which can have varied clinical manifestations. It is more common in females and usually has an insidious course. Most patients present with mild clinical symptoms, such as constipation, fatigue, and weakness. Symptoms are associated with a slight increase in thyroidstimulating hormone (TSH) levels and the presence of thyroid antibodies. However, overt hypothyroidism is uncommon. We hereby present an interesting case of rhabdomyolysis secondary to severe hypothyroidism due to Hashimoto's thyroiditis.
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