Crimean-Congo Hemorrhagic Fever Accompanied by Acalculous Cholecystitis and Pancytopenia: A Rare Case

To the Editor, Crimean-Congo hemorrhagic fever (CCHF) is a tick-borne zoonotic disease caused by a highly pathogenic virus, with a mortality rate ranging from 10% to 40% (1).Contrary to the high mortality rates reported in other countries, the mortality rate in Trkiye has been observed to be approximately 5% (2).Outbreaks of CCHF have been observed in Trkiye during specific periods, with the first case reported in our country in 2002 (3).Although most patients with CCHF exhibit symptoms such as myalgia, dizziness, arthralgia, photophobia, and diarrhea, bleeding manifestations-typically a hallmark of severe disease-may be delayed (4).The CCHF virus induces direct endothelial damage, including apoptosis and increased capillary permeability mediated by various cytokines.This endothelial dysfunction activates the coagulation cascade and contributes to multiorgan injury via proinflammatory cytokines (5).CCHF has been shown to involve a wide range of tissues, including the adrenal glands, liver, spleen, brain, bone marrow, lymph nodes, lungs, muscles, kidneys, cervix, and vascular endothelial cells (6).Here, we present a case of Crimean-Congo hemorrhagic fever characterized by severe pancytopenia and acalculous cholecystitis-an uncommon manifestation of organ involvement and a rare complication.A 38-year-old female patient presented with a 10-day history of fever, abdominal pain, and recurrent episodes of nausea and vomiting.She had no notable personal or family medical history, no history of medication use, and denied ingestion of unusual plants or mushrooms.The patient was involved in animal husbandry but reported no known tick exposure.On physical examination, the patient was alert and oriented.Tenderness was noted in the right upper quadrant of the abdomen.A petechial rash was observed on the body.No other pathological findings were detected.Laboratory investigations revealed pancytopenia, markedly elevated hepatic enzymes, and mild coagulation abnormalities (Figure 1A).Peripheral blood smear revealed no morphologically atypical or malignant cells.Cytological findings were within normal hematologic limits, and platelet morphology and distribution were consistent with the CBC results.The patient was monitored in the intensive care unit.Abdominal computed tomography (CT) revealed diffuse thickening of the gallbladder wall measuring 16 mm, accompanied by marked edema.Pericholedochal fluid accumulation was noted, and the gallbladder appeared hydropic.No calculi were observed within the gallbladder lumen or the extrahepatic biliary tree.The intrahepatic and extrahepatic bile ducts were of standard caliber.These findings were consistent with acute acalculous cholecystitis.Splenic vertical length was increased, measuring 150 mm, and perihepatic free fluid was identified (Figure 1).Oral intake was discontinued, and empirical antimicrobial therapy with intravenous meropenem was initiated.The patient also received platelet transfusions and fresh frozen plasma.In parallel with clinical suspicion for CCHF raised by the infectious diseases department, antiviral therapy with oral ribavirin was initiated (2000 mg loading dose, followed by 1000 mg four times daily for four days, then 500 mg four times daily for six days), alongside dexamethasone (16 mg intravenous once daily for three days).The diagnosis was confirmed by reverse transcription polymerase chain reaction (RT-PCR), with a cycle threshold (Ct) value of 34.32.At two-week follow-up post-treatment, the patient was asymptomatic and exhibited complete normalization of hematologic, hepatic, and coagulation parameters.