A 73-year-old Asian man was hospitalized in the Cardiac ICU with fever, thrombocytopenia, and pain in many parts of his body, including the chest, abdomen, lower back, and legs. His past medical history included hypertension and coronary heart disease, and he had three stents implanted. Home medications consisted of enalapril, aspirin, Plavix, atorvastatin, and isosorbide mononitrate sustained-release tablets. Physical examination revealed a blood pressure reading of 90/60 mmHg, a heart rate of 110 beats per minute, a body temperature of 38.9 C, normal lung sounds, and no swelling of the liver or spleen. The initial laboratory data are shown in  Table 1 . The results of computed tomography pulmonary angiography (CTPA) revealed that the enhanced lung texture in both lungs and scattered strips of high-density shadows, so a diagnosis of scattered pneumonia in both lungs was considered. Aortic computed tomography angiography (CTA) revealed atherosclerosis of the thoracic aorta and some branches. The electrocardiogram showed sinus tachycardia. Heart color Doppler ultrasound suggested that the right ventricle was enlarged and the left ventricular diastolic function was weakened. Arteriovenous ultrasound of the lower extremities revealed atherosclerosis in both limbs and an old thrombosis in the right calf muscles. Digital radiography of the knee joints revealed bone hyperplasia bilaterally. Abdominal computed tomography (CT) showed that the liver shadow was enlarged, and the abdominal fat space was cloudy. Color Doppler ultrasound of the abdomen indicated an enlarged gallbladder and cholestasis.
The patient was admitted to the hospital with a diagnosis of toxemia. Then, the patient received cefminox sodium for two days. A series of infectious disease examinations, including blood culture, urine culture, hepatitis B virus polymerase chain reaction (PCR), and a (1,3)-beta-D-glucan test, a galactomannan antigen test, and an epidemic hemorrhagic fever virus antibody test, were all negative, except the blood culture. Klebsiella pneumoniae was found in the blood culture. We then switched to treatment with meropenem on the third day. Due to the patient's further decline in platelets, a worsening creatinine level, and liver function damage, we conducted a series of tests concerning heparin-induced thrombocytopenia-related antibodies, anti-nuclear antibodies, three types of rheumatism, and anticardiolipin. The test results were all negative. A further ferritin assessment revealed a level of 2,925.3 mug/L (normal range: 20-300 mug/L), while a bone marrow biopsy suggested that the red and white blood cell counts were reduced and some blood cells were hemophagocytic. Other tests related to HLH were conducted, and the results were: soluble interleukin-2 receptor alpha chain, 20,229 pg/ml (normal range <6,400 pg/ml); natural killer cell activity, 14.43% (normal range >=15.11%); IL-10, 1,125.41 pg/ml (normal range <4.91 pg/ml); IL-6, 55.06 pg/ml (normal range <5.30 pg/ml); tumor necrosis factor alpha (TNF- alpha), 3.11 pg/ml (normal range <2.31 pg/ml). The IL-2 and IL-4 were within the normal range. In line with the HLH-2004 standard and a hemophagocytic (H) Score cut-off of 190 ( Table 2 ), the patient was diagnosed with HLH. The tumor markers of this patient were all negative, including carbohydrate antigen 724, cytokeratin 19 fragment, carcinoembryonic antigen, carbohydrate antigen 242, carbohydrate antigen 125, neuron-specific enolase, alpha-fetoprotein, free human chorionic gonadotropin, squamous cell carcinoma antigen, total prostate-specific antigen, free prostate-specific antigen, and carbohydrate antigen (199). No abnormal space-occupying lesions were found in imageology tests of each site, so tumor-related HLH was excluded first. The results of series of tests, including one for respiratory tract infection pathogens, a tuberculosis infection T cell spot test, a cytomegalovirus PCR assay, and an EBV PCR assay were all negative. Finally, the patient was diagnosed as having HLH associated with Klebsiella pneumoniae.
To identify the focus of the infection and devise an appropriate treatment plan, a whole-hospital discussion was carried out. Heart-related infections were excluded because there is no infective endocarditis or valvular heart disease was found with echocardiography. After comparing the lung CT before and after admission, the lung inflammation was mild and showed little change, so it was not consistent with HLH caused by primary infection. Liver abscess was also excluded by abdominal CT and color Doppler ultrasound. And patient's acute liver injury was caused by HLH. According to the patient's routine urine test and urine culture, the acute kidney injury of the patient was associated with multiple organ failure caused by HLH. Finally, the following plan was made: platelets, 1 IU, qd, for one week; dexamethasone, initially 10 mg/m2, qd, for two weeks, 5 mg/m2, qd, for two weeks, 2.5 mg/m2, qd, for two weeks, 1.25 mg/m2, qd, for one week; and meropenem, 0.5 g, qd, for two weeks. Due to economic reasons, the patient refused intravenous immunoglobulin.
The changes in significant laboratory test results during the whole treatment process are shown in  Figure 1 . By the third day of dexamethasone treatment, the symptoms of general pain had disappeared. The platelets increased gradually in the following week, while ferritin decreased to 1,150.6 mug/L, and serum creatinine, transaminase, and body temperature returned to normal levels.
However, one week later, the patient has fever, lower back pain, and knee pain again. Although laboratory tests and the blood culture results were normal. A repeat CT of the lungs revealed that the inflammation was better than before ( Figure 2 ). The patient mainly had lower back pain, and the magnetic resonance imaging (MRI) of the lumbar spine indicated that the possibility of abscess formation in L4 and L5 was high, and the possibility of inflammation and abscess formation in the right greater psoas muscle, iliopsoas muscle, and left greater psoas muscle was high ( Figure 3 ). The patient and his family members refused any further treatment and asked for him to be discharged. Three days after discharge, the patient underwent abscess drainage at a local hospital, and his condition gradually improved. Six months after discharge, the patient was followed up by telephone, and the patient said there was no fever, general pain, or other symptoms.