Noriko Ishihara

An esophageal squamous cell carcinoma patient with high serum granulocyte-colony stimulating factor level: report of a case

We present herein a case of a patient who was clinically diagnosed as having a granulocyte-colony stimulating factor (G-CSF)-producing tumor on the basis of the close correlation of the hematological parameters with the tumor status and his high serum G-CSF level. A 76-year-old male patient underwent transthoracic radical esophagectomy for advanced carcinoma of the lower esophagus. His leukocyte count and serum G-CSF level were markedly high at 24 260/μl and 134 pg/ml, respectively, before the operation. By immunohistochemical staining of the resected tumor, focal but obvious expression of G-CSF was demonstrated in the cytoplasm of cancer cells, and neutrophilic infiltration was histologically observed in adjacent struma of the tumor invasion front. After surgery, the leukocyte count decreased to a nearly normal level but increased again when the disease recurred in the pleura and lymph nodes 5 months later. Although palliative chemoradiotherapy decreased the leukocyte count to a normal level transiently, leukocyte count again markedly increased when metastatic disease occurred. The leukocyte count reached 78 060/μl the day before the patient died.

Two patients with severe alcoholic hepatitis accompanied by hypercytokinemia and granulocytic hyperelastasemia, successfully treated by intravenous infusion of urinastarine (Miraclid)

Abstract Severe alcoholic hepatitis (SAH) is not simply a disease of the liver, but it also causes infection and multiple organ failure, and therefore carries an extremely poor prognosis. We report the successful treatment of two patients with SAH. Case 1: The patient was a 55‐year‐old man. He was a heavy drinker whose alcohol intake had increased for some 3 years to 1.8 L sake a day. Slight clouding of consciousness, fever, and jaundice were evident on his admission to our hospital. Laboratory data showed leukocytosis with a predominance of polymorphonuclear leukocytes, and a decline in coagulability. He tested negative for various hepatitis virus markers. With the diagnosis of SAH made, steroid pulse therapy and bilirubin adsorption therapy were administered. The jaundice improved and the interleukin‐8 (IL‐8) level decreased. Continuous intravenous infusion of urinastarine (Miraclid) normalized the granulocyte elastase level. Improvement was also seen in coagulability, ascites, icterus and consciousness. Case 2: The patient was a 49‐year‐old man. He was a heavy drinker whose alcohol intake had increased for 1 month. Fever, jaundice, ascites, and mild disturbance of consciousness were evident at the time of admission. Examination on admission diagnosed SAH. Bilirubin adsorption and continuous intravenous infusion of urinastarine were initiated. As a result, circulating IL‐8 level was decreased and coagulability was improved. Therapy for granulocytic hyperelastasemia and hypercytokinemia supervening on SAH is a new effective approach on improvement in the disease.

Specific Gastric Blood Vessels in Sinistral Portal Hypertension

Advanced pancreatic cancer is a highly uncontrollable disease that is encountered throughout the world. Occlusion of the splenic vein as a result of hematemesis is suspected to be a cause sinistral portal hypertension (SPH) in patients with pancreatic cancer (1). We herein report the case of a patient with pancreatic cancer in whom the specific gastric blood vessel that caused bleeding was identified. Abdominal CT and macroscopic pathology showed a tumor of the pancreas that invaded the splenic vein (Picture 1). A large amount of melena was observed in the gastric varices of the

Hepatic splenosis mimicking hepatocellular carcinoma in a patient with chronic hepatitis C

A 51-year-old man was referred to us with a diagnosis of chronic hepatitis, secondary to hepatitis C infection after receiving blood transfusion at splenectomy for traffic accident at 16-year age. He had undergone ultrasonographic examination, and a homogeneous and slight hyperechoic mass, measuring 18 × 20 mm in diameter, was detected in liver segment IV (Figure 1). Contrast-enhanced computed tomography (CT) scan showing a marked hyper-attenuation of the lesion during the hepatic arterial phase and a fast wash-out during the venous phase, mimicking hepatocellular carcinoma (HCC) (Figure 2).