br Case report At that time her
Case report At that time, her laboratory examinations showed hemoglobin (Hb) of 10.4 g/dl (normal: 11.3–15.3), and platelets of 36,000/mm3 (normal: 150,000–400,000), and WBC count of 3800/mm3 (normal: 4000–11,000). The liver function showed serum albumin was 3.2 g/dl, total bilirubin was 1.7 mg/dl, alkaline phosphotate was 184 U/l (normal −190), aspartate aminotransferase (AST) was 70 U/l (normal: 8–38), alanine aminotransferase (ALT) was 56 U/l (normal: 10–35), alpha-fetal protein (AFP) was 624 ng/ml (normal <12), international normalized ratio (INR) was 1.52 (normal: 0.85–1.15). Her HBsAg was negative and anti-HCV was positive. Her Child-Pugh score was 7 (Child-Pugh class B). Abdominal ultrasonography showed one bulging tumor, 4.2 × 3.2 cm in size. The triple phase CT scan of the liver demonstrated an ill-defined low density and hypervascular soft tissue mass in the left lobe of liver (Couinaud\'s segement 4b, S4b), approximately 41 mm in diameter, with early enhancing in the arterial phase and washout in the delayed phase on the after hsp70 inhibitor medium CT, that showed compatibility with HCC (Fig. 1). Para-esophageal varices, multiple collateral vessels in the abdomen, mild ascites and splenomegaly were also noted. The diagnosis of HCC was determined based on a single positive imaging technique showing hypervascularization associated with more than 400 ng/ml of AFP level. In addition, the patient did not take any medications and surgical treatment in our clinic, and also did not return to our OPC to follow up her HCC progression. Over 2 years later, she returned to our OPC on 27th/July/2014 after developing abdominal distension and leg edema over the previous three weeks. The physical examination showed abdomen distension with ascites and pitting edema. Her AFP level was 11.8 ng/ml, serum albumin was 2.4 g/dl, total bilirubin was 1.7 mg/dl, AST was 61 U/l, ALT of was 38 U/l, alkaline phosphotate was 132 U/l. The following triple phase CT scan of the liver revealed no obvious mass in the liver, with a poor enhancing lesion over the previous HCC site (Fig. 2). Her liver cirrhosis status with progression was noted with clinic symptoms attacked. She denied any treatment (including invasive procedures, radiation, medications, and herb drugs) and was only treated with oral diuretics for controlling symptoms during these two years. She also reported no gastrointestine bleeding, shock, trauma, blood transfusion, or other special episodes. In addition, Genomic (chromosomal) DNA clone did not attend regular follow-up appointments due to personal reasons. Approximately thirty months after initial diagnosis, the last triple phase CT scan of the liver still revealed no obvious tumor recurrence (Fig. 3). Taken together, a patient with spontaneous remission of HCC was determined in this case.
Discussion Spontaneous remission of cancer is a rare phenomenon, and defined by Cole and Everson as partial or complete disappearance of a malignant tumor in the absence of any treatment, or in the presence of the therapy which is considered to be inadequate to exert a significant influence on neoplastic disease. Most malignant tumor with spontaneous regression occurs on renal cell carcinoma, neuroblastoma, melanoma, and choriocarcinoma; these constituted more than half of all cases. Incidence rate of spontaneous regression of cancer is estimated to be 1 in 60,000–100,000 cancer patients. Unfortunately, spontaneous regression of HCC is a more rare event, and the reported incidence rate is 1 in 140,000 cases of HCC. The first case of HCC with spontaneous regression is described by Johnson and colleagues in 1972. Until now, about 80 cases have been reported in English literature. The first biopsy-proven Taiwanese patient had been documented in 1992. After review the literatures and several clinical events were documented, including abstinence from alcohol, androgen withdrawal, persistent fever, pain, gastrointestinal bleed requiring transfusion, herbal therapies, use of vitamin K, anti-estrogen therapy, sepsis, blood transfusion, portal vein tumor thrombosis, angiography related angiospasm or arterial thrombosis. However, the most appropriate etiology to explain possible mechanisms for the above clinical events are still unclear.