2023年 · 第38卷第11期

The patient, a 50-year-old male, was admitted to hospital because "physical examination found liver space-occupying lesions for more than 2 years". Physical examination: A mass of about 4 cm was palpable under the xiphoid process, which was hard in texture, with clear borders, mild tenderness in the upper abdomen, without rebound pain and muscle tension. Tumor markers: AFP, PIVKA-II and CA19-9 were not elevated. Imaging examination: Ultrasound examination: A solid heterogeneous echo nodule was detected in the left lobe of the liver, about 5.8 cm ×3.3 cm in size, with irregular shape and unclear boundary; CT examination: Plain scan showed a patchy slightly lower density focus in the left lateral lobe of the liver, about 4.7 cm ×4.2 cm ×4.0 cm in size, and the boundary with the surrounding liver tissue was not clear. Heterogeneous enhancement in the arterial phase of the enhancement scan. Further enhancement in portal vein phase and delayed phase; MRI examination: T1WI showed a flake-like low signal in liver S3 mass (Figure 1A), T2WI showed a flake-like uneven slightly high signal in liver S3 mass (Figure 1B), DWI showed a flake-like high signal in liver S3 mass, ADC showed a flake-like low signal in liver S3 mass, with clear boundary, and spoke T1 and T2 double low signal inside. In the arterial phase of enhanced scanning, the liver S3 mass was flaky and unevenly enhanced, but the internal spoke signal was not enhanced (Figure 1C), and the portal vein phase and the delayed phase were further enhanced, but the internal spoke signal was not enhanced. "Laparoscopic left hemihepatectomy + cholecystectomy" under general anesthesia. The postoperative pathological specimens showed a 6.5 cm ×6.0 cm ×5.5 cm round tumor, which was hard in texture, with clear borders and gray-white color, and a star-shaped fibrous scar with poor borders could be seen in the center (Figure 2). After operation, he was given symptomatic and supportive treatment with anti-inflammatory, liver-protective, analgesic and fluid rehydration, and was successfully discharged from hospital. Postoperative pathology: moderately differentiated hepatocellular carcinoma (fibrolamellar type) (Figure 3). There was no abnormality in CT reexamination six months after operation.

A 22-year-old female was diagnosed with rectal cancer in September 2004, complaining of "blood in the stool for one and a half years". She underwent anterior rectal cancer resection. Postoperative pathology showed (rectal) ulcerative medium-poorly differentiated adenocarcinoma, about 8.0 cm ×6.0 cm ×0.8 cm in size, invading the whole thickness of the intestinal wall, and metastatic cancer was seen in mesenteric lymph nodes (3/22). Immunohistochemical examination showed: P53 (-), P120 (+ +), Her-1 (+ +), Her-2 (+ +), Ki-67 (-), TOPⅡ α (-). Five cycles of FOLFOX regimen chemotherapy were followed up for 5 years without recurrence. My grandmother died of "cancer" at the age of 40. In March 2004, the patient's mother was diagnosed with colon cancer at the age of 48 and died one year later. In August 2019, the patient underwent colonoscopy, which showed a bulging mass in the initial segment of ascending colon, ileocecal valve, and cecum, accounting for 4/5 of the circumference. The pathological diagnosis was adenocarcinoma, some of which were mucinous adenocarcinoma. PET-CT examination revealed malignant tumor of ascending colon with external invasion, hypermetabolism of FDG and metastasis of peri-intestinal lymph nodes. According to his history of rectal cancer and family history 15 years ago, he was diagnosed as Lynch syndrome-colorectal cancer before operation. Laparoscopic radical resection of right colon cancer and transverse ileocolostomy were performed. The postoperative pathology showed that the tumor size was 10.0 cm ×9.0 cm ×2.8 cm, moderately-poorly differentiated adenocarcinoma, some of which were mucinous adenocarcinoma (<50%), infiltrated into the subserous layer, and tumor thrombus was visible in the vessel (Figure 1). Immunohistochemical examination showed: CK20 (+), CK79 (-), EGFR (+), Ki-67 (70% +), MLH1 (protein expression loss), PMS2 (protein expression loss), MSH2 (protein expression), MSH6 (protein expression). EBV in situ hybridization: EBER (-). Paraintestinal lymph nodes 2/30. Mutation in exon 2 of KRAS gene was detected, but no mutation was detected in NRAS, PIK3CA and BRAF genes. Genetic test: PD-L1 negative. The tumor mutation burden (Muts/Mb) was 71.51, which was lower than 12% of patients with ascending colon cancer. Microsatellites detect microsatellite instability (MSI-H). Lynch syndrome-colorectal cancer was diagnosed according to family history of colon cancer, loss of tumor mismatch repair protein expression and genetic examination of MLH1 germline mutation. No other treatment was performed after operation. In August 2021, due to increased menstrual flow for 1 year, gynecological ultrasound showed: endometrial thickening, uterine parenchyma occupying space, and liquid opacity at the back of the uterus occupying space. Both pelvic enhanced MRI and PET-CT showed abnormal signals of right fallopian tube nodules, endometrium and cervical endometrium, significantly increased FDG uptake, and the possibility of malignant tumors (Figure 2A). Hysteroscopy, hysteroscopic segmented diagnosis and curettage, and cervical biopsy were performed. Pathological examination revealed (uterine cavity occupying space and cervical canal occupying space) endometrioid carcinoma grade I with mucus differentiation, and the pathological diagnosis was endometrial carcinoma, while the clinical diagnosis was right ovarian cancer. PD-1 inhibitor treatment was administered on 24 Sep 2021 with Keytruda 2.5 mg/kg once 3 weeks. After 3 cycles of immunotherapy, MRI reexamination on January 11, 2022 showed no endometrial thickening and no abnormal signal, and PET-CT examination showed no clear abnormal FDG metabolism lesions, which was considered to achieve complete remission after immunotherapy (Figure 2B). After 6 cycles of immunotherapy, reexamination of hysteroscopy showed no endometrial lesions, and endometrial biopsy showed secretory phase changes. At present, maintenance treatment with PD-1 inhibitor is continued.

The patient, a 52-year-old female, came to the outpatient clinic for "finding a right breast mass for more than 2 months". Physical examination: Both breasts were of normal size, symmetrical, without discharge, and a mass of 6 cm ×2 cm was palpable on the outside of the right breast, which was tough in texture, with unclear boundaries, poor activity, no adhesion to skin and muscles, and no mass was palpable in the left breast. No enlarged lymph nodes were palpable in bilateral cervical, supraclavicular and groin. Breast ultrasound showed that the "mass" in the upper quadrant of the right breast was touched with a hypoechoic mass of about 5.7 cm ×1.6 cm (Figure 1), with horizontal growth, irregular shape, clear boundary, poor smooth edge, even internal echo, no calcification, no subsequent change, and no obvious abnormal echo in the tissues around the lesion. CDFI: abundant blood supply visible internally, flow rate 19.62 cm/s, RI: 0.53, elasticity score 2. Several lymph node echoes were seen under the bilateral axillary, with the large left side being 2.9 cm ×1.2 cm and the large right side being 3.1 cm ×1.1 cm. Most of the cortex was thickened, the cortex-medulla boundary was clear, and CDFI: blood flow signal was increased. Hint: Right breast hypoechoic mass, BI-RADS class 4A. Mammography showed a patchy asymmetric dense shadow in the upper quadrant of the right breast (Figure 2), with a range of about 4.0 cm ×2.3 cm. Multiple swollen lymph nodes were seen under the right axillary, but no obvious swollen lymph nodes were seen under the left axillary. Hint: The right mammary mass is flaky asymmetric dense shadow, BI-RADS Class 4A. Serum IgG: 53.8 g/L, serum immunoglobulin G4 (IgG4): 50.2 g/L. An ultrasound-guided puncture biopsy of the mass was performed. Pathological examination showed: (puncture biopsy of the right breast mass) was sent for examination of breast tissue, with a large number of nodular infiltration of lymphocytes and plasma cells, and interstitial fibrous tissue proliferation and collagenization. Combined with the results of immunohistochemical examination, immunoglobulin G4-related sclerosing mastitis (IgG4-RM) was considered (Figure 3). After treatment with glucocorticoid, serum IgG and IgG4 decreased after re-examination 3 months later, and breast ultrasound showed that the original mass was significantly reduced.