Coexistence of ovarian serous papillary cystadenofibroma and type A insulin resistance syndrome in a 14-year-old girl: A case report.

BACKGROUND: Type A insulin resistance syndrome is a rare disorder caused by mutations in the gene encoding the insulin receptor. Its coexistence with ovarian serous papillary cystadenofibroma is even rarer. CASE SUMMARY: A 14-year-old girl developed type A insulin resistance syndrome and showed high fasting insulin, glucose, and hemoglobin A1c (HbA1c) levels. The girl suffered from ovarian serous papillary cystadenofibroma. The laboratory results were as follows: fasting insulin was 2624.90 pmol/L and HbA1c was 8.5%. A heterozygous missense mutation on exon 20 of the insulin receptor gene (c.3601C>T, Arg1201Trp) was observed. The histopathological diagnosis was a cystic lesion that extended to the upper right uterus, indicating a right ovarian serous papillary cystadefibroma accompanied by focal interstitial hyperplasia. The patient was treated with metformin for over 6 mo. Additionally, laparoscopic resection (bilateral) of the ovarian lesion and laparoscopic intestinal adhesiolysis were performed under general anesthesia. Diet therapy combined with exercise was then initiated. The patient had an uneventful recovery. The patient also showed improved blood glucose control, with reduced levels of fasting insulin (857.84 pmol/L) and HbA1c (7.0%). CONCLUSION: Insulin resistance may play a significant role in the induction of tumors. It is important to investigate further the association between insulin resistance and tumors and the underlying mechanism.

A rare case of pregnancy complicated by mesenteric mass: what does chylous ascites tell us?

Mesenteric fibromatosis is a rare benign nonmetastatic neoplasm that appears as a sporadic lesion or occurs in patients with familial polyposis, while chylous ascites associated with aggressive mesenteric fibromatosis during pregnancy has never been reported thus far. Here we present the case of a 28-year old pregnant woman, in whom an aggressive mesenteric fibromatosis with chylous ascites was detected, involving the jejunum, superior mesenteric artery (SMA) and superior mesenteric vein (SMV) and pancreas. One year after a successful surgical excision, the patient had no signs of recurrence. The authors report the case for its rarity and emphasize on combining clinicopathological, radiological and immunohistochemistry analysis for management of the disease.

[Expressions of matrix metalloproteinase-9 and tissue inhibitor of metalloproteinase-1 in ectopic and eutopic endometrium].

OBJECTIVE: To study the expression of matrix metalloproteinase-9(MMP-9) and tissue inhibitor of metalloproteinase-1 (TIMP-1) in ectopic and eutopic endometrium in patients with endometriosis. METHODS: The expressions of MMP-9 and TIMP-1 in ectopic and eutopic endometrium were detected by immunohistochemistry streptavidin-biotin peroxidase (SP) method in 45 patients with endometriosis (study group) and in 32 patients with uterine fibroid (control group). RESULTS: In the ectopic and eutopic endometrium of group and in the control group endometrium, the expression of MMP-9 was respectively 0.381, 0.336 and 0.276; the expression of TIMP-1 was respectively 0.239, 0.253, 0.267. As a result, the ratio of MMP-9/TIMP-1 in ectopic and eutopic endometrium of study group and in the control group endometrium was respectively 1.594, 1.293, 1.034. The difference of MMP-9, MMP-9/TIMP-1 in ectopic and eutopic and the control group endometrium was markedly significant (P < 0.01 or P < 0.05). The difference of the expression of TIMP-1 between ectopic and the control group endometrium was also markedly significant (P < 0.01). Higher expression of MMP-9 and lower expression of TIMP-1 in ectopic endometrium and higher expression of MMP-9 in eutopic endometrium occurred in the whole menses period, in which higher expression of MMP-9 in ectopic endometrium than in eutopic endometrium only took place in proliferative phase. CONCLUSION: The change of expression of MMP-9 and TIMP-1 in ectopic endometrium may be related to the pathogenesis of endometriosis.

[Expression of PTEN protein and its correlation with p27kip1 and cyclin D1 expression in primary breast cancer].

OBJECTIVE: To study the expression of phosphatase and tensin homology deleted on chromosometen ten (PTEN) protein, a tumor suppressor gene in breast cancer and its correlation with p27(kip1) and cyclin D1 expression. METHODS: PTEN protein expression, p27(kip1) and cyclin D1 protein expression were detected by immunohistochemical method in paraffin sections from 61 women with primary breast cancer. PTEN protein expression was compared with clinico-pathologic parameters as related to p27(kip1) and cyclin D1. RESULTS: PTEN, being shown in the cytoplasm, was negative in 6.6% (4/61), reduced in 41.0% (25/61) and positive in 52.5% (32/61) samples. PTEN expression level was correlated with axillary lymph node status, loss of estrogen receptor stain, recurrence and metastasis. On univariate analysis, the disease-free survival rate of patients with higher PTEN expression (> 50% cells stained) was better than those with lower expression (P = 0.0101). However, there was no correlation between p27(kip1), cyclin D1 expression or PTEN expression. CONCLUSION: PTEN, its lower expression being correlated with poor outcome of breast cancer patients, plays a prominent role in breast cancer. p27(kip1) or cyclin D1 may not be the primary downstream genes of PTEN in breast cancer.