Development and evaluation of the automated risk assessment system for multidrug-resistant organisms (autoRAS-MDRO).

BACKGROUND: A high proportion of infections acquired in hospitals are caused by multidrug-resistant organisms (MDROs). The priority in MDRO prevention is to detect high-risk patients and implement preventive intervention as soon as possible. AIM: To develop an automated risk assessment system for MDROs (autoRAS-MDRO) to screen for patients at MDRO infection risk and evaluate the predictive validity of the autoRAS-MDRO. METHODS: Data for 4200 variables were extracted from the electronic health records (EHRs) for constructing the MDRO risk-scoring algorithm, which was based on a logistic regression model. The autoRAS-MDRO was designed such that the MDRO risk classification (high, moderate, low risk) could be automatically displayed on the nursing Kardex screen in the EHRs system. For the development of the MDRO risk-scoring algorithm, 1000 patients with MDROs and 4000 patients without MDROs were selected; similarly, for the evaluation, 2173 and 8692 patients with and without MDROs, respectively, were selected. FINDINGS: The predictive validity of the autoRAS-MDRO was as follows: (i) at the 6-month evaluation: sensitivity, 81%; specificity, 79%; positive predictive value (PPV), 49%; negative predictive value (NPV), 94%; and Youden index, 0.60; (ii) at the 12-month evaluation: sensitivity 79%, specificity 78%, PPV 47%, NPV 94%, and Youden index, 0.57. CONCLUSION: The autoRAS-MDRO had moderate predictive validity. It could be useful in redirecting nurses' time and efforts required for MDRO risk assessment and implementation of infection control measures, and in reducing the incidence of MDRO infection in hospitals, thereby contributing to patient safety.

Human mismatch repair gene (hMSH2) product expression in relation to recurrence of transitional cell carcinoma of the urinary bladder.

BACKGROUND: Several convincing studies have shown that the hMSH2 gene plays major roles in mismatch repair by recognizing mismatched bases and preventing mutations during DNA replication. Loss of this function may result in the accumulation of DNA replication errors or even the mutator phenotype (which may be responsible for the multiple mutations required for multistep carcinogenesis), and it has been found to affect the prognosis of patients. Thus, the authors felt that it would be of interest to study the expression patterns of hMSH2 protein in malignant tumors and to assess the correlation of hMSH2 protein to various clinical and pathologic features in these patients. METHODS: The authors examined the expression patterns of hMSH2 protein in 115 patients with transitional cell carcinoma (TCC) of the urinary bladder by immunohistochemical technique using monoclonal antibody to hMSH2 protein. RESULTS: The group in which hMSH2 was preserved (>20% of nuclei were positive for staining by anti-hMSH2 antibody) included 86 of 115 (75%) of the TCCs, whereas the remaining 29 cases (25%) belonged to the group in which hMSH2 was preserved (< or = 20% of tumor nuclei were positive), including 2 negative cases. Univariate analysis indicated that reduced expression of hMSH2 protein was significantly more frequent in high grade tumors than in low grade tumors (P = 0.04). Furthermore, statistical multivariate analysis revealed that hMSH2 reduction was significantly related to the recurrence (P = 0.02). CONCLUSIONS: These results suggest that abnormal expression of hMSH2 protein might be involved in tumorigenic processes and in the progression of some TCCs, and that the loss of hMSH2 protein expression might be a useful predictor of recurrence of TCC.

Nonfunctioning adrenal cortical cancer and analysis of the steroidogenic activity of the tumor: a case report.

An adrenocortical cancer was detected by a CT scan in a 37-year-old woman, which did not have an excessive secretion of steroids or catecholamines. The tumor was enhanced inhomogeneously by the bolus injection of contrast medium, and magnetic resonance imaging (MRI) showed that the tumor was hypointense compared to the liver on a T1-weighted image and was diffusely hyperintense on a T2-weighted image. Histologically, the tumor consisted predominantly of compact cells with marked cellular and nuclear pleomorphism, but no capsular or vascular invasion were observed. An analysis of the steroidogenic activity of the tumor revealed that the activity of mitochondrial P450c11beta was extremely reduced in the tumor.

Aldosterone-producing adrenal cortical cancer: a case report and analysis of steroidogenic enzymes in the tumor.

A case of hyperaldosteronism caused by adrenal cortical cancer observed in a 32-year-old man was reported. The patient showed marked hypertension and hypokalemia, but neither obesity nor hyperglycemia was observed. Endocrine studies revealed hyperaldosteronism and concurrent excessive secretion of cortisol, but diurnal rhythms of plasma ACTH and cortisol were normal. Imaging studies revealed a large left adrenal mass, and the positive accumulation of radiolabelled material by adrenal scintigraphy was observed both in the tumor and the contralateral adrenal gland. The removed tumor was predominantly composed of dark compact cells with marked nuclear pleomorphism, and mitotic figures and sinusoidal invasion were also observed. The analysis of steroidogenic enzyme activities revealed that the activity of aldosterone-synthesizing enzyme (P-450aldo) which was usually undetectable in normal adrenal tissues and adenomas other than aldosterone-producing adenoma (APA) was detectable as one-third of that of APA. Although activities of other enzymes were reduced, the expression of P-450aldo activity was considered to be the specific character of this cancer.

ACTH-independent macronodular adrenocortical hyperplasia (AIMAH): report of two cases and the analysis of steroidogenic activity in adrenal nodules.

We report clinical findings and steroidogenic activities in adrenal tissues in 2 cases of AIMAH. Endocrine studies revealed an undetectable level of plasma ACTH and a diminished circadian rhythm of plasma cortisol. A significant increase in plasma cortisol levels in response to ACTH stimulation was observed in both cases. After the administration of metyrapone in one case, urinary excretion of 17-hydroxycorticosteroid (17-OHCS) significantly increased, although the plasma ACTH level did not respond. Computed tomography showed large masses in both adrenal glands, and bilateral uptake was identified on adrenal scintigraphy. The totals for the bilateral adrenal glands were 98 g and 105 g, respectively, and the left adrenal was larger than the right in both cases. Steroid content in the nodules measured by high performance liquid chromatography (HPLC) showed that the cortisol content was definitely lower than that in cortisol-producing adenoma (CPA) and even in normal adrenals. The activities of cytochrome P450c17, P450c21 and P450c11 were evaluated in one case, and all of them were reduced in the nodules. Especially that of P450c17 was remarkably reduced. These data suggest that cortisol production in AIMAH is inefficient, and that the cause of Cushing's syndrome may be related to the marked increase in the number of cells or bulk of the tumor.

The analysis of steroidogenic activity in non-hyperfunctioning adrenocortical adenoma.

The steroidogenic activities in non-hyperfunctioning adrenal adenoma (NHFA) have not yet been fully examined. Steroid content both in adenoma and its non-tumorous adjacent adrenal tissue was measured by the HPLC system in 8 cases of NHFA and 2 cases of preclinical Cushing's syndrome (PCS). Activities of cytochrome P450c17alpha, P450c21, P450c11beta, P450c18 and aldosterone-synthesizing enzyme (P450aldo) were also determined by the enzyme reconstitution system. Steroid content in NHFA varied but no significant difference was seen between NHFA and normal control adrenals. Activities of all P450s except P450aldo were confirmed in NHFA, but they were almost equivalent to those in normal control adrenals. As no significant difference between NHFA and normal controls was observed in either steroid contents or P450s activities, the steroidogenic activity of NHFA is considered to be comparable to that of normal adrenals.

[E-cadherin expression and histopathological features in renal cell carcinomas].

E-cadherin, a member of the cadherin family, plays a major role in cell-cell adhesion of normal epithelium. Recent studies have demonstrated that heterogeneous expression, reduction or loss of E-cadherin is involved in invasion and metastasis of cancer cells. In this study, the localization of E-cadherin in the normal human kidney and the relationship between E-cadherin expression and histopathological features in renal cell carcinomas was examined immunohistochemically. Renal cell carcinoma tissues and normal kidney counterparts were obtained from 20 patients. E-cadherin in the normal kidney was detected in the cell-cell border of the distal tubules, collecting duct and Bowman's capsule but not in the proximal tubules. E-cadherin expression was reduced in all the clear cell type renal cell carcinomas with compact or cystic configuration (n = 15), while it was well preserved in all the papillary type (n = 3) and chromophobe cell type (n = 1) renal cell carcinomas. Different expression patterns between primary site and metastasis, i.e., homogeneously weak in primary tumor and heterogeneously positive in metastatis, was observed in a case of clear cell type renal cell carcinoma. Different patterns of expression between clear and non-clear cell type, or between papillary and non-papillary type, together with strong expression in chromophobe type might reflect the origin of each type of renal cell carcinoma. Further studies will clarify whether the change in expression of E-cadherin is associated with the prognosis of renal cell carcinoma.