Hepatorenal Syndrome: Definitions, Diagnosis, and Management.

Hepatorenal syndrome (HRS) is a hemodynamically driven process mediated by renal dysregulation and inflammatory response. Albumin, antibiotics, and ß-blockers are among therapies that have been studied in HRS prevention. There are no Food and Drug Administration-approved treatments for HRS although multiple liver societies have recommended terlipressin as first-line pharmacotherapy. Renal replacement therapy is the primary modality used to bridge to definitive therapy with orthotopic liver transplant or simultaneous liver-kidney transplant. Advances in our understanding of HRS pathophysiology and emerging therapeutic modalities are needed to change outcomes for this vulnerable population.

Lung cancer metastasis to the breast mimicking inflammatory breast carcinoma on imaging.

While metastatic disease to the breast has been documented from many primary neoplasms with incidence ranging from 0.2% to approximately 2.7% among reported clinical cases, breast cancer metastases resulting from a primary lung neoplasm is significantly less commonly reported in the literature. Routes of metastatic spread of lung neoplasms include both hematologic and lymphatic routes. We present a case of biopsy proven lymphangitic spread of primary lung neoplasm to the ipsilateral breast and axillary nodes mimicking inflammatory breast cancer. It remains crucial to differentiate between extramammary diseases with metastatic deposits in the breast from a primary breast neoplasm as treatment remains very different between these entities. As in this case, the pathologic, histologic, and immunohistochemistry analyses are critical in determining the origin of the malignant cells and formulating a treatment plan.

Deficits in visual working-memory capacity and general cognition in African Americans with psychosis.

On average, patients with psychosis perform worse than controls on visual change-detection tasks, implying that psychosis is associated with reduced capacity of visual working memory (WM). In the present study, 79 patients diagnosed with various psychotic disorders and 166 controls, all African Americans, completed a change-detection task and several other neurocognitive measures. The aims of the study were to (1) determine whether we could observe a between-group difference in performance on the change-detection task in this sample; (2) establish whether such a difference could be specifically attributed to reduced WM capacity (k); and (3) estimate k in the context of the general cognitive deficit in psychosis. Consistent with previous studies, patients performed worse than controls on the change-detection task, on average. Bayesian hierarchical cognitive modeling of the data suggested that this between-group difference was driven by reduced k in patients, rather than differences in other psychologically meaningful model parameters (guessing behavior and lapse rate). Using the same modeling framework, we estimated the effect of psychosis on k while controlling for general intellectual ability (g, obtained from the other neurocognitive measures). The results suggested that reduced k in patients was stronger than predicted by the between-group difference in g. Moreover, a mediation analysis suggested that the relationship between psychosis and g (i.e., the general cognitive deficit) was mediated by k. The results were consistent with the idea that reduced k is a specific deficit in psychosis, which contributes to the general cognitive deficit.

The Processing-Speed Impairment in Psychosis Is More Than Just Accelerated Aging.

Processing speed is impaired in patients with psychosis, and deteriorates as a function of normal aging. These observations, in combination with other lines of research, suggest that psychosis may be a syndrome of accelerated aging. But do patients with psychosis perform poorly on tasks of processing speed for the same reasons as older adults? Fifty-one patients with psychotic illnesses and 90 controls with similar mean IQ (aged 19-69 years, all African American) completed a computerized processing-speed task, reminiscent of the classic digit-symbol coding task. The data were analyzed using the drift-diffusion model (DDM), and Bayesian inference was used to determine whether psychosis and aging had similar or divergent effects on the DDM parameters. Psychosis and aging were both associated with poor performance, but had divergent effects on the DDM parameters. Patients had lower information-processing efficiency ("drift rate") and longer nondecision time than controls, and psychosis per se did not influence response caution. By contrast, the primary effect of aging was to increase response caution, and had inconsistent effects on drift rate and nondecision time across patients and controls. The results reveal that psychosis and aging influenced performance in different ways, suggesting that the processing-speed impairment in psychosis is more than just accelerated aging. This study also demonstrates the potential utility of computational models and Bayesian inference for finely mapping the contributions of cognitive functions on simple neurocognitive tests.