To compare the time course of clinical recurrences and reoperations following primary resections for fistulization versus fibrostenotic obstruction in ileal Crohn's disease, we performed a retrospective cohort study of 71 patients undergoing their first resection at The Mount Sinai Hospital between 1961 and 1984. Among these 71 patients, 35 were classified as fistulizing and 36 as fibrostenotic. Follow-up was 93% complete through 1990, with a median follow-up of 73 months to reoperation and 105 months to last contact. The fistulizing and fibrostenotic patients experienced virtually identical numbers of clinical recurrences: 25 from the former group and 24 from the latter. The recurrences appeared very slightly earlier among the fistulizing than among the fibrostenotic group, but the difference did not approach statistical significance. Only 18 patients came to reoperation during follow-up: 12 from the fistulizing and 6 from the fibrostenotic group. The earliest reoperation in the fistulizing group occurred at 14 months and in the fibrostenotic group at 44 months. There was a trend for earlier reoperation in the fistulizing group, but the difference was not statistically significant. Different clinical patterns of Crohn's disease have yet to be correlated with distinctive subclinical biologic markers.

The serum-ascites albumin difference is reported to be superior to ascitic total protein, ascitic-to-serum total protein ratio, lactic dehydrogenase, and ascitic-to-serum lactic dehydrogenase ratio in differentiating between ascites from liver disease and malignant ascites, S-A greater than 1.1 reflecting portal hypertension. We analyzed ascitic fluid from 46 consecutive patients with chronic liver disease, 28 patients with ascites associated with malignancy, 10 patients with right-sided heart failure, 4 patients with hypothyroidism, and 6 patients with miscellaneous causes of ascites to determine if this albumin difference is indeed a more valuable parameter. Analysis of our data confirms with a larger number of patients that the serum-ascites albumin difference is a more reliable indicator of transudative ascites, better termed portal hypertensive ascites. Malignant ascites without liver metastases had features of nonportal hypertensive ascites, and the serum-ascites albumin difference confirms this. The characteristics of malignant ascites associated with liver metastases, however, resemble those of the portal hypertensive ascites complicating liver disease. This new parameter is also helpful in distinguishing congestive heart failure with high protein ascites and portal hypertensive ascitic features from malignant ascites without liver metastases. Of particular note, myxedematous ascitic fluid, classically categorized as exudative, had an S-A greater than 1.1, indicating the possible role of portal hypertension in the development of ascites in these patients.

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A 76-year-old female presented with bright red rectal bleeding. Endoscopic evaluation revealed a polypoid lesion sprouting hair in the sigmoid colon. Histologically the resected polyp was composed of elements of all three germ layers, fulfilling the criteria for a teratoma. The differential diagnosis of this benign polyp and its significance are discussed.

Background Coronavirus disease 2019 (COVID-19) patients can develop pulmonary fibrosis (PF), which is associated with impaired outcome. We assessed specific leukocytic transcriptome profiles associated with PF and the influence of early dexamethasone (DEXA) treatment on the clinical course of PF in critically ill COVID-19 patients. Methods We performed a pre-post design study in 191 COVID-19 patients admitted to the Intensive Care Unit (ICU) spanning two treatment cohorts: the pre-DEXA- (n = 67) and the DEXA-cohort (n = 124). PF was identified based on radiological findings, worsening of ventilatory parameters and elevated circulating PIIINP levels. Longitudinal transcriptome profiles of 52 pre-DEXA patients were determined using RNA sequencing. Effects of prednisone treatment on clinical fibrosis parameters and outcomes were analyzed between PF- and no-PF-patients within both cohorts. Results Transcriptome analyses revealed upregulation of inflammatory, coagulation and neutrophil extracellular trap-related pathways in PF-patients compared to no-PF patients. Key genes involved included PADI4, PDE4D, MMP8, CRISP3, and BCL2L15. Enrichment of several identified pathways was associated with impaired survival in a external cohort of patients with idiopathic pulmonary fibrosis. Following prednisone treatment, PF-related profiles reverted towards those observed in the no-PF-group. Likewise, PIIINP levels decreased significantly following prednisone treatment. PF incidence was 28% and 25% in the pre-DEXA- and DEXA-cohort, respectively (p = 0.61). ICU length-of-stay (pre-DEXA: 42 [29–49] vs. 18 [13–27] days, p < 0.001; DEXA: 42 [28–57] vs. 13 [7–24] days, p < 0.001) and mortality (pre-DEXA: 47% vs. 15%, p = 0.009; DEXA: 61% vs. 19%, p < 0.001) were higher in the PF-groups compared to the no-PF-groups within both cohorts. Early dexamethasone therapy did not influence these outcomes. Conclusions ICU patients with COVID-19 who develop PF exhibit upregulated coagulation, inflammation, and neutrophil extracellular trap-related pathways as well as prolonged ICU length-of-stay and mortality. This study indicates that early dexamethasone treatment neither influences the incidence or clinical course of PF, nor clinical outcomes.