At the heart of the problem: congestive cardiac failure as a cause of ascites: A narrative review

Heart failure leading to cardiac ascites is an extremely rare and underrecognized entity in clinical practice. Recognizing cardiac ascites can be difficult, especially since patients presenting with ascites may have more than 1 etiology. Various biomarkers are available to aid in the diagnosis of cardiac ascites, though with differing sensitivities and specificities. Such biomarkers include serum albumin, ascitic albumin and protein, as well as serum N-terminal pro-brain natriuretic peptide (NT-proBNP). While serum NT-proBNP is a powerful biomarker in distinguishing the etiology of ascites and monitoring treatment progression, its cost can be prohibitive in low-resource settings. Clinicians practicing under these circumstances may opt to rely on other parameters to manage their patients. We go on further to report a series of 3 patients with cardiac ascites to illustrate how these biomarkers may be employed in the management of this patient population. Clinicians should always keep in mind the differential diagnosis of cardiac failure as a cause of ascites. The resolution of cardiac ascites may serve as a surrogate clinical marker for response to antifailure therapy in lieu of NT-proBNP at resource-scarce centers.     

Infestation of Tunga penetrans in villages near Zomba Central Hospital

An outbreak of Tunga Penetrans (Jigger Flea) infestation affecting a number of villages near to a Central Hospital in Malawi is described. Due to the large number of affected individuals, high parasitic load, and extended duration of infection an alternative to the recommended approach of surgical removal of the flea was required. Benzyl benzoate paint and liquid paraffin had been used in local Primary Healthcare settings previously and topical treatment with antiparasitic agents has been advocated in the literature, particularly for severe infestation. Benzyl benzoate and liquid paraffin were applied topically to four adults with numerous jigger flea burrows, and their progress assessed regularly. After completion of 7 days of treatment patients noted that fleas were dislodging spontaneously, and that embedded parasites had not increased in size to the same extent that untreated fleas had in previous infestations. Following confirmation of the viability of its implementation in a resource-poor setting, this treatment regimen has subsequently been adopted by the local branch of the District Health Office for distribution to infected communities.     

Minactivin expression in human monocyte and macrophage populations

Adherent monolayer cultures of human blood monocytes, peritoneal macrophages, bone marrow macrophages, and colonic mucosa macrophages were examined for their ability to produce and secrete minactivin, a specific inactivator of urokinase-type plasminogen activator. All except colonic mucosa macrophages produced and secreted appreciable amounts of minactivin, but only blood monocytes were stimulated by muramyl dipeptide (adjuvant peptide) to increase production. The minactivin from each of these populations could be shown to preferentially inhibit urokinase-type plasminogen activator and not trypsin, plasmin, or "tissue"-type plasminogen activator (HPA66). A plasminogen-activating enzyme present in monocyte cultures appeared unaffected by the presence of minactivin and could be shown to be regulated independently by dexamethasone.