Therapeutic approaches in hypertriglyceridemia-induced acute pancreatitis: A literature review of available therapies and case series.

Hypertriglyceridemia-induced acute pancreatitis (HGAP) is the third most common etiology of acute pancreatitis. HGAP can be attributed to genetic disturbances in triglyceride metabolism or multiple secondary causes. Here, we presented three cases for HGAP and explored different therapeutic approaches for treating HGAP. A case series of three patients who presented with HGAP and underwent different therapeutic approaches was conducted. The first patient was a 37-year-old male who presented with nonsevere HGAP; he was treated with conservative therapy with insulin and heparin infusion, which resulted in clinical and laboratory improvement. The second patient was a 64-year-old male with human immunodeficiency virus on multiple highly active antiretroviral therapy. He presented with severe HGAP and multiorgan failure. After initiation of therapeutic plasma exchange, his HGAP resolved. The third patient was a 28-year-old male who presented with recurrent episodes of HGAP; his conservative therapy failed and was eventually escalated to therapeutic plasma exchange (TPE). HGAP can be attributed to genetic disturbances of lipid or secondary etiologies. A nonsevere form of HGAP can be managed with conventional therapy including insulin and heparin; however, severe HGAP may require TPE.

Extensive necrotizing fasciitis from Fournier's gangrene.

Fournier's gangrene is rapidly progressive necrotizing fasciitis that mainly affects the male perineum. Despite the advancement in surgical intervention, Fournier's gangrene carries high rates of mortality. Here, we present a 51-year-old male with hypertension and history of alcohol abuse presented to the emergency department with scrotal pain and swelling for a one-week period without preceding trauma to perineal area. He underwent emergent surgical debridement for and extensive necrotizing fasciitis. Early initiation of antibiotics, surgical intervention and good wound care postoperatively were cornerstone in his recovery.

A conserved cysteine residue in the third transmembrane domain is essential for homomeric 5-HT3 receptor function.

The cysteine (Cys) residue at position 312 in the third transmembrane domain (M3) is conserved among 5-hydroxytryptamine type 3 (5-HT(3)) receptor subunits and many other subunits of the nicotinic acetylcholine (nACh) related Cys-loop receptor family, including most of the gamma-aminobutyric acid type A (GABA(A)) and glycine receptor subunits. To elucidate a possible role for the Cys-312 in human 5-HT(3)A receptors, we replaced it with alanine and expressed the 5-HT(3)A(C312A) mutant in HEK293 cells. The mutation resulted in an absence of 5-HT-induced whole-cell current without reducing homopentamer formation, surface expression or 5-HT binding. The 5-HT(3)A(C312A) mutant, when co-expressed with the wild-type 5-HT(3)A subunit, did not affect functional expression of receptors, suggesting that the mutant is not dominant negative. Interestingly, co-expression of 5-HT(3)A(C312A) with 5-HT(3)B led to surface expression of heteropentamers that mediated small 5-HT responses. This suggests that the Cys-312 is essential for homomeric but not heteromeric receptor gating. To further investigate the relationship between residue 312 and gating we replaced it with amino acids located at the equivalent position within other Cys-loop subunits that are either capable or incapable of forming functional homopentamers. Replacement of 5-HT(3)A Cys-312 by Gly or Leu (equivalent residues in the nACh receptor delta and gamma subunits) abolished and severely attenuated function, respectively, whereas replacement by Thr or Ser (equivalent residues in nACh receptor alpha7 and GABA(A) subunits) supported robust function. Thus, 5-HT(3)A residue 312 and equivalent polar residues in the M3 of other Cys-loop subunits are essential determinants of homopentameric gating.