Ibuprofen Associated Acute Vanishing Bile Duct Syndrome and Toxic Epidermal Necrolysis in an Infant

Acute vanishing bile duct syndrome, a rare but rapidly progressive destruction of the intrahepatic bile ducts with unknown pathogenesis, is most often a drug- or toxin-related. Toxic epidermal necrolysis is a serious dermatologic condition and a potentially life threatening disease, which is drug or infection induced. Ibuprofen associated acute vanishing bile duct syndrome and toxic epidermal necrolysis have not been reported previously in infants. We report a 7-month-old infant with ibuprofen associated toxic epidermal necrolysis, followed by severe and rapidly progressive vanishing bile duct syndrome. She recovered totally with supportive care.     

Acne Knowledge of Hispanic Parents of Teenagers with Mild to Moderate Acne

We performed a cross‐sectional study of Hispanic and non‐Hispanic parents of children with acne using a survey designed to determine their level of awareness of acne and its treatment; 82% of Hispanic parents and 40% of non‐Hispanic parents agreed that a health care provider should treat mild acne (p < 0.001). Hispanic parents of adolescents with acne agreed more frequently than non‐Hispanic parents that children with mild and moderate acne should be taken to a health care provider for treatment, but they tended not to visit health care providers. Future studies should aim to determine the reasons for this discrepancy, after which culturally sensitive educational programs can be developed to address this disparity.     

Different effects of five depigmentary compounds,rhododendrol, raspberry ketone,monobenzone, rucinol and AP736 on melanogenesis and viability of human epidermal melanocytes

Numerous medications are used to treat hyperpigmentation. However, several reports have indicated that repeated application of some agents, such as rhododendrol (RD), raspberry ketone (RK) and monobenzone (MB), can be toxic to melanocytes. Although these agents had severe side effects in human trials, no current in vitro methods can predict the safety of such drugs. This study assessed the in vitro effects of five depigmentary compounds including leukoderma‐inducing agents. In particular, we determined the effects of different concentrations and exposure times of different depigmentary agents on cell viability and melanogenesis in the presence and absence of ultraviolet B (UVB) radiation. Concentrations of RD, RK and MB that inhibit melanogenesis are similar to concentrations that are cytotoxic; however, concentrations of rucinol (RC) and AP736 that inhibit melanogenesis are much lower than concentrations that are cytotoxic. Furthermore, the concentrations that cause toxic effects depend on exposure duration, and prolonged exposure to RD, RK and MB had more cytotoxic effects than prolonged exposure to RC and AP736. The cytotoxic effects of RD and RK appear to be mediated by apoptosis due to increased expression of caspase‐3 and caspase‐8; UVB radiation increased the cytotoxicity of these agents and also increased caspase activity. Our results indicate that different leukoderma‐inducing compounds have different effects on the viability of normal epidermal melanocytes and suggest that the in vitro assay used here can be used to predict whether an investigational compound that induces leukoderma may lead to adverse effects in human trials.     

Oncogenic mutations of thyroid hormone receptor β

The C-terminal frame-shift mutant of the thyroid hormone receptor TRβ1, PV, functions as an oncogene. An important question is whether the oncogenic activity of mutated TRβ1 is uniquely dependent on the PV mutated sequence. Using four C-terminal frame-shift mutants—PV, Mkar, Mdbs, and AM—we examined that region in the oncogenic actions of TRβ1 mutants. Remarkably, these C-terminal mutants induced similar growth of tumors in mouse xenograft models. Molecular analyses showed that they physically interacted with the p85α regulatory subunit of PI3K similarly in cells. In vitro GST-binding assay showed that they bound to the C-terminal Src-homology 2 (CSH2) of p85α with markedly higher avidity. The sustained association of mutants with p85α led to activation of the common PI3K-AKT-ERK/STAT3 signaling to promote cell proliferation and invasion and to inhibit apoptosis. Thus, these results argue against the oncogenic activity of PV being uniquely dependent on the PV mutated sequence. Rather, these four mutants could favor a C-terminal conformation that interacted with the CSH2 domain of p85α to initiate activation of PI3K to relay downstream signaling to promote tumorigenesis. Thus, we propose that the mutated C-terminal region of TRβ1 could function as an “onco-domain” and TRβ1 is a potential therapeutic target.     

Amylase level after pancreaticoduodenectomy in predicting postoperative pancreatic fistula

BackgroundIt is new clinical interest higher serum amylase level with pancreatitis after pancreaticoduodenectomy (PD) correlates with postoperative pancreatic fistula (POPF). Nevertheless, its evidence and study were scarce. We aimed to investigate correlation of serum amylase level immediate after PD and POPF occurrence.MethodsOf 163 patients who underwent PD at between January 2009 and December 2019, retrospective analysis was conducted to identify risk factors including serum amylase level immediate after PD for POPF occurrence.ResultsOverall incidence of POPF (25/163) was 15.3%. The patients occurred a POPF had significantly higher level of serum amylase on POD0 compared to in whom without a POPF (414 vs 253, p < 0.001). In univariate analysis, ASA classification, post pancreatectomy acute pancreatitis (POAP, serum amylase on POD0 >285IU/L) and Fistula Risk Grade were correlated with POPF occurrence. In multivariable analysis, Fistula risk grade and POAP were significantly associated with developing POPF.ConclusionIn patients with higher serum amylase (>285IU/L) on POD0 with higher fistula risk grade, comprehensive management to achieve mitigation of POPF is important.