Post-cricoid web is an uncommon cause for dysphagia and is most frequently reported in middle-aged women. Triad of web, iron deficiency anemia (IDA), and dysphagia is known as Plummer-Vinson syndrome (PVS). Literature on PVS is very limited. Here we report the first prospective study of PVS with predefined diagnostic criteria and management plan. Adults with dysphagia or those incidentally found to have esophageal web were prospectively enrolled between July 2011 and June 2013. Participants were evaluated with hemogram, barium swallow, and esophagogastroduodenoscopy. PVS was diagnosed if a person had IDA and a post-cricoid web in barium swallow and/or endoscopy. Patients were managed with dilation using through-the-scope controlled radial expansion balloon followed by oral iron and folic acid supplementation. Thirty-seven patients (age, median [range] 40 [19-65] years; 32 [86%] women) were enrolled. Thirty-one symptomatic patients had dysphagia grade 1 (n = 12, 39%), 2 (n = 13, 42%), and 3 (n = 6, 19%) for a median (range) duration of 24 (4-324) months. Barium swallow, done in 29, showed web in 25 which were either circumferential or anterior in position. Twenty-nine (29/31, 94%) patients had complete and two had partial response after the first session of endoscopic dilatation without any complication. Dysphagia recurred in three (10%) of the 30 patients who were followed for a median (range) of 10 (1-24) months. Esophageal-web related dysphagia in patients with PVS responds favorably after single session of endoscopic dilation.

Amla increased the protein expression of liver FXR, LXRα, PPARα and their downstream proteins Insig-2, ABCA1 and LDLR. This property of amla to modulate some of the key proteins involved in lipid metabolism promises its usefulness as a preventive agent for dyslipidemia and hepatic steatosis.

Amla (Emblica officinalis) has antidiabetic, hypolipidemic, anti-inflammatory, and antioxidant properties, but its effect on free radical induced red cell damage and membrane and plasma protein alterations has not been adequately addressed. The aim of the present study was to evaluate the antioxidant property of amla against oxidative stress-induced red cell damage and plasma protein alterations. Red blood cells (RBCs) were preincubated with different concentrations of amla extract (50, 100, 150, and 200 μg/mL) and then treated with physiological (5 mM) and pathological (50 mM) concentrations of glucose for 24 h. In another in vitro study the plasma was pretreated with different concentrations of amla extract and then incubated with 2, 2'-Azo-Bis (2-methylpropionamidine) dihydrochloride (AAPH) for 2 h. After the incubation RBC-malondialdehyde (MDA), RBC-reduced glutathione (GSH), RBC indices, RBC morphometric study, plasma MDA, protein carbonylation, total protein, and albumin were estimated. The antioxidant property of amla was assessed by DPPH assay. RBC-MDA levels were significantly decreased and RBC-GSH levels were significantly increased with higher concentration of amla extract (150 and 200 μg/mL). Red cell count and its indices were improved with the increasing concentration of amla. In addition, at higher concentration, amla restored the RBC membrane integrity. The plasma in vitro study also showed that amla improved the plasma MDA, protein carbonylation, total protein, and albumin levels. Amla extract effectively protected the RBCs and plasma proteins from the reactive oxygen species induced oxidative damage. Liquid chromatography-mass spectrometry (LC-MS) analysis of the extract revealed the presence of gallic acid, quinic acid, and quercetin as the major constituents in addition to the other flavonoids.

Amla decreased low-density lipoprotein cholesterol and increased HDL cholesterol in ovariectomized rats fed chow or fructose. In ovariectomized and fructose-fed rats, it prevented insulin resistance aside from subduing the rise in TG. Amla may be explored for its use in preventing dyslipidemia in postmenopausal women.