Obesity is a global public health problem. Obese persons are likely to develop complications like degenerative joint diseases, diabetes mellitus, dyslipidemia, cardiovascular diseases, fatty liver,cancer of esophagus and pancreas resulting in reduced life expectancy, poor quality of life and burden to economy. A subset of obese subjects does not develop metabolic abnormalities and they are described as metabolically healthy obese (MHO). This entity is a debatable one, and not well accepted. Here we review the merits and demerits of MHO. This is a narrative review and we have not applied advanced statistical procedures. The review articles by Stefan, Bluher and the cross-references are widely quoted in this article. Apart from this, we collected full-text articles from “PubMed,” and “ClinicalKey” platforms using the search term “Metabolically healthy obesity.” As evident in the literature, MHO is a significantly prevalent condition (10%–20%) with wide variation depending on the criteria used. This condition is subject to conversion to unhealthy with risk for development of cardio-metabolic abnormalities like diabetes and DL. The impact of intervention is remarkable but equivocal. MHO should not be considered a safe condition. The transit nature of MHO offers an opportunity for intervention. MHO is an eye-opener for future research.

Acute fatty liver of pregnancy (AFLP) is a rare cause of catastrophic liver dysfunction and failure in late pregnancy. Defective mitochondrial fatty acid oxidation (FAO) seems to be the underlying pathogenic mechanism. Stressors of both late pregnancy (increased maternal dependence on fats as energy source) and fetus with homozygous defect in mitochondrial FAO, precipitate AFLP in a woman who was previously asymptomatic. Mitochondrial disorders exhibit significant clinical heterogeneity, but many of these primary and secondary disorders have liver as the primary organ affected. The liver injury pattern in these patients also has a varied spectrum and course. Unlike other primary mitochondrial disorders affecting the liver, AFLP represents a potentially completely reversible form of liver injury. Thus, AFLP behaves as a secondary mitochondrial disorder precipitated by inciting factors from fetus and placenta. In this review, we attempt to highlight the varied aspects of mitochondrial dysfunction in AFLP. Mitochondrial injury is the mainstay of pathogenesis and can be recognized in typical clinical features and histopathological findings in patients with AFLP. We also present the consequent impact of recognizing underlying mitochondrial injury on clinical diagnosis and management strategies employed in AFLP.

The diet, microbiota, and gut epithelium primarily determine gut health. Two fundamental physiochemical factors that regulate and coordinate the interaction between these three determinants of gut health are the redox potential (Eh) and pH. The Eh-pH coordinates determine the solubility, bioavailability, and toxicity of macronutrients and micronutrients. There is spatial heterogeneity in the redox potential, pH, and microbial composition/density both along and across the lumen of the Gastrointestinal (GI) tract. The optimal functioning of any compartment within the GI tract depends on its Eh-pH coordinates. Any abnormal deviation will likely result in pathophysiology and a shift in its resident flora to suit the altered Eh-pH state. Diet and digested products have a significant influence in regulating the local Eh-pH coordinates along with the microbiome and the mucosal secretions. This review emphasizes the importance and the need for simultaneous Eh-pH assessment of the lumen and mucosa of various compartments of GI tract in diagnosis and treatment. Since pH is a well-studied variable in the context of the gut, this minireview will focus on the relation between redox potential and gut health/disease.

Background and Aim: Diuretic doses for the optimal management of ascites may be influenced by the patient profile and conditions. We undertook this study to map the usage of common diuretics, alone or in combination, for the management of patients with decompensated cirrhosis and to determine the prevalence of adverse effects with the administered regimens and factors that predict the need for paracentesis while on diuretics. Methods: This prospective study was done in an outpatient clinic among patients with known liver cirrhosis, irrespective of etiology, belonging to Child-Pugh Class B or C, with mild to moderate ascites and no dyselectrolemia on diuretics. The primary outcome of the study was the need for paracentesis. The type and dose of diuretic at this instance were noted. Results: A total of 200 patients (168 male), predominantly from southern Indian states, formed the study group. The median model for endstage liver disease score was 18 and 70% of cases required paracentesis within 3 months. The single diuretic agent was used in 18% of cases while combination of two diuretics was used in 82%. Spironolactone was the most common single agent used (26, 72.2%). The combination of furosemide and spironolactone was the most common diuretic combination used (89.6%, 147 cases). One hundred and thirty patients (65%) reported the adverse effects to diuretics. Renal dysfunction and electrolyte disturbances were the most common adverse effects. Adverse effects to diuretic use and frequency of large volume paracentesis were significantly more common in patients taking furosemide 40 mg and spironolactone 100 mg per day. Conclusions: Indian patients with decompensated chronic liver disease do not appear to tolerate the high doses of diuretics and 65% of them develop diuretic-related adverse effects. There is a need to formulate the guidelines for the optimal management of ascites in decompensated chronic liver disease in the Indian setting.

Background and Aims: Immunization against hepatitis A, hepatitis B, and pneumococcus has been recommended in patients with cirrhosis of the liver. This questionnaire survey was undertaken to determine the rates of vaccination against these organisms in a cohort of patients with liver disease in India. Methods: We included all patients who were willing for the study and had been seen by a gastroenterologist/hepatologist at least once. Patients offering incomplete information were excluded from the study. Serological tests for confirmation of immunological response were not done. Details of counseling and vaccination status for hepatitis B, hepatitis A, and pneumococcal infection were noted. Results: A total of 305 patients (272 males, 89%) formed the study cohort. The median age was 60 years (range 27–76 years) and the median duration of liver disease was 12 months (1–120 months). The median model of end stage liver disease (MELD) was 14 (range 7–35). Only 37 (12.1%) patients reported that they had been counseled for vaccination against these infections. The rates of vaccination were very low (<10%). Conclusion: Very dismal vaccination rates were noted in Indian patients with liver cirrhosis.

Background: Severe acute pancreatitis is the result of a cytokine storm induced by pancreatic inflammation. Mutations in the heat-shock protein 70 (HSP70) gene can induce excessive cytokine secretion in the context of inflammation. We undertook this study to determine whether common single-nucleotide polymorphisms (SNPs) in the HSP70 gene were associated with severe acute pancreatitis. Methods: One hundred and twenty-seven consecutive patients with acute pancreatitis admitted to the hospital were evaluated and followed up for clinical outcomes. DNA from venous blood was extracted, and the following SNPs were genotyped – rs1061581 (HSPA1B), rs2227956 (HSPA1 L), rs1008438 (HSPA1A), and rs1043618 (HSPA1A). Polymerase chain reaction-restriction fragment length polymorphism was used for genotyping at the first two loci, while allele-specific polymerase chain reaction was used to genotype the two latter SNPs. Results: None of the four hP70 gene polymorphisms that were studied showed any significant difference between acute mild and acute severe pancreatitis. However, the T allele in rs2227956 showed a trend to association with severe pancreatitis (P = 0.08), as did the TT genotype (0.09). Conclusion: HSP70 gene polymorphisms did not significantly associate with the severity of illness in acute pancreatitis.