Over the past decade, the Nomenclature Committee on Cell Death (NCCD) has formulated guidelines for the definition and interpretation of cell death from morphological, biochemical, and functional perspectives. Since the field continues to expand and novel mechanisms that orchestrate multiple cell death pathways are unveiled, we propose an updated classification of cell death subroutines focusing on mechanistic and essential (as opposed to correlative and dispensable) aspects of the process. As we provide molecularly oriented definitions of terms including intrinsic apoptosis, extrinsic apoptosis, mitochondrial permeability transition (MPT)-driven necrosis, necroptosis, ferroptosis, pyroptosis, parthanatos, entotic cell death, NETotic cell death, lysosome-dependent cell death, autophagy-dependent cell death, immunogenic cell death, cellular senescence, and mitotic catastrophe, we discuss the utility of neologisms that refer to highly specialized instances of these processes. The mission of the NCCD is to provide a widely accepted nomenclature on cell death in support of the continued development of the field.

https://biblio.ugent.be/publication/8555786/file/8555788.pdf

Molecular mechanisms of cell death: recommendations of the Nomenclature Committee on Cell Death 2018.

In 2009, the Nomenclature Committee on Cell Death (NCCD) proposed a set of recommendations for the definition of distinct cell death morphologies and for the appropriate use of cell death-related terminology, including 'apoptosis', 'necrosis' and 'mitotic catastrophe'. In view of the substantial progress in the biochemical and genetic exploration of cell death, time has come to switch from morphological to molecular definitions of cell death modalities. Here we propose a functional classification of cell death subroutines that applies to both in vitro and in vivo settings and includes extrinsic apoptosis, caspase-dependent or -independent intrinsic apoptosis, regulated necrosis, autophagic cell death and mitotic catastrophe. Moreover, we discuss the utility of expressions indicating additional cell death modalities. On the basis of the new, revised NCCD classification, cell death subroutines are defined by a series of precise, measurable biochemical features.

/pdf/molecular-definitions-of-cell-death-subroutines-q5g428rlyi.pdf

Molecular definitions of cell death subroutines: recommendations of the Nomenclature Committee on Cell Death 2012

Practice guidelines in acute pancreatitis.

https://www.spg.pt/wp-content/uploads/2015/11/2013-ACG_Guideline_AcutePancreatitis_September_2013.pdf

American College of Gastroenterology guideline: management of acute pancreatitis.

Autophagy is a mechanism by which cellular material is delivered to lysosomes for degradation, leading to the basal turnover of cell components and providing energy and macromolecular precursors. Autophagy has opposing, context-dependent roles in cancer, and interventions to both stimulate and inhibit autophagy have been proposed as cancer therapies. This has led to the therapeutic targeting of autophagy in cancer to be sometimes viewed as controversial. In this Review, we suggest a way forwards for the effective targeting of autophagy by understanding the context-dependent roles of autophagy and by capitalizing on modern approaches to clinical trial design.

/pdf/targeting-autophagy-in-cancer-2pjcn0h04a.pdf

Targeting autophagy in cancer

Recurrent acute pancreatitis (RAP) is defined as more than two attacks of acute pancreatitis (AP) without any evidence of underlying chronic pancreatitis (CP). As the known causes of AP are generally taken care of, RAP usually occurs in the idiopathic group, which forms 20%-25% of cases of AP. The causes of idiopathic RAP (IRAP) can be mechanical, toxic-metabolic, anatomical, or miscellaneous. Microlithiasis commonly reported from the West is not a common cause of IRAP among Indian patients. Pancreas divisum (PD) is now believed as a cofactor, the main factor being associated genetic mutations. The role of Sphincter of Oddi dysfunction (SOD) as a cause of IRAP remains controversial. Malignancy should be ruled out in any patient with IRAP > 50 years of age. Early CP can present initially as RAP. The work-up of patients with IRAP includes a detailed history and investigations. Primary investigations include liver function tests (LFT), serum calcium and triglyceride, abdominal ultrasonography (USG) and contrast-ehhanced computed tomography (CECT) abdomen. Endoscopic ultrasound (EUS), magnetic resonance cholangiopancreatography (MRCP) and possibly endoscopic retrograde cholangiopancreatography (ERCP) are indicated in the secondary phase if the work-up is negative after the primary investigations. EUS is advised usually 6-8 weeks after an acute episode. Treatment of patients with IRAP is aimed at the specific aetiology. In general, empirical cholecystectomy should be discouraged with the availability and widespread use of EUS. Endoscopic sphincterotomy is advised if there is strong suspicion of SOD. Minor papilla sphincterotomy should be carried out in those with PD but with limited expectations. Regular follow-up of patients with IRAP is necessary because most patients are likely to develop CP in due course.

http://www.tropicalgastro.com/filedownload.aspx?id=601

Recurrent acute pancreatitis: an approach to diagnosis and management

Plummer Vinson syndrome is a constellation of postcricoid esophageal webs, iron deficiency anemia, dysphagia and koilonychia. We describe some unusual manifestations in three patients with this syndrome; these were clubbing instead of koilonychia, tortuous esophagus in addition to presence of esophageal webs, and celiac disease.

Plummer Vinson syndrome: unusual features.

Anti tubercular drug related hepatotoxicity is common. The mechanism of injury and factors predisposing to its development are not fully understood. Forty patients with anti tubercular drugs related hepatotoxicity were studied to see the clinical and biochemical profile of these patients and to find out the significance of acetylator phenotype in the development of hepatotoxicity. Mean age of patients with liver damage (37.82 +/- 10.0 years) was similar to those without liver damage (36.48 +/- 12.5 years). Pyrazinamide appeared to increase the hepatotoxicity of isoniazid and rifampicin. The percentage of rapid acetylators and slow acetylators among patients with hepatotoxicity (70% and 30% respectively) was similar to controls (66.6% rapid and 33.3% slow acetylators). Acetylator phenotype probably has no role in anti tubercular drugs induced hepatotoxicity.

/pdf/anti-tubercular-treatment-induced-hepatotoxicity-does-3wnuwzp6fg.pdf

Anti tubercular treatment induced hepatotoxicity: does acetylator status matter?

A 45-year-old male presented with severe abdominal pain, hyperamylasaemia and a bulky pancreas In addition, he had deep jaundice and markedly raised serum transaminases, and his serum was positive for IgM anti-hepatitis E virus (HEV) antibodies The common aetiologies of acute pancreatitis were excluded The patient ran a benign course for both acute viral hepatitis and acute pancreatitis, and recovered completely Acute pancreatitis caused by HEV infection has been reported only occasionally

Acute pancreatitis associated with acute hepatitis E infection.

OBJECTIVE. The purpose of this article is to present the pathologic and clinical features of IgG4-related sclerosing cholangitis (ISC), illustrate the associated imaging findings, and discuss treatment of the disorder. CONCLUSION. ISC is an inflammatory disorder involving the biliary system and resulting in strictures. Although often associated with autoimmune pancreatitis, it may be an isolated disease. Differentiation of ISC from other forms of cholangitis and cholangiocarcinoma is difficult but necessary for management. Imaging is important in diagnosing and assessing the extent of disease and planning a management strategy.

https://www.ajronline.org/doi/pdf/10.2214/AJR.19.21519

Pramod Kumar Garg

Papers

Recurrent acute pancreatitis: an approach to diagnosis and management

Plummer Vinson syndrome: unusual features.

Anti tubercular treatment induced hepatotoxicity: does acetylator status matter?

Acute pancreatitis associated with acute hepatitis E infection.

IgG4-Related Sclerosing Cholangitis: A Clinical and Imaging Review