ReviewPostgraduate medical journal1995
The pathogenesis of chronic pancreatitis.
Review in Postgraduate medical journal, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
2 citing papers in PubMed, 15 citations in OpenAlex.
- Association of matrix metalloproteinase-7 (-181A/G) promoter polymorphism in chronic pancreatitis.The Indian journal of medical research · 2014Article
- Tropical pancreatitis.Journal of gastroenterology · 2007Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
To date, there is no consensus on the evolution of chronic pancreatitis. Comfort's initial proposal of acute pancreatitis progressing to chronic pancreatitis was discarded by protagonists of the 'separate' theory. Sarles thus stresses the de novo evolution of chronic pancreatitis-acinar protein hypersecretion associated with an imbalance of pancreatic stone promoting and inhibiting factors. However, the 'necrosis-fibrosis sequence' hypothesis of Kloppel and Mallet resurrects the probability of acute pancreatitis leading to chronic pancreatitis. Dimagno offers a unifying concept that the degree of acinar injury determines the natural history of pancreatitis. Uninhibited release of toxic free radicals could be a common end point for various aetiologies resulting in acute or chronic pancreatitis. The pathogenesis of chronic calcifying pancreatitis of the tropics is possibly no different from alcoholic chronic pancreatitis. Neurocrine and paracrine mechanisms have been offered to explain pain out of proportion to radiological and histological pancreatic abnormalities in minimal change chronic pancreatitis.
Indexed as
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.