Last update 01 Nov 2024

Baritosis

Last update 01 Nov 2024

Basic Info

Synonyms

BARITOSIS, Baritosis, Baritosis (disorder)

+ [13]

Introduction

A rare type of pneumoconiosis caused by long standing exposure to barium dust. It is characterized by the formation of fine dense lesions in the lung parenchyma. The lesions do not affect the lung function and disappear without treatment after the exposure to barium dust stops.

Drugs associated with Baritosis

GMA-106

Target

GIPR x GLP-1R

Mechanism

GIPR antagonists [+1]

Active Org.

Zhengda Pharmaceutical (Guangzhou) Co., Ltd. [+3]

Originator Org.

Gmax Biopharm LLC

Active Indication

Diabetes Mellitus [+4]

Inactive Indication-

Drug Highest PhasePhase 2

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

BEBT-809

Target

GPR75

Mechanism

GPR75 inhibitors

Active Org.

Originator Org.

Active Indication

Inactive Indication

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

BEBT-808

Target

GLP-1R

Mechanism

GLP-1R agonists

Active Org.

Originator Org.

Active Indication

Inactive Indication

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with Baritosis

100 Translational Medicine associated with Baritosis

0 Patents (Medical) associated with Baritosis

Literatures (Medical) associated with Baritosis

01 Sep 2021·Clinical Case Reports

Barium‐induced pneumatosis intestinalis in a patient with anti‐synthetase syndrome

Article

Author: Mukai, Tomoyuki ; Yamamoto, Shintaro ; Morita, Yoshitaka ; Fujita, Shunichi

AbstractPneumatosis intestinalis is defined as the presence of gas in the bowel wall. The combination of the two risks, pre‐existing connective tissue diseases and barium contrast examination, may trigger pneumatosis intestinalis, albeit at a low incidence. Clinicians should be aware of the condition for proper differential diagnosis.

01 Jul 2020·JCSM Rapid Communications

The wasting‐associated metabolite succinate disrupts myogenesis and impairs skeletal muscle regeneration

Article

Author: Samani, Adrienne ; Ducharme, Alexandra M. ; Jatoi, Aminah ; Doles, Jason D. ; Hogan, Kelly A. ; Arneson‐Wissink, Paige C.

AbstractBackgroundMuscle wasting is a debilitating co‐morbidity affecting most advanced cancer patients. Alongside enhanced muscle catabolism, defects in muscle repair/regeneration contribute to cancer‐associated wasting. Among the factors implicated in suppression of muscle regeneration are cytokines that interfere with myogenic signal transduction pathways. Less understood is how other cancer/wasting‐associated cues, such as metabolites, contribute to muscle dysfunction. This study investigates how the metabolite succinate affects myogenesis and muscle regeneration.MethodsWe leveraged an established ectopic metabolite treatment (cell permeable dimethyl‐succinate) strategy to evaluate the ability of intracellular succinate elevation to (i) affect myoblast homeostasis (proliferation and apoptosis), (ii) disrupt protein dynamics and induce wasting‐associated atrophy, and (iii) modulate in vitro myogenesis. In vivo succinate supplementation experiments (2% succinate and 1% sucrose vehicle) were used to corroborate and extend in vitro observations. Metabolic profiling and functional metabolic studies were then performed to investigate the impact of succinate elevation on mitochondria function.ResultsWe found that in vitro succinate supplementation elevated intracellular succinate about 2‐fold and did not have an impact on proliferation or apoptosis of C2C12 myoblasts. Elevated succinate had minor effects on protein homeostasis (~25% decrease in protein synthesis assessed by O‐propargyl‐puromycin staining), and no significant effect on myotube atrophy. Succinate elevation interfered with in vitro myoblast differentiation, characterized by significant decreases in late markers of myogenesis and fewer nuclei per myosin heavy chain positive structure (assessed by immunofluorescence staining). While mice orally administered succinate did not exhibit changes in overall body composition or whole muscle weights, these mice displayed smaller muscle myofiber diameters (~6% decrease in the mean of non‐linear regression curves fit to the histograms of minimum feret diameter distribution), which was exacerbated when muscle regeneration was induced with barium chloride injury. Significant decreases in the mean of non‐linear regression curves fit to the histograms of minimum feret diameter distributions were observed 7 and 28 days post injury. Elevated numbers of myogenin positive cells (three‐fold increase) supportive of the differentiation defects observed in vitro were observed 28 days post injury. Metabolic profiling and functional metabolic assessment of myoblasts revealed that succinate elevation caused both widespread metabolic changes and significantly lowered maximal cellular respiration (~35% decrease).ConclusionsThis study broadens the repertoire of wasting‐associated factors that can directly modulate muscle progenitor cell function and strengthens the hypothesis that metabolic derangements are significant contributors to impaired muscle regeneration, an important aspect of cancer‐associated muscle wasting.

07 Apr 2020·Journal of the Belgian Society of Radiology

Gastrointestinal and Peritoneal Barium Granulomas in Old Patient

Author: Shen, XueHua ; Alwalid, Osamah

Teaching point: Barium granuloma is a rare but potentially risky complication of barium studies that should be prevented, especially in susceptible patients.

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Baritosis

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