Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0206061 (interstitial pneumonia)
 6,105 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A patient on home total parenteral nutrition (TPN) developed a diffuse granulomatous interstitial pneumonitis secondary to calcium phosphate deposition. Calcium and phosphorus concentrations in the TPN formula were not unusually high, indicating that other factors contributed to calcium phosphate crystallization. The effects of duration of storage of the TPN formulation, solution temperature, pH, and magnesium concentration on calcium phosphate precipitation are discussed.
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PMID:Pulmonary deposition of calcium phosphate crystals as a complication of home total parenteral nutrition. 249 52

Acute toxicosis developed in a group (n = 35) of fattening hogs and replacement gilts that had excessive vitamin D3 inadvertently added to their feed. All of the pigs were lethargic, and emesis was evident in about half of the pigs 1 to 2 days after they consumed the feed. On the 2nd day, 3 of the pigs died. The remaining pigs were given a different ration. Five additional pigs died during the next 2 weeks. Clinical toxicosis also was observed in 1 of 2 feeder pigs fed the suspect feed in the laboratory and in 2 of 2 pigs fed the suspect feed by the company that had mixed the feed. Gross necropsy findings consistently observed were hemorrhagic gastritis and diffuse interstitial pneumonia. Myocardial degeneration and nephrosis were seen in, respectively, 1 of 6 and 4 of 6 pigs necropsied. Histologically, necrosis and mineralization of variable severity were observed in the fundic gastric mucosa, lungs, kidneys, bone, heart, and small blood vessels of the lungs and heart. Less necrosis and more mineralization were observed in pigs that survived longer than 6 days. The 2 pigs fed the suspect feed in the laboratory had increased concentrations of serum calcium from the 3rd to the 9th days or the 1st to the 3rd days, after feeding the suspect feed. Serum phosphorus concentrations were increased from the 1st until the 2nd or 3rd day, and serum magnesium concentrations were increased from the 1st or 2nd to the 3rd day after feeding the suspect feed.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Acute toxicosis in swine associated with excessive dietary intake of vitamin D. 632 15

Dimethyl hydrogen phosphite (DMHP) is used as an intermediate in the production of insecticides and herbicides, as an additive to lubricants, and as a stabilizer in oil and plaster and was considered for use as a chemical to simulate the physical (but not the biologic) properties of anticholinesterase agents. Results of 13-week gavage studies in F344/N rats (0-400 mg DMHP/kg body weight) and in B6C3F1 mice (0-1,500 mg DMHP/kg body weight) were used to identify short-term toxicity and to establish doses for the 2-year toxicology and carcinogenesis studies. In these studies, dimethyl hydrogen phosphite (greater than 97% pure) was administered for 103 weeks in corn oil by gavage to groups of 50 male F344/N rats and to groups of 50 male and female B6C3F1 mice at doses of 0, 100, or 200 mg/kg and to groups of 50 female F344/N rats at doses of 0, 50, or 100 mg/kg. In the 2-year studies, survival of high dose male rats and high dose male mice was lower (P<0.05) than that of the vehicle controls (male rats: vehicle control, 39/50; low dose, 29/50; high dose, 23/50; male mice: 42/50; 34/50; 32/50). At the end of the studies, mean body weights were lower than those of the corresponding vehicle controls for high dose male rats (-15%), for high dose female rats (-5%), and for high dose male mice (-5%). Dimethyl hydrogen phosphite caused dose-related increases in nonneoplastic and neoplastic lesions of the lung in male and female rats. In high dose male rats, there were increased incidences of lung neoplasms, including squamous cell carcinomas (0/50; 0/50; 5/50), alveolar/bronchiolar adenomas (0/50; 0/50; 5/50), and alveolar/bronchiolar carcinomas (0/50; 1/50; 20/50). In high dose female rats, there was a marginal increase in the incidence of alveolar/bronchiolar carcinomas of the lung (0/50; 1/49; 3/50). Hyperplasia of the lung and chronic interstitial pneumonia were increased in dosed male rats and in high dose female rats. Dimethyl hydrogen phosphite caused increases in forestomach lesions in male and female rats. In male rats, there was an increased incidence of forestomach neoplasms, including squamous cell papillomas (0/50; 1/50; 3/50) and squamous cell carcinomas (0/50; 0/50; 3/50). High dose male rats had increased incidences of hyperkeratosis and hyperplasia of the forestomach. In high dose female rats, the incidence of forestomach hyperplasia was increased. Neoplastic lesions of the forestomach (a squamous cell papilloma and a squamous cell carcinoma) were found in two high dose female rats. Mineralization of the cerebellum was seen in high dose male rats (12/49) and in no other group. Focal calcification of the testis occurred at increased incidence in dosed male mice in the 2-year studies (2/50; 9/47; 24/50). Compound-related testicular atrophy was seen in male mice in the 13-week study. Dimethyl hydrogen phosphite did not induce any neoplasms in male or female mice. Dimethyl hydrogen phosphite was not mutagenic in Salmonella typhimurium strains TA98, TA100, TA1535, or TA1537 in the presence or absence of Aroclor 1254-induced male Sprague-Dawley rat or Syrian hamster liver S9. This chemical did not induce sex-linked recessive lethal mutations in Drosophila melanogaster. An audit of the experimental data was conducted for these carcinogenic studies on dimethyl hydrogen phosphite. No data discrepancies were found that influenced the final interpretations. Under the conditions of these gavage studies, there was clear evidence of carcinogenicity in male rats receiving dimethyl hydrogen phosphite, as shown by increased incidences of alveolar/bronchiolar adenomas, alveolar/bronchiolar carcinomas, and squamous cell carcinomas of the lung and of neoplasms of the forestomach. There was equivocal evidence of carcinogenicity in female F344/N rats receiving dimethyl hydrogen phosphite, as shown by marginally increased incidences of alveolar/bronchiolar carcinomas of the lung and of neoplasms of the stomach. There was no evidence of carcinogenicity in male or female B6C3F1 mice receiving dimethyl hydrogen phosphite at doses of 100 ogen phosphite at doses of 100 or 200 mg/kg for 103 weeks. Synonyms: phosphonic acid, dimethyl ester (9CI); dimethyl phosphite; dimethyl phosphorus acid; methyl phosphonate; dimethyl phosphonate; dimethoxyphosphine oxide; TL 585; DMHP; phosphorous acid, dimethyl ester; dimethylphosphite; dimethyl phosphonate; dimethylphosphorous acid; bis(hydroxymethyl) phosphine oxide
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PMID:NTP Toxicology and Carcinogenesis Studies of Dimethyl Hydrogen Phosphite (CAS No. 868-85-9) in F344/N Rats and B6C3F1 Mice (Gavage Studies). 1274 16

Calcinosis of juvenile dermatomyositis (JDM) is a crucial problem because it is refractory to various therapies. An 11-year-old boy who had been treated for JDM with interstitial pneumonia developed calcinosis of both legs despite treatment with corticosteroid and cyclosporin A. Images of his knees showed massive calcinosis with restricted range of motion. Probenecid was used to reduce calcinosis, resulting in remarkable improvement of calcinosis accompanied by normalization of serum phosphorus level and disability after 17 months of administration. We suggest that probenecid is useful for the treatment of calcinosis of JDM.
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PMID:Efficacy of probenecid for a patient with juvenile dermatomyositis complicated with calcinosis. 1688 Nov 25