Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0032285 (pneumonia)
 54,520 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 60-year-old laboratory technician developed pulmonary infiltrates consistent with chemical pneumonitis following accidental exposure to a mixture of hydrogen bromide and phosphorus tribromide. A protracted clinical course ensued consistent with bronchiolitis obliterans. These problems may have been avoided if the potential for subsequent damage had been realized at the time of the initial exposure. Health personnel must be aware of the potentially delayed effects of accidental exposures to respiratory irritants.
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PMID:Chemical pneumonitis due to exposure to bromine compounds. 338 40

Rabbits and rats were exposed to single doses of smoke from pyrotechnic mixtures containing red phosphorus. The survivors were observed for up to 14 days. Most of the histological changes observed were found in the respiratory tract and they included abnormalities in the larynx and trachea, alveolitis and, in a few cases, frank pneumonia.
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PMID:Histological changes produced by exposure of rabbits and rats to smokes produced from red phosphorus. 671 94

In radiation of the thorax, the lung has been shown to be a major dose-limiting organ. The early and late responses of the lung to radiation has been reviewed, with primary emphasis on the following cell types: type II pneumocyte, type I pneumocyte, pulmonary endothelial cell and macrophage. The earliest observable and quantifiable cellular response to radiation is exhibited by the type II pneumocytes as a decrease in lamellar bodies and a corresponding increase in surfactant content of the alveolar lavage. By 18-63 weeks following exposure, several type II cells, restored in their lamellar body population, undergo degeneration and sloughing into alveolar spaces. Type I pneumocytes generally exhibit little change, although some investigators describe alveolar denudation due to degenerating type I cells. Macrophages decrease in numbers following irradiation, returning to normal populations by 4 weeks. These changes correspond closely to the changes in alveolar lavage phospholipid phosphorus. Descriptions of radiation-induced damage to endothelial cells are variable. However, blebbing and vacuolation appear to be late developing responses, although altered permeability may be earlier in its expression. Radiation pneumonitis and fibrosis are the two major clinical and experimental responses of the lung to radiation following exposures of greater than 12 Gy. The former appears to involve type II cells, macrophages and pulmonary endothelial cells, and for the latter macrophages, fibroblasts, type II pneumocytes and the pulmonary endothelial cells are involved. The two events are not interdependent, and may not necessarily be interrelated.
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PMID:Morphologic changes reflecting early and late effects of irradiation of the distal lung of the mouse: a review. 716 57

Carboxypeptidase M (CPM) cleaves the C-terminal arginine and lysine of peptides; it is expressed in the lung, especially on the plasma membrane of alveolar type I cells. Here, we report on CPM in human bronchoalveolar lavage (BAL) collected from 69 patients and analyzed for activity, cell number and type, and protein level. Seventy-six percent of CPM activity, measured at pH 7.5 with 5-dimethylamino-naphthalene-1-sulfonyl-alanyl-arginine (Dansyl-Ala-Arg) substrate, was immunoprecipitated with polyclonal antibody to purified human enzyme. In patients without active lung disease, CPM activity in BAL was 7.69 (+/- 2.12) nmol/h/mg protein, but in patients with acute pneumonia, it was 29.25 (+/- 4.06) (p < 0.01). In patients with Pneumocystis carinii pneumonia, CPM activity was elevated to 26.00 (+/- 4.85) (p < 0.01) and in patients with lung cancer, to 30.95 (+/- 4.12) (p < 0.01). The activity was not associated with the cellular elements of BAL. The highest specific activity was in the large aggregate fraction of surfactant, which also contained the highest concentration of phosphorus. Transmission electron microscopy of this fraction revealed the presence of typical lamellar bodies and tubular myelin structures. The high CPM activity may stem from its induction and release in acute lung disease. In addition, CPM may be a marker of infection with certain pathogens and an indicator of type I cell injury in parenchymal lung diseases.
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PMID:Carboxypeptidase M activity is increased in bronchoalveolar lavage in human lung disease. 763 39

An 81-year-old woman was hospitalised because of pneumonia in December 1989. In February 1991, an iliac bone biopsy was performed on the suspicion of disturbed bone metabolism due to chronic renal failure. Since she developed anemia due to continuous bleeding from the surgical wounds, saccharated iron oxide was administered beginning in March. Hypophosphatemia was noted 23 days after the beginning of administration. Due to the possibility of osteomalacia, active vitamin D was given but the hypophosphatemia persisted. Following an EDTA-2 Na load test performed to evaluate the reabsorption of phosphorus in the renal tubules, it was considered that the patient had a functional disorder of the parathyroid glands and that reabsorption of phosphorus was interrupted in the renal tubules. Furthermore, abnormal distributions of phosphorus seemed to occur in the same areas where sucrose was metabolized and iron was stored. Therefore, it was considered that these abnormalities induced hypophosphatemia following the intravenous administration of saccharated iron oxide. In addition to these actions, the possibility remained that phosphate absorption was inhibited in the small intestine by calcium lactate.
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PMID:[A case of hypophosphatemia induced by intravenous administration of saccharated iron oxide]. 785 46

A 46-year-old male patient underwent long-term hemodialysis treatment had suffered from calciphylaxis (defined by Selye), such symptoms as advanced systemic vascular calcification, rapid progression of gangrene on both fingers and toes, disturbance of consciousness, and sclerosis and obstruction of the superficial vein after venipuncture during 11.5 years of dialysis. Furthermore, he had a long history (30 years) of heavy smoking. He died as a result of sepsis due to pneumonia after 12.5 years of dialysis. He had received dialysis treatment using a small amount of dialysate (50 liters on a recirculating system) for 8.5 years and had been dialysed 2 and 2 or 3 times a week for 10 years. As a result of this insufficient dialysis treatment, his characteristic laboratory data showed hypocalcemia, hyperphosphatemia, elevated calcium-phosphorus product, advanced metabolic acidosis, hyperalkaliphosphatemia and elevated serum parathyroid hormone. Autopsy revealed the following: 1) enlargement parathyroid gland enlarged in two (4.0 g and 2.0 g, respectively) showing adenomatous hyperplasia presenting cord-like arrangement of chief cells and water-clear cells, 2) systemic medial calcification in radial, ulnar, renal, mesenteric and brain arteries, and 3) Berline-blue positive iron deposit in calcified arteries in mesenteric and parathyroid tissue. From these results, we concluded that factors (challengers) related to the appearance of calciphylaxis might be as follows: 1) advanced secondary hyperparathyroidism, 2) long-term uremic state, 3) administration of VD2 and VD3, 4) iron salt injection, and 5) a long history of heavy smoking. We speculated that these challengers might act synergistically to cause calciphylaxis.
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PMID:[A long-term hemodialysis patient complicated with systemic calciphylaxis]. 823 Aug 23

Chronic toxicity of indium arsenide (InAs) and indium phosphide (InP) was studied in male Syrian golden hamsters which received InAs or InP particles containing a total dose of 7.5 mg of arsenic or phosphorus by intratracheal instillations once a week for 15 weeks. As a control, hamsters were treated with the vehicle, phosphate buffer solution. During their total life span, the cumulative body weight gain of hamsters in the InAs group was suppressed significantly compared with that in the control group, but not in the InP group when compared with that in the control group. Concerning the histopathological findings of the lung, the incidence rates of proteinosis-like lesions, alveolar or bronchiolar cell hyperplasia, pneumonia, emphysema and metaplastic ossification observed in the InAs or InP group were significantly higher than those observed in the control group. From these results, it would seem that InAs and InP produced severe damage to the lungs of hamsters.
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PMID:Chronic toxicity of indium arsenide and indium phosphide to the lungs of hamsters. 869 Mar 34

Patients with end-stage renal disease commonly develop secondary hyperparathyroidism. Calcitriol may be administered to such patients to decrease the synthesis and secretion of parathyroid hormone (PTH) and to help maintain calcium and phosphorus homeostasis. However, the doses of calcitriol required to suppress serum PTH concentrations can lead to hypercalcemia or hyperphosphatemia in many patients undergoing hemodialysis. Paricalcitol is a new vitamin D analogue that is safe and effective in suppressing elevated concentrations of PTH in patients with established hyperparathyroidism who are maintained on chronic hemodialysis. As with vitamin D, the biologic action of paricalcitol is mediated through activation of the vitamin D receptor (VDR). The VDR functions as a ligand-induced transcription factor regulating the rate of expression of genes that are involved in controlling not only calcium homeostasis and bone remodeling but also hormone secretion, inhibition of cell growth, and induction of cell differentiation. In vitro studies have shown that paricalcitol inhibits PTH secretion from bovine parathyroid cells in a dose-dependent manner. Studies in renally insufficient rats demonstrated that paricalcitol caused approximately 10 times less elevation of serum calcium concentrations than calcitriol. In clinical studies, paricalcitol effectively decreased PTH by about 60% over a 12-week period. Mean serum concentrations of calcium were significantly increased but remained within the normal range. There were occasional (5/414 determinations) transient elevations in serum calcium above the upper limit of normal in some (5/401) patients. Serum phosphorus values did not change significantly compared with baseline, although they tended to be slightly higher in the paricalcitol-treated group than in the group receiving placebo. Elevations of the calcium-times-phosphorus product were relatively few but occurred more often in the paricalcitol than in the placebo group. The terminal half-life of paricalcitol was 5 to 7 hours in healthy subjects; in patients undergoing hemodialysis, it was 14 hours. Adverse events associated with paricalcitol use included, among others, chills, feeling unwell, fever, sepsis, palpitations, dry mouth, gastrointestinal bleeding, nausea, vomiting, edema, light-headedness, and pneumonia. Paricalcitol should be considered as an alternative to calcitriol in the treatment of patients who are undergoing maintenance hemodialysis for end-stage renal disease, as it has a decreased potential to induce hypercalcemia and hyperphosphatemia. Additional studies are required to determine the long-term effects of therapy.
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PMID:Paricalcitol, a new agent for the management of secondary hyperparathyroidism in patients undergoing chronic renal dialysis. 1032 13

Calciphylaxis is a rapidly developing, fatal process of vascular calcium deposition with prominent cutaneous manifestation. We treated a long-term haemodialysis patient who developed an analogous disorder limited to the lungs. A 57-year-old man was admitted for initiation of peritoneal dialysis because limited cardiac reserve precluded further haemodialysis. He was treated successfully for pneumonia until hypoxia and progressive hypercalcaemia developed. (99m)Tc-methylene disphosphonate scintigraphy showed diffusely increased pulmonary uptake. Death supervened despite aggressive and successful treatment of hypercalcaemia. Autopsy studies included immunohistochemistry and morphometric studies of bone. Alveolar capillary walls showed diffuse calcium deposition. Both gross and microscopical findings differed from those of typical metastatic calcification in dialysis patients. Immunoreactivity for parathyroid hormone-related protein was present in the lesions. Bone histomorphometry indicated mild osteitis fibrosa. Pneumonia is believed to have caused local synthesis of parathyroid hormone-related protein that, along with high calcium x phosphorus product, contributed to calcium deposition. By analogy with the cutaneous process we termed the deposition "pulmonary calciphylaxis".
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PMID:Acute respiratory failure due to "pulmonary calciphylaxis" in a maintenance haemodialysis patient. 1117 29

A 50-year-old Japanese female with chronic renal failure who had been on continuous ambulatory peritoneal dialysis developed fulminant systemic cutaneous necrosis that began as painful livedo reticularis-like skin lesions on her thighs. Because of disseminated vascular calcification within the muscular layer of her lower limbs, we eventually diagnosed her with calciphylaxis. The skin necrosis progressed rapidly, and she died of sepsis and pneumonia on the 53rd hospital day. In addition to her long-lasting severe hyperparathyroidism and extremely elevated serum phosphorus and calcium levels, mechanical, frictional stimulation inflicted on the local skin and administration of corticosteroids were suspected to have precipitated the calciphylaxis. Our lack of awareness of this disease in its early stages resulted in our missing the chance to do a parathyroidectomy that might have changed the course. It is important to know the clinical features of this rare disease in order to make a diagnosis as early as possible.
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PMID:Fulminant and relentless cutaneous necrosis with excruciating pain caused by calciphylaxis developing in a patient undergoing peritoneal dialysis. 1128 Apr 61


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