Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038362 (stomatitis)
 8,852 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The coincidence of skin eruption and remission induced by gold has not previously been reported. In 50 out of 247 patients with rheumatoid arthritis treated with gold salts (Solganal) between 1977 and 1987 treatment was stopped owing to adverse reactions. Skin rashes were present in 31 patients, 10 had nephropathy, and nine patients had aphthous stomatitis. All 31 patients who developed skin eruption entered a concomitant clinical and laboratory remission. The remission satisfied the American Rheumatism Association preliminary criteria and was accompanied by a significant decrease of mean erythrocyte sedimentation rate from 43 (SD 13) to 25 (11) mm/h. Disease was exacerbated in 23 patients after three to 60 months. Eight patients are in remission at present, five to 68 months after gold treatment was discontinued. In contrast, no remission was noticed among the 19 patients with nephropathy or stomatitis.
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PMID:Association between gold induced skin rash and remission in patients with rheumatoid arthritis. 214 Feb 55

Inorganic bismuth salts are poorly soluble in water: solubility is influenced by the acidity of the medium and the presence of certain compounds with (hydr)oxy or sulfhydryl groups. The analysis of bismuth in biological material is not standardised and is subject to large variation; it is difficult to compare data from different studies, and older data should be approached with caution. The normal concentration of bismuth in blood is between 1 and 15 micrograms/L, but absorption from oral preparations produces a significant rise. Distribution of bismuth in the organs is largely independent of the compound administered or the route of administration: the concentration in kidney is always highest and the substance is also retained there for a long time. It is bound to a bismuth-metal binding protein in the kidney, the synthesis of which can be induced by the metal itself. Elimination from the body takes place by the urinary and faecal routes, but the exact proportion contributed by each route is still unknown. Elimination from blood displays multicompartment pharmacokinetics, the shortest half-life described in humans being 3.5 minutes, and the longest 17 to 22 years. A number of toxic effects have been attributed to bismuth compounds in humans: nephropathy, encephalopathy, osteoarthropathy, gingivitis, stomatitis and colitis. Whether hepatitis is a side effect, however, is open to dispute. Each of these adverse effects is associated with certain bismuth compounds. Bismuth encephalopathy occurred in France as an epidemic of toxicity and was associated with the intake of inorganic salts including bismuth subnitrate, subcarbonate and subgallate. In the prodromal phase patients developed problems in walking, standing or writing, deterioration of memory, changes in behaviour, insomnia and muscle cramps, together with several psychiatric symptoms. The manifest phase started abruptly and was characterised by changes in awareness, myoclonia, astasia and/or abasia and dysarthria. Patients recovered spontaneously after discontinuation of bismuth. Intestinal lavage, forced diuresis and haemodialysis have been tried without positive effects on the clinical condition of the patient or on blood bismuth concentration, and the use of dimercaprol as an antidote has produced reports of both positive and negative findings. To confirm the diagnosis of bismuth encephalopathy, it is essential to find elevated bismuth concentrations in blood, plasma, serum or CSF. A safety level of 50 micrograms/L and an alarm level of 100 micrograms/L have been suggested in the past, but no proof is available to support the choice of these levels.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Pharmacokinetics and toxicity of bismuth compounds. 268 29

From 1980 to 1988 235 koalas were necropsied and 67 were found to have urinary tract disease. Six affected koalas out of 48 were derived from wildlife parks around Sydney while 61 of 187 were derived from free living populations on the central and north coasts of New South Wales. Sixteen had cystitis alone, 5 had cystitis and associated renal disease only, 16 females had cystitis with genital disease, 23 had urinary disease in combination with other systemic disease and 7 had renal disease only. Overall 49 animals had cystitis (30 females and 19 males; 47 being free living) with 12 of these having renal extension (all free living). Cystitis tended to be active but chronic while associated renal disease was mainly designated as hydronephrosis and pyelonephritis. Other forms of renal disease included lymphosarcoma, oxalate nephrosis, acute and chronic nephritis, and microabscessation related to septicaemia. Female genital disease associated with cystitis was commonly vaginitis and metritis. Paraovarian cysts were detected with and without metritis. Other diseases occurring with urinary tract disease included conjunctivitis, dermatitis/stomatitis, pneumonia and hepatic disease. The higher prevalence of urinary tract disease in free living koalas, especially cystitis, is in contrast to captive koalas and may reflect the interaction between disease cause and habitat.
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PMID:A survey of urinary tract disease in New South Wales koalas. 273 Apr 73

Pathologic evaluations of pigeons dying between September 1984 and August 1985 are reported for a production colony of 1200-1800 White Carneau and Show Racer pigeons ranging in age from hatchlings to 12 years. Infectious diseases were the common causes of death in pigeons younger than 1 year; salmonellosis and nephritis were the common causes in pigeons 1-3 years old; and neoplasia and reproductive organ disorders were the common causes in pigeons older than 3 years. Monthly mortality was 2-4% in pigeons fed a cholesterol-containing diet and 0.9% in those fed noncholesterol-containing pellet diets. The increased deaths in the cholesterol-fed birds were attributed primarily to end-stage renal disease and atherosclerosis with secondary complications. The most frequently observed clinical entity in pigeons younger than 6 months was pseudomembrane formation on the oral and pharyngeal mucosa, termed pseudomembranous stomatitis. The definitive etiologic factor was not determined. Although all affected pigeons had similar gross lesions, the cases fell into one of three subsets, suggestive of bacterial, fungal, or viral etiologies. Chronic nephritis occurring as end-stage renal disease was more severe in pigeons fed a cholesterol-containing diet.
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PMID:Survey of the pathologic findings in a large production colony of pigeons, with special reference to pseudomembranous stomatitis and nephritis. 381 11

Lead, cadmium, mercury and arsenic are widely dispersed in the environment. Adults are primarily exposed to these contaminants in the workplace. Children may be exposed to toxic metals from numerous sources, including contaminated air, water, soil and food. The chronic toxic effects of lead include anemia, neuropathy, chronic renal disease and reproductive impairment. Lead is a carcinogen in three animal species. Cadmium causes emphysema, chronic renal disease, cancer of the prostate and possibly of the lung. Inorganic mercury causes gingivitis, stomatitis, neurologic impairment and nephrosis, while organic mercurials cause sensory neuropathy, ataxia, dysarthria and blindness. Arsenic causes dermatitis, skin cancer, sensory neuropathy, cirrhosis, angiosarcoma of the liver, lung cancer and possibly lymphatic cancer.
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PMID:Occupational and community exposures to toxic metals: lead, cadmium, mercury and arsenic. 716 33

The notable glomerular feature of human immunodeficiency virus (HIV)-associated nephropathy (HIVAN) is the collapse of the capillary tuft with marked glomerular epithelial cell hyperplasia. These data suggest a loss of normal podocyte function, which is associated with a loss of the podocyte differentiation markers, Wilm's tumor (WT-1), synaptopodin, podocalyxin, and common acute lymphoblastic leukemia antigen (CALLA). We have previously shown that HIV-1 expression can induce these changes in HIV-1 transgenic mice. To identify which HIV-1 gene product(s) are responsible for the phenotypic changes in podocytes, we created multiple mutated HIV-1 constructs and then pseudotyped them with vesticular stomatitis virus glycoprotein (VSVG) envelope to enhance the tropism of these mutant viruses. In addition to gag/pol, the mutant viruses lacked one of the following, env, nef, rev, vif, vpr, or vpu. In addition, we generated single gene expressing pseudotyped viruses to complement the scanning mutation approach of our viral parental construct. Murine podocytes were then infected with one of the viral constructs either lacking or expressing the various HIV-1 genes. We found that HIV-1 nef was necessary and sufficient for proliferation of podocytes and down-regulation of synaptopodin and CALLA. These data suggest that Nef induces many of the changes we observe in HIV transgenic model and, as a result, this now defines the pathway for exploration of host responses to HIV-1 infection.
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PMID:Critical role for Nef in HIV-1-induced podocyte dedifferentiation. 1453 2

Uremic stomatitis represents a relatively uncommon intraoral complication seen, mostly, in cases of end-stage renal disease or undiagnosed/untreated chronic renal failure. Its incidence has decreased due to the advent of renal dialysis. Clinically uremic stomatitis is characterized by the presence of painful plaques and crusts that are usually distributed on the buccal mucosa, dorsal or ventral surface of the tongue, gingiva, lips, and floor of the mouth. Treatment consists of improvement of urea blood concentration and the underlying renal failure, supported by increased oral hygiene with antiseptic mouthwashes and antimicrobial/antifungal agents if necessary. Although uremic stomatitis occurs in patients with end-stage renal disease, we report a case of a patient who exhibited an ulcerative form of uremic stomatitis related to the sudden relapse of uremia, although not in an advanced stage of her renal disease. A description of the clinical and microscopic appearance is given along with our hypothesis for the pathogenesis of the disease.
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PMID:Ulcerative uremic stomatitis associated with untreated chronic renal failure: report of a case and review of the literature. 1663 72

HIV-associated nephropathy (HIVAN) is the most common cause of chronic renal failure in HIV-infected patients. Tubulointerstitial inflammation is a prominent component of the histopathology of HIVAN. The pathogenesis of HIVAN is a result of infection of renal epithelial cells, but the cellular response to this infection remains poorly defined. In these studies, we used oligonucleotide microarrays to identify differentially expressed genes in renal tubular epithelial cells from a patient with HIVAN at three time points after infection with vesicular stomatitis virus-pseudotyped gag/pol-deleted HIV-1. Very few genes were differentially expressed 12 and 24 hours after infection. Three days after infection, however, 47 genes were upregulated by at least 1.8-fold. The most prominent response of these cells to HIV-1 expression was production of proinflammatory mediators, including chemokines, cytokines, and adhesion molecules. Many of the upregulated genes are targets of interleukin 6 and nuclear factor kappa B regulation, suggesting a central role for these proteins in the response of tubular epithelial cells to HIV-1 infection. Analysis of kidneys from HIV-1 transgenic mice revealed upregulation of many of the proinflammatory genes identified in the microarray studies. These studies provide novel insights into the mechanisms by which HIV-1 infection of tubular epithelial cells leads to tubulointerstitial inflammation and progressive renal injury.
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PMID:HIV-1 infection initiates an inflammatory cascade in human renal tubular epithelial cells. 1676 88

Chronic renal failure is a relatively common systemic disease. Systemic abnormalities such as anemia, platelet disorders and hypertension as well as oral manifestations including xerostomia, uremic stomatitis, periodontal disease and maxillary and mandibular radiographic alterations can be observed in individuals with chronic renal disease. In view of its frequent occurrence and the need of knowledge by dentists dealing with this condition, this paper discusses the most important issues regarding chronic renal failure, addressing its systemic and oral manifestations and the dental management of chronic renal patients. A case report is presented.
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PMID:Systemic conditions, oral findings and dental management of chronic renal failure patients: general considerations and case report. 1692 47

Diabetic nephropathy (DN) is the leading cause of end-stage renal disease requiring dialysis in the Western world. Clinical studies reveal that stringent control of blood glucose levels reduces the risk of most diabetic complications, underscoring the importance of understanding the cellular response to hyperglycemia. Our work identifies a new pathway of potential significance in this response, linking hyperglycemia to the stimulation of constitutive protein secretion via a pathway involving munc13 and rab34. These two proteins have previously been shown to interact at the Golgi via the munc13 homology domain 2 (MHD2). In the present study, using cultured rat mesangial cells (RMC), we show that high glucose-induced upregulation of endogenous munc13-2 increases secretion of the model protein, vesicular stomatitis virus glycoprotein-green fluorescent protein (VSVG-GFP), while small interfering (si)RNA-mediated knockdown of either munc13-2 or rab34 abolishes this effect. Similarly, increased secretion of VSVG-GFP is observed following transfection of HeLa cells with wild-type munc13-2, but not when HeLa cells are transfected with a mutant protein in which the MHD2 domain is deleted. Finally, we show that high glucose-stimulated secretion of fibronectin in RMC is abolished by siRNA knockdown of munc13-2. Collectively, our results demonstrate that the mechanistic basis for our observed high glucose-induced protein secretion is through interaction of munc13 and rab34, indicating a potentially critical role for this newly described pathway in the pathogenesis of DN.
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PMID:Rab34 and its effector munc13-2 constitute a new pathway modulating protein secretion in the cellular response to hyperglycemia. 1964 Oct 95


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