Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0847097 (acidity)
 15,165 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Although dermatology now has the most extensive group of systemic medications available for the treatment of skin diseases at any time, GCSs remain the most important agents for managing inflammatory disorders. It is important that the dermatologist have a broad knowledge of guidelines for clinical use, pharmacology, and adverse effects of these drugs. Acute and chronic side reactions should be well recognized. An understanding of the HPA axis and reasons for administering GCSs in different ways is of great value. A good medical history should be taken on any patient treated with GCSs, including knowledge of conditions that would make GCSs inadvisable and other concomitant systemic medications that might produce drug interactions. During the course of therapy, physical examination should include all systems pertinent to side effects caused by these agents, including frequent evaluations of weight and blood pressure. Blood chemistries should be performed on a regular basis, including glucose, electrolytes, and serum lipids. Osteoporosis is one of the most significant adverse affects to be evaluated, with bone mineral density studies recommended on an annual basis for persons continuing on GCS therapy. If hip or other joint pain develops, MR imaging is the most specific and sensitive radiologic examination for evaluating the possibility of osteonecrosis. An ophthalmology examination should be performed every 6 to 12 months to detect early cataract or glaucoma development. Any early signs of infection should be evaluated by appropriate smears, wet preparations, and cultures. Many other studies, including gastrointestinal and pulmonary examinations, may be dictated by specific acute situations. It is important to begin early prevention of the bone loss that occurs with GCS-induced osteoporosis. The 1996 guidelines of the American College of Rheumatology, including adequate calcium and vitamin D intake, should be followed. Hormonal replacement, a bisphosphonate, calcitonin, or a thiazide diuretic may be indicated. Restriction of sodium in the diet is important, as well as adequate potassium intake. The diet should be low in saturated fat and calories and should be high in vegetable protein. Because osteoporosis is so prevalent with GCSs, keeping the patient as active as possible with mild-to-moderate exercise is important. Whenever possible, exposure to persons with infectious processes should be avoided, and proper treatment should be instituted at the initial signs of systemic or cutaneous infection. Oral doses of GCSs are best taken with food to prevent gastrointestinal irritation, and agents for gastric acidity occasionally may be indicated. Significant trauma should be prevented, as should severe exposure to the sun. Many situations may call for consultation with other medical or surgical subspecialists. The patient must be aware of the importance of regular physician evaluations and reporting of any adverse effects while on long-term GCSs. A good relationship and understanding between the patient and physician are vital in minimizing potential problems from these agents. If the dermatologist maintains the proper guidelines of care, patients on GCSs have the highest benefits and lowest risks possible.
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PMID:Update on systemic glucocorticosteroids in dermatology. 1115 87

Associations with free-living protozoa (FLP) have been implicated in the persistence of foodborne pathogenic bacteria in food-related environments. To date however no information is available on the presence of FLP in the gastrointestinal tract (GIT) of pigs, which represents an important reservoir for zoonotic foodborne bacteria and hence a potential location for associations with FLP. This is at least partly due to the lack of adequate protocols to recover FLP from intestinal content and feces. In the present study different protocols to recover FLP from the porcine GIT and feces were tested. The most effective protocols were then applied to explore the presence of live FLP in the pig GIT and feces. A filtration based protocol was identified as the most suitable method to recover viable FLP from the porcine GIT and feces. Cultivable FLP were recovered from different parts of the GIT, suggesting at least a transient presence of FLP in this habitat. Free-living amoebae species (Acanthamoeba spp., Hyperamoeba sp., Vannella sp., Vermamoeba vermiformis, hartmannellids and vahlkampfiids) but also ciliates (Colpoda sp. and Tetrahymena/Glaucoma lookalike) and flagellates (cercomonads, bodonids and glissomonads) were recovered and cultured from pig intestinal content. Acanthamoeba hatchetti and Filamoeba sinensis were isolated for the first time from pig intestinal content. Despite high gastric acidity, non-cyst forming amoeba species were also detected which suggests survival of their trophozoites in the animal GIT.
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PMID:Free-living protozoa in the gastrointestinal tract and feces of pigs: Exploration of an unknown world and towards a protocol for the recovery of free-living protozoa. 2736 81

Carbonic anhydrase inhibitors are a common cause of normal anion gap metabolic acidosis; however, development is less commonly associated with ophthalmic administration of these agents. We report a case of a premature neonate who was being treated at our institution with betaxolol, dorzolamide, and latanoprost ophthalmic products for suspected bilateral congenital glaucoma. In addition, the patient was also receiving caffeine, ursodiol, and acidified liquid human milk fortifier. The patient developed a normal anion gap metabolic acidosis, and both dorzolamide ophthalmic solution and the acidified human milk fortifier were considered potential causes. Upon discontinuation of the dorzolamide ophthalmic solution and the switching of liquid human milk fortifiers, the normal anion gap metabolic acidosis gradually resolved. As a result of the pH and acidity, the acidified liquid human milk fortifier is thought to be associated with an anion gap acidosis; therefore, dorzolamide is suspected to be the primary cause of a normal gap acidosis. This case demonstrates that systemic effects can occur with ophthalmic administration of dorzolamide in a premature neonate. Ophthalmic agents should not be overlooked as a potential cause of systemic toxicity.
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PMID:Metabolic Acidosis with Ophthalmic Dorzolamide in a Neonate. 2745 5