Latest Treatment of Gout
Gout affects about 0.25 of the population of Europe and North America. Drugs are effective in management and some drugs can precipitate attacks. Patients with gout but no visible tophi have a urate pool that is 2-3 times normal and since this exceeds the amount that can be carried in solution in the extracellular fluid, microcrystalline deposits forming tissues including the joints patients with tophi have a urate pool that may be 15-26 times normal. Hyperuricaemia and gout from whatever cause (e.g. metabolic, renal disease, neoplasia) depends essentially on two processes, (1) overproduction and (2) underexcretion of urate. Both mechanisms may operate in the same patient but decreased renal clearance contributes to hyperuricaemia in most patients with gout. Drugs may influence these processes as follows Underexcretion of urate is caused by all diuretics (except spironolactone), aspirin, ethambutol, pyr-azinamide, nicotinic acid, and alcohol (which increases urate synthesis and also...
Acute gout Acute gout is usually treated with an NSAID in full dose. Any such drug which is tolerated may be used (except aspirin which in low dose promotes urate retention, see below) indomethacin is often chosen because of its strong anti-inflammatory action and efficacy. If treatment is started early, the attack may be terminated in a few hours. Colchicine is useful if NSAIDs are contraindicated. If neither colchicine nor NSAIDs are tolerated, oral prednisolone 40 mg d and tapered over a week is also effective. It requires only a moment's thought to appreciate that the uricosurics and allopurinol will not relieve an acute attack of gout. Recurrent gout, tophaceous gout, and gout causing renal damage (gouty nephropathy) Treatment is initiated if the serum urate consistently exceeds 0.6 mmol 1 and the patient has had three or more attacks of acute gout in a year. Allopurinol should be started in a quiescent period because it will prolong an attack of gout if started during one, and...
Rubner measured the heats of combustion of a number of different proteins, fats, and carbohydrates in a bomb calorimeter and also studied the heat of combustion of urine passed by a dog, a man, a boy, and a baby. He realised that the heat of combustion of protein in a bomb calorimeter was greater than its caloric value in the body because the body oxidises proteins only to urea, creatinine, uric acid, and other nitrogenous end-products, all of which can be further oxidised 5 .
In 1987, Lee et al. (15), from the M.D. Anderson Medical Center, identified the following poor prognostic features for CLL (1) age more than 60 yr, (2) serum alkaline phosphatase greater than 80 U dL, (3) serum uric acid greater than 7.0 mg dL, (4) serum lactate dehydrogenase (LDH) greater than 325 U dL, and (5) presence of external lymphadenopathy. Patients were divided into three categories (a) low risk, LDH less than 325 U dL and the presence of one of the prognostic features mentioned above (b) intermediate risk, LDH less than 325 U dL and two to three poor prognostic features listed above or LDH more than 325 U dL with one poor prognostic feature and (c) high risk, LDH greater than 325 U dL and the presence of two poor prognostic features or all of the aforementioned poor prognostic features. The median survival times were 10, 6, and 2 yr for low-, intermediate-, and high-risk groups, respectively.
An assay for uric acid involves the enzyme urate oxidase, which catalyzes the following reaction Uric acid + O2 + 2H2O Allantoin + H2O2 + CO2 (3.1) While allantoin is difficult to measure spectrophotometrically, uric acid possesses a strong UV absorption with a maximum at 293 nm (molar absorptivity 1.22 x 104 M 1cm 1) Uric acid quantitation thus involves monitoring the
Verts uric acid into allantoin, which is highly soluble in urine. It is an efficient way of promptly reducing serum uric acid levels, thus preventing uric acid nephropathy and preserving renal function, allowing a better excretion of the other cell metabolites such as potassium and phosphorus. Strict clinical and metabolic monitoring of patients during the lysis phase is essential.
Euvolemic hyponatremia is most commonly caused by SIADH. Nonphysiologic nonosmotically mediated (therefore inappropriate ) secretion can occur in the setting of pulmonary disease, CNS disease, pain, in the postoperative period, or as part of a paraneoplastic syndrome. Because of retention of free water, patients actually have mild (although clinically inap-parent) volume expansion. Additionally, if they have a normal dietary sodium intake, the kidneys do not retain sodium avidly. Therefore, modest natriuresis occurs so that the urine sodium level is elevated to 20 mmol L. SIADH is a diagnosis of exclusion the patient must be hyposmolar but euvolemic, with urine that is not maximally dilute (osmolality 150-200 mosm L), urine sodium 20 mmol L, and normal adrenal and thyroid function. Some laboratory clues to SIADH are low BUN and low uric acid levels. Unless the patient has severe neurologic symptoms, the treatment of SIADH is water restriction.
Glucocorticoids, unlike mineraldocorticoids, restore glomerular filtration rate (GFR) and renal plasma flow to normal following adrenalectomy. They also facilitate free-water excretion (clearance) and uric-acid excretion. Of Glucocorticoids have also been found to have psychoneural effects following chronic hyper- or hypo-cortisol secretion. In these cases patients may initially become euphoric and then psychotic, paranoid, and finally depressed. In addition, cortisol increases gastric flow and gastric secretion, while it decreases gastric mucosal-cell proliferation. The latter two effects can lead to peptic ulceration following chronic cortisol treatment.
The application of biochemical testing for medical testing began about 100 years ago. One of the first clinical chemists, Dr. Otto Folin, developed quantitative analytical methods for urine analytes of urea, ammonia, creatinine, uric acid, electrolytes, and acidity. He also developed early blood tests, including those for ammonia and creatinine, using the Jaffe method. Dr. Folin helped to establish the clinical significance of renal function and metabolic tests and published the first reference ranges for uric acid, nonprotein nitrogen (NPN), and protein in blood. He helped to develop methods for testing glucose and total serum protein in body fluids.
Measurements of total nitrogen intake and output can be used to calculate protein nutritional status (Leverton & Gram 1949 Hegsted 1978). This approach is based on principles of chemical mass-balance, and although practical matters concerning collecting total nitrogen waste make this method difficult to implement, measurements of nitrogen balance generally permit a reliable determination of protein homeostasis. Use of the method requires special consideration since urinary nitrogen may occur in the forms of urea and ammonia (derived from amino acid and protein catabolism) and uric acid and creatinine (derived from nonprotein sources), and since nitrogen may be lost in faeces, sweat and other products (Figure 10.1). To facilitate studies, investigators have proposed correction factors that account for the relationship between total urinary nitrogen and urinary urea nitrogen (Mackenzie et al. 1985) and for miscellaneous non-urinary nitrogen losses (Calloway et al. 1971).
Given certain physicochemical conditions, crystals can deposit within the tubular lumen. Methotrexate, for example, is relatively insoluble at low pH and can precipitate in the distal nephron when the urine is acid. Similarly the uric acid produced by the metabolism of nucleic acids released during rapid tumour cell lysis can cause a fatal urate nephropathy. This was a particular problem with the introduction of chemotherapy for leukaemias until the introduction of allopurinol it is now routinely given before the start of chemotherapy to block xanthine oxidase so that the much more soluble uric acid precursor, hypoxanthine, is excreted instead. Crystal-nephropathy is also a
The chimpanzee (25) has also been used to evaluate certain diuretics. In this animal, the effect of the compound on uric acid excretion can also be studied, because apes, like humans, are devoid of hepatic uricase and therefore maintain a relatively high level of circulating serum urate (26). Chimpanzees have also been used in the study of uricosuric agents (25), but tests with such large animals obviously present numerous problems. Attempts have also been made to block the enzyme uricase in rats by administering potassium oxonate and thus to obtain higher serum uric acid levels (27).
Calibration of the cytochrome c electrode is not trivial since the radical is a short-lived species. Investigations of the biocatalytic generation of superoxide by the xanthine oxidase catalyzed conversion of hypoxanthine to uric acid showed that a steady state situation can be achieved in solution 53 . The continuous generation of the radical is counterbalanced by the spontaneous dismutation. This situation continues until the substrate of the generation reaction (hypoxanthine) will be consumed. The steady state radical concentration in solution corresponds to a steady state oxidation current detected at the electrode. A kinetic analysis showed that this sensor current can be linearly correlated to the square root
Figure 22.7 Catabolism of purine nucleotides to uric acid. Figure 22.7 Catabolism of purine nucleotides to uric acid. Figure 22.7 shows pathways of purine catabolism leading to uric acid. As seen in the figure, AMP and GMP can both be hydrolyzed from their phosphates by nucleotidase, ultimately yielding the bases hypoxanthine and xanthine, respectively. Hypoxanthine is converted to xanthine by xanthine oxidase and xanthine is converted to uric acid, also by xanthine oxidase. In addition, AMP can be degraded first in a deamination to form IMP, which loses its phosphate to become inosine. Inosine, in turn, is converted to hypOxanthine. Uric acid, the end point of purine degradation in primates, is excreted. Most other animals, however, oxidize uric acid to allantoin, hydrolyze allantoin to allantoic acid and subsequently convert allantoic acid to urea or other possible excretion products, depending on the animal (Figure 22.8). See also Excessive Uric Acid in Purine Degradation,...
See also Reactive Oxygen Oxygen Metabolism and Human Disease Superoxide Dismutase Catalase Glutathione Peroxidase
Large scale production of reactive oxygen species has the potential to inflict considerable damage on the tissues in which they are produced, a situation called oxidative stress. Antioxidant compounds, such as glutathione, vitamin C and vitamin E, and uric acid provide non-enzymatic protection against oxidative stress because they can scavenge ROS before the ROS can cause damage. Alternatively, antioxidant compounds can prevent oxidative damage from spreading, such as the chain reaction of lipid peroxidation. Vitamin E is the principal lipid-soluble antioxidant compound and plays an important role in preventing membrane damage. .' -Carotene and other carotenoid compounds related to vitamin A are lipid-soluble antioxidants that also play roles in free radical trapping. Glutathione plays an important role in cellular antioxidant protection. Vitamin C (ascorbic acid) is present in far higher amounts in cellular fluids and probably plays the predominant role in extracellular antioxidant...
The safest urine pH to avoid kidney stones is close to 6. Be I ow this value, uric acid stones are most likely to form. Ca-phosphate stones precipitate in alkaline urine. By driving NH4+ excretion with a high distal H+ secretion, a considerable quantity of H+ can be elimi nated at a urine pH close to 6.0. By excreting organic anions rather than HCO3 , a considerable quantity of HCO3-can also be eliminated at a urine pH close to 6.0 (see Figure 2). Avoiding uric acid kidney stones Uric acid is the waste product of purine meiabo-lism 47 . The free acid form, uric acid, rather than total urates is the critical component for kidney stone formation because uric acid is sparingly soluble in water (Equation 4). Because the pK of uric acid in the urine at 3 7 C is close to 5.3 47 , precipitation of uric acid can be avoided without increasing the urine volume by raising the urine pH to 6 at the same to tal urate excretion rate 48 . Urate + H+ o Uric acid...
Or malignant nephritis - inflammation of the kidney nephrolithiasis - presence of calculi in the urinary tract urate nephrolithiasis indicates the presence of uric acid in the stone nephrotoxicity - damage to the kidneys neurohypophysis - the posterior or back portion of nitrogen ingested and that excreted noncompetitive immunoassay - immunoassay that does not contain reagent antigen competing with patient antigen nonprotein nitrogen - catabolites of protein and nucleic acid metabolism, including urea, ammonia, creatinine, creatine, and uric acid
Microtubules in eukaryotic cells are important for the maintenance and modulation of cell shape and the disposition of intracellular elements during the growth cycle and mitosis. It may thus come as no surprise that the inhibition of microtubule polymerization can block many normal cellular processes. The alkaloid colchicine (see figure), a constituent of the swollen, underground stems of the autumn crocus (Colchicum autumnale) and meadow saffron, inhibits the polymerization of tubulin into microtubules. This effect blocks the mitotic cycle of plants and animals. Colchicine also inhibits cell motility and intracellular transport of vesicles and organelles (which in turn blocks secretory processes of cells). Colchicine has been used for hundreds of years to alleviate some of the acute pain of gout and rheumatism. In gout, white cell lyso-somes surround and engulf small crystals of uric acid. The subsequent rupture of the lysosomes and the attendant lysis of the white cells initiate an...
Vasoconstrictors, principally noradrenaline. While this hyposensitivity may be a consequence of the sodium depletion, thiazides are generally more effective antihypertensive agents than loop diuretics, despite causing less salt loss, and evidence suggests an independent action of thiazides on an unidentified ion-channel on vascular smooth muscle cell membranes. Maximum effect on blood pressure is delayed for several weeks and other drugs are best added after this time. Adverse metabolic effects of thiazides on serum potassium, blood lipids, glucose tolerance, and uric acid metabolism led to suggestions that they should be replaced by newer agents not having these effects. It is, however, now recognised that unnecessarily high doses of thiazides have been used in the past and that with low doses, e.g. bendro-fluazide (bendroflumethiazide) 1.25-2.5 mg d or less (or hydrochlorothiazide 12.5-25 mg), thiazides are both effective and well-tolerated. Moreover, they are not only by far the...
Depending on the patient's age (see above) use either a p Blocker or thiazide Diuretic as firstline therapy, unless there is a compelling reason to avoid these (e.g. asthma and gout, respectively). If the first drug is effective but not tolerated, switch to the other member of the pair i.e. ACE inhibitor (or AIIRA) instead of P-blocker, Calcium blocker instead of diuretic.
Adverse effects include hyperuricaemia and arthralgia, which is relatively frequent with daily but less so with intermittent dosing and, unlike gout, affects both large and small joints. Pyrazinoic acid, the principal metabolite of pyrazinamide, inhibits renal tubular secretion of urate. Symptomatic treatment with an NSAID is usually sufficient and it is rarely necessary to discontinue pyrazinamide because of arthralgia. Hepatitis, which was particularly associated with high doses, is not a problem with modern short-course schedules. Sideroblastic anaemia and urticaria also occur.
Polarization immunoassay (FPIA), the serum of the same patient was found to contain 3.0 mM salicylate, a value that is above the recommended therapeutic range of 1.1-2.2 mM. After direct urine injection (Fig. 1A), MECC revealed an overloaded, completely unresolved electropherogram in which the presence of salicylate was difficult to identify. However, after 10-fold dilution (Fig. 1B,C), clear separation of salicylate and two of its metabolites, gentisic acid and salicyluric acid, were obtained. In addition, an endogenous marker substance, uric acid, could also be identified. For all four compounds, there was excellent agreement of the normalized absorbance spectra with those of pure compounds (Fig. 1D-G) allowing identification as well as purity assessment of these zones. Comparison of panels A and B also reveals the impact of the sample matrix, showing that detection time by itself is not adequate for analyte identification. However, in conjunction with multiwavelength detection it...
Of the patients are asymptomatic and seek medical attention solely because an enlarged spleen is found on routine physical examination, or because of an abnormal peripheral blood smear. Those patients who become symptomatic suffer from fatigue, symptoms related to an enlarged spleen, gout due to elevated uric acid levels, and constitutional symptoms such as weight loss, night sweats, fatigue, and peripheral edema. The latter represent advanced symptoms. Pressure of a large spleen on the stomach may lead to delayed gastric emptying and early satiety.21 Myeloid metaplasia may occur in unusual sites, such as the pulmonary, gastrointestinal, and central nervous systems. Although extramedullary hematopoiesis occurs frequently in the lymph nodes, it rarely accounts for significant nodal enlargement.
In menstrual cycle, 439, 439f, 440, 441f source of, 389t Gonads, 438. See also Ovary Testis Gout, 229 anion gap, 222-223, 223f BUN-to-creatinine ratio, 212, 212t creatinine clearance, 203-205 electrolyte analysis, 220-224, 223f fractional excretion of sodium, 214 hemolysis effects on, 219-220 osmolality, 228 urea, 211-212, 212t uric acid, 229-230 urinary albumin, 210-211 urinary protein, 210 Kinetic spectrophotometry, 106t, 107-109 Kinetics, of enzymes, 23-25, 24f in drug metabolism, 507-508 in spectrophotometry, 23-25, 24f Km (Michaelis constant), 24, 24f
Uric acid, and ascorbic acid were minimized. Similarly, Luong et al. 95 have used 3-aminopropyltriethoxysilane (APTES) as both a solubilizing agent for carbon nanotubes and an immobilization matrix for GOx to construct a mediatorless, highly efficient glucose sensor. In this study, a well-defined redox response from glucose was observed at -0.45 V (vi. Ag AgCl) whereas no response was seen for three common interfering species, namely uric acid, ascorbic acid, and acetaminophen, at a concentration corresponding to the physiological level of 0.1 mM.
Nephrolithiasis is a disorder in which small stones - usually formed from calcium and oxalate - precipitate in the kidney. If they pass into the ureter they cause irritation, spasm, and may block the flow of urine. The pain of a kidney stone is intense it typically starts suddenly in the lower back and radiates down and around toward the groin. In general, the more calcium and oxalate in the urine, the greater the chances of developing kidney stones. Uric acid in the urine can be the seed around which calcium oxalate stones develop. The risk of kidney stones can be strongly influenced by dietary factors.5
Diuretic therapy may lead to a number of metabolic and electrolyte disorders. In general, these disturbances are mild but can be life-threatening in certain cases. Some of the common adverse effects observed with diuretic treatment are hypokalemia, hyperuri-cemia, and glucose intolerance. Diuretics that possess a site of action proximal to the collecting tubules, such as the loop and thiazide diuretics, induce potassium loss an average loss cf 0.5-0.7 meq L generally results with long-term therapy (30). In most young hypertensive patients, this reduction does not present any problem however, in older patients or patients with preexisting heart disease, it may lead to the occurrence of ventricular arrhythmias. Combinations with potassium-sparing diuretics are frequently used to minimize the effect. Dietary potassium supplements may also be prescribed. In patients receiving long-term diuretic therapy, serum uric acid concentrations increase on average 1.3 mg L as the result of a...
Or NMDA receptors has three main actions. First, activation of lipases in the cell membrane increases arachidonic acid release, which leads to increases in reactive oxygen species. Calcium then activates nitric oxide synthase to increase nitric oxide levels. Finally, calcium activates proteases, lipases, and endonucleases that can damage structural and functional elements in neuronal cells. Reactive oxygen species and nitric oxide also can form peroxynitrite by reacting with superoxide. Peroxynitrite is a powerful oxidant which has many and varied effects in neurons and other cell types, including depletion of cell thiol groups, lipid peroxidation, mobilization of cell calcium, impaired mitochondrial function correlated with muscular contractile failure in rat diaphragms, and modification of synaptic proteins.52-57 Uric acid is a peroxynitrite scavenger and protects cells against this powerful oxidant. In granule cells of the cerebellum, uric acid protects against CN-induced apoptotic...
220.127.116.11 Side Effects and Contraindications. Vincristine causes severe tissue necrosis upon extravasation (123).Neurotoxicity is a significant potential problem with vincristine and is often treated in part by reducing the dose of the drug (347). Myelosuppression also occurs but to a lesser extent and this effect should be monitored to prevent significant toxicity to the patient. Gout can occur with vincristine administration and can be controlled by use of allopuri-nol. The other side effects of vinblastine are common to antitumor agents (alopecia, ulceration, nausea, diarrhea, etc.).
See also The Importance of PRPP, De Novo Biosynthesis of Purine Nucleotides, Excessive Uric Acid in Purine Degradation, De Novo Pyrimidine Nucleotide Metabolism, Nucleotide Salvage Synthesis, Deoxyribonucleotide Biosynthesis, Biosynthesis of Thymine Deoxyribonucleotides, Salvage Routes to Deoxyribonucleotide Synthesis
In an attempt to improve on these clinical staging systems, a host of prognostic factors have been studied. In 1982 Rozman et al. (60) showed the prognostic value of the ALC in Rai stage I and II and in Binet stage A and B. Survival is shortened in both clinical stages when the ALC is greater than 50 x 109 cells L. In 1987 Lee et al. (61), using a regression model as well as uric acid and lactate dehydrogenase (LDH) levels, were able to separate risk groups within a given clinical Rai stage, but this approach does not appear to have been widely used (61). In 1987 Mandelli et al. (62) drew attention to the ALC ( 60 x 109 cells L) and the size of a given lymph node and spleen and likewise were able to improve on the present staging systems. It is of interest that they defined their first stage as a benign monoclonal lymphocytosis. Using plastic embedding methods, in 1974 Gray et al. (63) were one of the first groups to investigate bone marrow pattern
Remove sample from red cells after blood clots or plasma has been spun down. The peroxidase assay can be susceptible to increases in uric acid, ascorbic acid, bilirubin, hemoglobin, or other reducing substances. Samples should have only the normal amount of these substances present.
The role of peroxynitrite in the nerve degeneration causing multiple sclerosis (MS) has been brought into focus with the observation that patients with gout hardly ever develop MS, suggesting that the chronic uric acid elevation causing gout also prevents the development of MS.
The recognition of tumor cells and how the unmanipulated immune system can be activated in a developing tumor, even though tumor-specific antigens may be expressed as distinct recognition molecules on the surface of tumor cells, have been controversial topics in the oncology field. As a hypothesis of the so-called danger theory, discussed in detail in Chapter 3, it was considered that cellular transformation did not provide sufficient proinflammatory signals to activate the immune system in response to a developing tumor. In the absence of such signals, there is often no immune response, and tolerance may develop. However, studies have indicated that danger signals, such as buildup of uric acid, presence of potential toll-like receptor ligands (e.g., heat shock proteins), the occurrence of a ligand transfer molecule in the signaling cascade induced by CpG DNA, and the presence of extracellular matrix (ECM) derivatives, may induce proinflam-matory responses that activate innate immune...
Panel, uric acid, LDH, prothrombin time, partial thromboplastin time, fibrinogen, and chest X-ray (with posterior anterior and lateral views). HLA typing (serology) should also be performed in case a patient becomes alloimmunized to random donor platelet transfusions and requires HLA-matched platelets during his or her treatment course. HLA typing at the DNA level should be performed on any patient who may be a stem cell transplant candidate in the future. It is best for HLA typing to be done prior to the initiation of chemotherapy, when more cells are present. A multiple gated acquisition scan should be done to assess cardiac function, as induction chemotherapy regimens for AML include an anthracycline. In addition, an indwelling venous catheter (i.e., Hickman catheter) should be placed for blood draws, blood product transfusions, fluid management, and antibiotic administration.2 A lumbar puncture is not a routine part of the work-up unless there is clinical suspicion for CNS...
For carbohydrates and fats, the final metabolic oxidation products are the same as those found in physical oxidation (CO2 + H2O), while for proteins the metabolic products that are eliminated in the urine (urea, creatinine, uric acid, and other nitrogenous compounds) still contain energy.
His complete blood count (CBC) was normal the blood uric acid concentration was abnormally high. His urine specimen was very dark yellow with a high specific gravity of 1.034, pH of 5.0, and the presence of blood. The microscopic examination of the urine showed a moderate amount of red blood cells and a few white blood cells. Moderate levels of crystals were seen in the urine. The technologist checked the LIS. The patient had been diagnosed with urate nephrolithiasis in the past. The technologist knew that most renal calculi are calcium oxalate, calcium phosphate, uric acid, cystine, or a mixture of these substances.24
Several strategies have been developed to deal with hemolytic anemia. The most important is monitoring the Hb at wk 2 and 4, and monthly, while patients are on treatment. Because the hemolysis is dose-dependent, reduction of ribavirin dose is advisable when the Hb falls below 10 gm dL. Patients on 1200 mg of ribavirin should reduce to 800 mg, and those on 1000 mg should reduce to 600 mg d. The authors advise against attempting to increase the ribavirin dose after reduction, and there is evidence to suggest that the efficacy of ribavirin is still maintained with the reduced dose. If the Hb falls below 8.5 gm dL, the authors recommend stopping ribavirin completely. In certain situations, such as in patients with HIV co-infection and cirrhosis, when continuation of therapy may be warranted, erythropoetin, 40,000 U wk, can be used to maintain the Hb above 10 gm dL, and should be started once the Hb falls below 10 gm dL. The hemolytic effect of ribavirin can also be attenuated by the use...
The lignan podophyllotoxin (27) is an ancient folk remedy (classically used for treatment of gout) found in the May apple, Podophyllum peltatum (265,266).Interestingly podophyllotoxin binds to tubulin at a site distinct from that occupied by taxol and the vinca bases, although its molecular mode of action does not involve this in any obvious way, and modern clinical interest lies in its isomers instead. The isopodophyllotoxins are semisynthetic analogs resulting from acid-catalyzed reaction with suitably protected sugars followed by additional transformations. This results in attachment of the sugars to the ring system, with opposite stereochemistry to podophyllotoxin itself. Etoposide
Antioxidants provide protection against oxidative damage from reactive oxygen species, such as superoxides, hydroxyl radicals, hydrogen peroxide (see here). Biological compounds that provide such protection include substances, such as vitamin A, vitamin C, and vitamin E, uric acid, glutathione and enzymes, such as superoxide dismutase, catalase, glutathione peroxidase. Many antioxidants act by scavenging reactive oxygen molecules or by chemically reducing oxidized compounds.
The product of the kidneys is urine, a watery solution of waste products, salts, organic compounds, and two important nitrogen compounds uric acid and urea. Uric acid results from nucleic acid decomposition, and urea results from amino acid breakdown in the liver. Both of these nitrogen products can be poisonous to the body and must be removed in the urine.
The fluid moving from the distal tubules into the collecting duct contains materials not needed by the body. This fluid is referred to as urine. Urea, uric acid, salts, and other metabolic waste products are the main components of urine. The urine flows through the ureters toward the urinary bladder. When the bladder is full, the urine flows through the urethra to the exterior.
Several published studies (Ma et al., 1997 Moreira et al., 1997 Wolthuis et al., 1999) have examined the effects of HBOC-201 on routine clinical laboratory tests however, since instruments and methodologies change as techniques are developed and advancements are made, these data should be verified with current instrumentation. Wolthuis et al. (1999) found that HBOC-201 did not interfere with routine hemocytometry, hemostasis analysis or detection of RBC agglutination. HBOC-201 was found to affect direct bilirubin, creatine kinase MB-fraction, creatine kinase, gamma-glutamyl transferase, magnesium and uric acid analysis. A second study examined the concentration dependence of HBOC-201 interference on 22 chemistry tests performed with Ektachem Vitros and Hitachi analyzers (Moreira et al., 1997). Assays that were not color-dependent (sodium, potassium, chloride) were not affected by the presence of HBOC-201 in the specimens. Measurement of aspartate aminotransferase, calcium, urea...
Increased potassium excretion and the elevation of plasma uric acid levels, as was observed with the thiazides, are also seen with the loop diuretics. These diuretics also increase calcium and magnesium excretion. The calciuric action of these agents has led to their use in symptomatic hypercalcemia (301).Many of the hypersensitivity and metabolic disorders seen with the thiazides are also seen with loop diuretics. The development cf transient or permanent deafness is a serious but rare complication observed with this class of agents. It is believed to arise from the changes in electrolyte composition of the endolymph (302). It usually occurs when blood levels of these drugs are very high.
Hysteria, rheumatism, gangrene and gout. It has also been employed as an antidote to strychnia, but with doubtful results. It is regarded as a medicine in impotence (Dymock et al, 1890). The Hindus consider camphor to be aphrodisiacal, but the Muhammadans hold a contrary opinion both regard it as a valuable application to the eyelids in inflammatory conditions of the eye (Watt, 1885 Morton, 1977).
Tumor lysis syndrome is usually seen 1-5 days after the initiation of chemotherapy in patients with AML and high circulating blast counts.25 In response to chemotherapy, leukemic cells lyse, leading to hyper-phosphatemia, hyperkalemia (or hypokalemia), hypo-calcemia, an elevated lactate dehydrogenase (LDH), and hyperuricemia. Hyperuricemia results from breakdown of nucleotide precursors in leukemic cells to hypoxanthine and xanthine, and subsequent conversion to uric acid.25 Renal failure can occur secondary to precipitation of calcium phosphate crystals or uric acid in the renal tubules.25-28 Patients at risk for tumor lysis should be aggressively hydrated and started on allop-urinol. Allopurinol, an inhibitor of xanthine oxidase, decreases the production of uric acid.25 Rasburicase, a novel recombinant form of urate oxidase, converts uric acid to allantoin.25 Allantoin is five to ten times more soluble than uric acid, thus allowing for more rapid urinary excretion.25 29 Rasburicase...
Obstructive uropathy Ultrasonography is the technique of choice for initial evaluation of suspected obstructive uropathy. In addition to detection of hydronephrosis in a nonen-hanced study, CT can define the anatomic site, degree, and cause of obstruction with nonen-hancing imaging. Retroperitoneal fibrosis is suspected by increased attenuation within fat tissue that suggests encasement of the ureters. A dilated ureter is identified as a column of water surrounded by a thin tube. Extrinsic masses compressing the ureters, intraluminal masses, or stones may also be visualized. Regardless of composition, calculi have high attenuation rates (600 HU for calcium and 180 - 500 for uric acid) when compared to tissue (30 - 60 HU). Therefore, all uric acid and
Xanthine oxidase can oxidize xanthine further to uric acid, as well (Figure 22.7) Allopurinol, which is similar to hypoxanthine (see here), is used to treat gout because it inhibits xanthine oxidase, leading to accumulation of hypoxanthine and xanthine, both of which are more soluble and more readily excreted than uric acid (the causative agent of gout). See also Purine Degradation, Excessive Uric Acid in Purine Degradation Allopurinol is a drug that is used to treat gout. It is similar to hypoxanthine (see here) and inhibits xanthine oxidase, leading to accumulation of hypoxanthine and xanthine, both of which are more soluble and more readily excreted than uric acid, the compound responsible for causing gout. See also Excessive Uric Acid in Purine Degradation
With many drugs there are differences in pharmacodynamics and pharmacokinetics according to whether their use is in a single dose or over a brief period (acute pharmacology) or long term (chronic pharmacology). The proportion of the population taking drugs continuously for large portions of their lives increases as tolerable suppressive and prophylactic remedies for chronic or recurrent conditions are developed e.g. for arterial hypertension, diabetes mellitus, mental diseases, epilepsies, gout, collagen diseases, thrombosis, allergies and various infections. In some cases long-term treatment introduces significant hazard into patients' lives and the cure can be worse than the disease if it is not skilfully managed. In general the dangers of a drug are not markedly increased if therapy lasts years rather than months exceptions include renal damage due to analgesic mixtures, and carcinogenicity.
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