Home Remedies for Gout
Mucosal organisms or their breakdown products may permeate the intestinal wall if the mucosal barrier function is breached. This barrier may be compromised by many pathological states and processes. The mucosa at the tip of the villi are particularly prone to ischaemia due to the counter-current exchange mechanism of the vessels. Shunting of blood during low flow states may lead to ischaemia affecting the tips of the villi alone. Subtle mucosal damage, which is only detectable microscopically, may occur following mild ischaemia. In transient hypoperfusion or hypoxia, the mucosal injury is more pronounced during reperfusion when the oxygen supply is re-established. This is due to damage by the putative deleterious oxygen radicals which are generated mainly via the xanthine oxidase pathway. Xanthine oxidase occurs naturally as the dehydrogenase but in ischaemia it is converted by proteolysis to the oxidase form. This latter form then catalyses a reaction which utilizes oxygen to convert...
Like many other groups of birds, hornbills are hunted for food and consumed for medicine. In Africa, parts of the ground-hornbill are eaten to improve health and sagacity, whereas in India, the great hornbill, the Indian pied hornbill, and the Indian gray hornbill are rendered into oils that supposedly aid in childbirth and relieve gout and joint pains. In Indonesia, the meat of the Sumba hornbill is roasted and eaten to relieve rheumatism and asthma. Because they are easily tamed, hornbills are captured and traded for pets or exhibition. Unlike any other group of birds, however, hornbills play special roles in the folklore and ceremonies of the countries where they occur. Long, elegant tail feathers are the most sought-after hornbill part, but heads and casques are also coveted. The Nishis people of Arunachal Pradesh, India, attach the upper beak of the great hornbill to rattan bopiah caps as traditional male headgear. Neighboring Wanchos of eastern Arunachal use the warm,...
As mentioned, lithium represents a common treatment for bipolar disorder. Lithium salts were first used therapeutically in the nineteenth century as remedies for sleeplessness and gout. Since the report of their efficacy in the treatment of bipolar disorder in the late 1940s by John Cade, lithium has been widely used in the treatment of acute manic symptoms and mood episode prophylaxis 21 . As mentioned, a number of double-blind studies have confirmed lithium's efficacy both in the acute treatment of mania, and for mania prophylaxis 14 . Further, multiple studies have suggested that lithium may be useful for both the acute and prophylactic treatment of depression (see 22 and 23 for meta-analysis and review). Unfortunately, many of the studies addressing monotherapy antidepressant effects had with some methodological shortcomings in particular, low sample sizes and the use of crossover study designs. In clinical experience, lithium's antidepressant effects as monotherapy may be modest,...
Xanthine oxidase (XO EC 22.214.171.124) catalyzes the oxidation of hypoxanthine and xanthine to uric acid (Structure 1), Hypoxanthine + H2O + O2 uric acid + H2O2 neously isomerizes to some keto form of xanthine that can be catalyzed by XO to the enol form of uric acid, which then spontaneously isomerizes to some keto form of uric acid. The isomeric forms of the substrates make interpretation of the kinetic results difficult, as the enol form of xanthine and the keto form of uric acid may be competitive inhibitors of XO. Other purines and adenine are oxidized more slowly (Table 1). A number of aldehydes (Table 1) are oxidized also to the corresponding carboxylic acids by XO. Xanthine + NAD+ uric acid + NADH + H+ (2) Xanthine + O2 uric acid + H2O2 (3)
In 1902, Schardinger (11) determined that fresh milk decolorized Methylene Blue. In 1922, Morgan et al. (12) reported that bovine milk converted hypoxanthine and xanthine into uric acid under both aerobic and anaerobic (when Methylene Blue was included) conditions. They found the same activity in liver, spleen, and lungs of rats and cows. The activity, which they named xanthine oxidase,'' was destroyed by boiling. In 1924, Dixon and Thurlow (13) partially purified XO and did
A number of methods are available to determine XO activity. Using xanthine as the substrate, the rate of oxidation of xanthine to uric acid can be followed by the rate of Methylene Blue reduction (under anaerobic conditions), by cytochrome c reduction (aerobically), by oxygen uptake (oxygen electrode use), or by the rate of uric acid formation (increase in absorbance at 290 nm). The easiest, and perhaps best assay is to follow the rate of uric acid formation from xanthine, in the presence of O2, in a recording spectrophotometer at 290 nm, pH 8.3, 25 C (8). The molar extinction coefficient, em, 9.6 x 103 M-1 cm-1. xanthine + O2 uric acid + H2O2 (8) Only initial rates should be used ( 5 conversion of xanthine to uric acid) in analyses, as H2O2 slowly inactivates the enzyme. Catalase can be added to remove the H2O2 when reaction times need to be extended (when low concentrations of XO are present).
In a very limited number of experimentally-induced models of cell death, GRP94 is released during necrotic, but not apoptotic, cell death (Basu et al., 2000 Berwin et al., 2001). These findings are of particular interest to the Danger Model (Matzinger, 2002), and the molecular identification of pathological cell death-derived molecular signals, such as uric acid and lysophosphatidyl choline (lyso-PC) (Lauber et al., 2003 Shi et al., 2003). Uric acid and lyso-PC have been shown to stimulate macrophage migration and the activation of macrophage pro-inflammatory responses (Lauber et al., 2003 Shi et al., 2003). However, there is controversy as to whether apoptotic cells themselves, though through different signals, are also capable of eliciting an inflammatory response (Gallucci and Matzinger, 2001 Ip and Lau, 2004).
PRV is frequently discovered incidentally when a complete blood count is performed for another reason. When symptoms are present, they are usually nonspecific. Fatigue, headache, and diaphoresis are common. Pruritis, often following a hot shower, is a frequent complaint. Up to 15 of patients may present with a thrombotic episode. Thrombotic cerebrovascular accidents, coronary artery thrombosis, Budd-Chiari syndrome, and pulmonary embolus all occur. Cavernous sinus thrombosis may also occur in untreated or poorly controlled disease. Erythromelalgia is specific to PRV and ET, and it is associated with an elevated platelet count and paradoxical vasodilation. It is characterized by redness, warmth, and a burning pain affecting the digits and responds promptly to aspirin. Gout may be a presenting manifestation of an MPD. There is an increased incidence of peptic ulcer disease in patients with PRV. Iron deficiency may occur and may initially mask the diagnosis. An elevated hematocrit with...
When evaluating the triggering agent, it must be observed that other medicaments could have caused the crystalluria, and only resulted in nephrolithiasis on combination with indinavir (e.g. ampicillin, acyclovir, aspirine, ciprofloxacin, methotrexate, vitamin C, sulfonamide and also other drugs that lead to an increase in uric acid).
The most common adverse event associated with patients receiving filgrastim relative to placebo-treated patients is bone pain (15-39 vs 0-21 ) (93). This dose-related adverse event appears to begin shortly after beginning treatment with filgrastim and may occur again or worsen just before neutrophilic recovery among patients who have previously received myelosuppressive chemotherapy (93). Both filgrastim and sargramostim can cause benign transient increases in serum concentrations of lactic dehydrogenase (LDH), alkaline phosphatase, and uric acid. Although the mechanisms of these increases are poorly understood, they are probably related to increased cell turnover in chemotherapy (94). The administration of sargramostim is associated with heightened activities of several cytokines (such as IL-1, IL-6, tumor necrosis factor-a, and leukotrienes), which may explain some of the asymmetry in that HGF's adverse event profile relative to that of filgrastim. In particular, the presence of...
To understand bat body adaptations for flight, it may be instructive to examine bird bodies. Bird bodies are designed for mass reduction. They do this in a number of ways. They have lost teeth and the accompanying heavy jaws and jaw musculature over evolutionary time. They have thin, hollow, and strong bones. Many bones are fused or reduced in size. The long bony tail of their ancestors has been greatly reduced to the small vestigial pygostyle. Birds have a series of air sacs in the body that serve to reduce weight. They do not have a urinary bladder to store urine nor do they have a urethra. The kidneys excrete uric acid into the cloaca where it is mixed with intestinal contents to produce the white guano associated with birds. Birds have lost one ovary, and lay eggs so they do not have to carry a fetus. The most distinctive feature of birds is their feathers, which provide lift, insulate them against heat or cold, streamline the body, and reduce mass.
Xanthine oxidase (XO, EC 126.96.36.199 see Chapters 19 and 42 for detailed information) is widely distributed in animals, plants, and microorganisms. It catalyzes the oxidation of hypoxanthine to xanthine and xanthine into uric acid. In addition XO is able to oxidize a wide range of purines, aldehydes, and pteridines with concomitant reduction of O2 to H2O2. Under certain conditions XO also produces the highly reactive superoxide anion. Bovine milk is very rich in XO
GRP94 is acting an innate immune adjuvant than as a cross-presentation antigen. This conclusion is, however, far from established and is, as noted, controversial. An open question that remains is whether or not GRP94 elicits this activation alone or only in concert with other danger signals. Available data demonstrate that tumor-derived peptides are not per se required for function however, in these experiments, GRP94 was provided to the mouse in the presence of irradiated, i.e., dying cells. As such, cells would be expected to release many of the well characterized danger signals, including uric acid and lysophosphatidyl choline. The precise molecular basis for immune activation remains to be defined.
Colchicine (from the autumn crocus Colchicium autumnale L., an alpine flower) is used to treat acute gout, but can also arrest cells in metaphase by tubulin-depolymerisation. Metaphase-cells have their chromosomes fully condensed and aligned at the equatorial plate of the cell. Thus white blood cells or amniotic cells, stimulated into mitosis by phytohaemagglutinin and
Carbohydrate has a protein-sparing effect. However, dietary protein intake must be balanced, as large amounts can cause gout or kidney stones in some individuals, as purine breaks down to uric acid, and high concentrations can crystallize in the kidneys and joints. Moreover, excess nitrogen is a burden for the kidneys and animal food proteins are also rich in fat, especially saturated types, which cause cardiovascular disease and obesity. According to the ADA dietary guidelines, 'the intake of protein in the usual range does not appear to be associated with the development of diabetic nephropathy, although it is advisable to avoid intakes superior to 20 per cent of the total daily energy'.
Both filgrastim and rHuGM-CSF have been safe and well tolerated in patients with hematologic toxicities. Medullary bone pain, reported in up to 24 of patients, was the only consistently observed adverse reaction attributed to filgrastim therapy. Mild-to-moderate spontaneously reversible increases in uric acid, lactate dehydrogenase, and alkaline phosphatase have been reported in filgrastim-treated patients (27-58 of patients) (38,65-72).
Dose-dependent, predictable, and spontaneously reversible increases in serum alkaline phosphatase, lactic dehydrogenase, and uric acid were reported. No serious clinical sequelae were reported in association with biochemistry abnormalities.
Free radical production is enhanced in both the ischemic core and penumbral following stroke injury, and this is believed to cause much of the damage seen in the core as well as penumbra. There are many agents that either block free radical production or inhibit its activation that have been shown to be very effective in experimental models. Uric acid is a well-known natural antioxidant present in fluids and tissues. Administration of uric acid resulted in a highly significant reduction in ischemic damage and improved behavioral outcome (Yu et al., 1998). Edaravone, Tetramethylpyrazine, alpha-phenyl-N-tert-butyl-nitrone, FR210575, and NXY-59 are other free radical inhibitors that were effective against experimental stroke injury. EGb-761 is a free radical scavenger derived from a concentrated extract of Ginkgo that is currently in a phase 2 clinical trial (Legos et al., 2002). Clinical trials with free radical scavengers have had limited success after acute ischemic stroke, but have...
10.5.7 xanthine oxidase and uric acid Xanthine oxidoreductase (XOR), a metalloflavoprotein, catalyzes the oxidation of the purine bases hypoxanthine and xanthine to uric acid. XOR is a site for ROS generation in the cell (128) (Figure 10.1). High levels of XOR activity resulting in ROS production has now been shown to play an important role in reperfusion injury and in congestive heart failure (129). Xanthine oxidase and its reaction product uric acid are therefore now considered to be important biomarkers for oxidative stress and cardiovascular diseases (129,130). Uric acid in urine, serum, and plasma is measured using a spectrophotometric assay based on phosphotungstic acid reagent (131) however, for improved specificity and characterization, HPLC methods have been used recently (132,133). The most popular assay method for xanthine oxidoreduc-tase involves the spectrophotometric measurement of urate production at 292 nm, using xanthine or hypoxanthine as the substrate (134). A...
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