The Biotech Medical Laboratories & Research Center

12/05/2019

25/09/2013

Urinalysis
Urinalysis can reveal diseases that have gone unnoticed because they do not produce striking signs or symptoms. Examples include diabetes mellitus, various forms of glomerulonephritis, and chronic urinary tract infections.
The most cost-effective device used to screen urine is a paper or plastic dipstick. This microchemistry system has been available for many years and allows qualitative and semi-quantitative analysis within one minute by simple but careful observation. The color change occurring on each segment of the strip is compared to a color chart to obtain results. However, a careless doctor, nurse, or assistant is entirely capable of misreading or misinterpreting the results. Microscopic urinalysis requires only a relatively inexpensive light microscope.
MACROSCOPIC URINALYSIS
The first part of a urinalysis is direct visual observation. Normal, fresh urine is pale to dark yellow or amber in color and clear. Normal urine volume is 750 to 2000 ml/24hr.
Turbidity or cloudiness may be caused by excessive cellular material or protein in the urine or may develop from crystallization or precipitation of salts upon standing at room temperature or in the refrigerator. Clearing of the specimen after addition of a small amount of acid indicates that precipitation of salts is the probable cause of tubidity.
A red or red-brown (abnormal) color could be from a food dye, eating fresh beets, a drug, or the presence of either hemoglobin or myoglobin. If the sample contained many red blood cells, it would be cloudy as well as red.
URINE DIPSTICK CHEMICAL ANALYSIS
pH
The glomerular filtrate of blood plasma is usually acidified by renal tubules and collecting ducts from a pH of 7.4 to about 6 in the final urine. However, depending on the acid-base status, urinary pH may range from as low as 4.5 to as high as 8.0. The change to the acid side of 7.4 is accomplished in the distal convoluted tubule and the collecting duct.
Specific Gravity (sp gr)
Specific gravity (which is directly proportional to urine osmolality which measures solute concentration) measures urine density, or the ability of the kidney to concentrate or dilute the urine over that of plasma. Dipsticks are available that also measure specific gravity in approximations. Most laboratories measure specific gravity with a refractometer.
Specific gravity between 1.002 and 1.035 on a random sample should be considered normal if kidney function is normal. Since the sp gr of the glomerular filtrate in Bowman's space ranges from 1.007 to 1.010, any measurement below this range indicates hydration and any measurement above it indicates relative dehydration.
If sp gr is not > 1.022 after a 12 hour period without food or water, renal concentrating ability is impaired and the patient either has generalized renal impairment or nephrogenic diabetes insipidus. In end-stage renal disease, sp gr tends to become 1.007 to 1.010.
Any urine having a specific gravity over 1.035 is either contaminated, contains very high levels of glucose, or the patient may have recently received high density radiopaque dyes intravenously for radiographic studies or low molecular weight dextran solutions. Subtract 0.004 for every 1% glucose to determine non-glucose solute concentration.
Protein
Dipstick screening for protein is done on whole urine, but semi-quantitative tests for urine protein should be performed on the supernatant of centrifuged urine since the cells suspended in normal urine can produce a falsely high estimation of protein. Normally, only small plasma proteins filtered at the glomerulus are reabsorbed by the renal tubule. However, a small amount of filtered plasma proteins and protein secreted by the nephron (Tamm-Horsfall protein) can be found in normal urine. Normal total protein excretion does not usually exceed 150 mg/24 hours or 10 mg/100 ml in any single specimen. More than 150 mg/day is defined as proteinuria. Proteinuria > 3.5 gm/24 hours is severe and known as nephrotic syndrome.
Dipsticks detect protein by production of color with an indicator dye, Bromphenol blue, which is most sensitive to albumin but detects globulins and Bence-Jones protein poorly. Precipitation by heat is a better semiquantitative method, but overall, it is not a highly sensitive test. The sulfosalicylic acid test is a more sensitive precipitation test. It can detect albumin, globulins, and Bence-Jones protein at low concentrations.
In rough terms, trace positive results (which represent a slightly hazy appearance in urine) are equivalent to 10 mg/100 ml or about 150 mg/24 hours (the upper limit of normal). 1+ corresponds to about 200-500 mg/24 hours, a 2+ to 0.5-1.5 gm/24 hours, a 3+ to 2-5 gm/24 hours, and a 4+ represents 7 gm/24 hours or greater.
Glucose
Less than 0.1% of glucose normally filtered by the glomerulus appears in urine (< 130 mg/24 hr). Glycosuria (excess sugar in urine) generally means diabetes mellitus. Dipsticks employing the glucose oxidase reaction for screening are specific for glucos glucose but can miss other reducing sugars such as galactose and fructose. For this reason, most newborn and infant urines are routinely screened for reducing sugars by methods other than glucose oxidase (such as the Clinitest, a modified Benedict's copper reduction test).

Ketones
Ketones (acetone, aceotacetic acid, beta-hydroxybutyric acid) resulting from either diabetic ketosis or some other form of calorie deprivation (starvation), are easily detected using either dipsticks or test tablets containing sodium nitroprusside.
Nitrite
A positive nitrite test indicates that bacteria may be present in significant numbers in urine. Gram negative rods such as E. coli are more likely to give a positive test.
Leukocyte Esterase
A positive leukocyte esterase test results from the presence of white blood cells either as whole cells or as lysed cells. Pyuria can be detected even if the urine sample contains damaged or lysed WBC's. A negative leukocyte esterase test means that an infection is unlikely and that, without additional evidence of urinary tract infection, microscopic exam and/or urine culture need not be done to rule out significant bacteriuria.

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MICROSCOPIC URINALYSIS
Methodology
A sample of well-mixed urine (usually 10-15 ml) is centrifuged in a test tube at relatively low speed (about 2-3,000 rpm) for 5-10 minutes until a moderately cohesive button is produced at the bottom of the tube. The supernate is decanted and a volume of 0.2 to 0.5 ml is left inside the tube. The sediment is resuspended in the remaining supernate by flicking the bottom of the tube several times. A drop of resuspended sediment is poured onto a glass slide and coverslipped.

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Examination
The sediment is first examined under low power to identify most crystals, casts, squamous cells, and other large objects. The numbers of casts seen are usually reported as number of each type found per low power field (LPF). Example: 5-10 hyaline casts/L casts/LPF. Since the number of elements found in each field may vary considerably from one field to another, several fields are averaged. Next, examination is carried out at high power to identify crystals, cells, and bacteria. The various types of cells are usually described as the number of each type found per average high power field (HPF). Example: 1-5 WBC/HPF.

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Red Blood Cells
Hematuria is the presence of abnormal numbers of red cells in urine due to: glomerular damage, tumors which erode the urinary tract anywhere along its length, kidney trauma, urinary tract stones, renal infarcts, acute tubular necrosis, upper and lower uri urinary tract infections, nephrotoxins, and physical stress. Red cells may also contaminate the urine from the va**na in menstruating women or from trauma produced by bladder catherization. Theoretically, no red cells should be found, but some find their way into the urine even in very healthy individuals. However, if one or more red cells can be found in every high power field, and if contamination can be ruled out, the specimen is probably abnormal.

RBC's may appear normally shaped, swollen by dilute urine (in fact, only cell ghosts and free hemoglobin may remain), or crenated by concentrated urine. Both swollen, partly hemolyzed RBC's and crenated RBC's are sometimes difficult to distinguish from WBC's in the urine. In addition, red cell ghosts may simulate yeast. The presence of dysmorphic RBC's in urine suggests a glomerular disease such as a glomerulonephritis. Dysmorphic RBC's have odd shapes as a consequence of being distorted via passage through the abnormal glomerular structure.
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White Blood Cells
Pyuria refers to the presence of abnormal numbers of leukocytes that may appear with infection in either the upper or lower urinary tract or with acute glomerulonephritis. Usually, the WBC's are granulocytes. White cells from the va**na, especially in the presence of va**nal and cervical infections, or the external urethral meatus in men and women may contaminate the urine.

If two or more leukocytes per each high power field appear in non-contaminated urine, the specimen is probably abnormal. Leukocytes have lobed nuclei and granular cytoplasm.
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Epithelial Cells
Renal tubular epithelial cells, usually larger than granulocytes, contain a large round or oval nucleus and normally slough into the urine in small numbers. However, with nephrotic syndrome and in conditions leading to tubular degeneration, the number sloughed is increased.

When lipiduria occurs, these cells contain endogenous fats. When filled with numerous fat droplets, such cells are called oval fat bodies. Oval fat bodies exhibit a "Maltese cross" configuration by polarized light microscopy.
Transitional epithelial cells from the renal pelvis, ureter, or bladder have more regular cell borders, larger nuclei, and smaller overall size than squamous epithelium. Renal tubular epithelial cells are smaller and rounder than transitional epithelium, and their nucleus occupies more of the total cell volume.

Squamous epithelial cells from the skin surface or from the outer urethra can appear in urine.

Their significance is that they represent possible contamination of the specimen with skin flora.
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Casts
Urinary casts are formed only in the distal convoluted tubule (DCT) or the collecting duct (distal nephron). The proximal convoluted tubule (PCT) and loop of Henle are not locations for cast formation. Hyaline casts are composed primarily of a mucoprotein (Tamm-Horsfall protein) secreted by tubule cells. The Tamm-Horsfall protein secretion (green dots) is illustrated in the diagram below, forming a hyaline cast in the collecting duct:

Even with glomerular injury causing increased glomerular permeability to plasma proteins with resulting proteinuria, most matrix or "glue" that cements urinary casts together is Tamm-Horsfall mucoprotein, although albumin and some globulins are also incorporated. An example of glomerular inflammation with leakage of RBC's to produce a red blood cell cast is shown in the diagram below:

The factors which favor protein cast formation are low flow rate, high salt concentration, and low pH, all of which favor protein denaturation and precipitation, particularly that of the Tamm-Horsfall protein. Protein casts with long, thin tails formed at the junction of Henle's loop and the distal convoluted tubule are called cylindroids. Hyaline casts can be seen even in healthy patients.

Red blood cells may stick together and form red blood cell casts. Such casts are indicative of glomerulonephritis, with leakage of RBC's from glomeruli, or severe tubular damage.

White blood cell casts are most typical for acute pyelonephritis, but they may also be present with glomerulonephritis. Their presence indicates inflammation of the kidney, because such casts will not form except in the kidney.

When cellular casts remain in the nephron for some time before they are flushed into the bladder urine, the cells may degenerate to become a coarsely granular cast, later a finely granular cast, and ultimately, a waxy cast. Granular and waxy casts are be believed to derive from renal tubular cell casts. Broad casts are believed to emanate from damaged and dilated tubules and are therefore seen in end-stage chronic renal disease.



The so-called telescoped urinary sediment is one in which red cells, white cells, oval fat bodies, and all types of casts are found in more or less equal profusion. The conditions which may lead to a telescoped sediment are: 1) lupus nephritis 2) malignant hypertension 3) diabetic glomerulosclerosis, and 4) rapidly progressive glomerulonephritis.
In end-stage kidney disease of any cause, the urinary sediment often becomes very scant because few remaining nephrons produce dilute urine.
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Bacteria
Bacteria are common in urine specimens because of the abundant normal microbial flora of the va**na or external urethral meatus and because of their ability to rapidly multiply in urine standing at room temperature. Therefore, microbial organisms found in all but the most scrupulously collected urines should be interpreted in view of clinical symptoms.
Diagnosis of bacteriuria in a case of suspected urinary tract infection requires culture. A colony count may also be done to see if significant numbers of bacteria are present. Generally, more than 100,000/ml of one organism reflects significant bacteriuria. Multiple organisms reflect contamination. However, the presence of any organism in catheterized or suprapubic tap specimens should be considered significant.

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Yeast
Yeast cells may be contaminants or represent a true yeast infection. They are often difficult to distinguish from red cells and amorphous crystals but are distinguished by their tendency to bud. Most often they are Candida, which may colonize bladder, urethra, or va**na.


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Crystals
Common crystals seen even in healthy patients include calcium oxalate, triple phosphate crystals and amorphous phosphates.

Very uncommon crystals include: cystine crystals in urine of neonates with congenital cystinuria or severe liver disease, tyrosine crystals with congenital tyrosinosis or marked liver impairment, or leucine crystals in patients with severe liver disease or with maple syrup urine disease.
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Miscellaneous
General "crud" or unidentifiable objects may find their way into a specimen, particularly those that patients bring from home.
Spermatozoa can sometimes be seen. Rarely, pinworm ova may contaminate the urine. In Egypt, ova from bladder infestations with schistosomiasis may be seen.

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METHODS OF URINE COLLECTION
1. Random collection taken at any time of day with no precautions regarding contamination. The sample may be dilute, isotonic, or hypertonic and may contain white cells, bacteria, and squamous epithelium as contaminants. In females, the specimen may cont contain va**nal contaminants such as trichomonads, yeast, and during me**es, red cells.
2. Early morning collection of the sample before ingestion of any fluid. This is usually hypertonic and reflects the ability of the kidney to concentrate urine during dehydration which occurs overnight. If all fluid ingestion has been avoided since 6 p.m. the previous day, the specific gravity usually exceeds 1.022 in healthy individuals.
3. Clean-catch, midstream urine specimen collected after cleansing the external urethral meatus. A cotton sponge soaked with benzalkonium hydrochloride is useful and non-irritating for this purpose. A midstream urine is one in which the first half of the bladder urine is discarded and the collection vessel is introduced into the urinary stream to catch the last half. The first half of the stream serves to flush contaminating cells and microbes from the outer urethra prior to collection. This sounds easy, but it isn't (try it yourself before criticizing the patient).
4. Catherization of the bladder through the urethra for urine collection is carried out only in special circumstances, i.e., in a comatose or confused patient. This procedure risks introducing infection and traumatizing the urethra and bladder, thus producing iatrogenic infection or hematuria.
5. Suprapubic transabdominal needle aspiration of the bladder. When done under ideal conditions, this provides the purest sampling of bladder urine. This is a good method for infants and small children.
Summary
To summarize, a properly collected clean-catch, midstream urine after cleansing of the urethral meatus is adequate for complete urinalysis. In fact, these specimens generally suffice even for urine culture. A period of dehydration may precede urine collection if testing of renal concentration is desired, but any specific gravity > 1.022 measured in a randomly collected specimen denotes adequate renal concentration so long as there are no abnormal solutes in the urine.
Another important factor is the interval of time which elapses from collection to examination in the laboratory. Changes which occur with time after collection include: 1) decreased clarity due to crystallization of solutes, 2) rising pH, 3) loss of ketone bodies, 4) loss of bilirubin, 5) dissolution of cells and casts, and 6) overgrowth of contaminating microorganisms. Generally, urinalysis may not reflect the findings of absolutely fresh urine if the sample is > 1 hour old. Therefore, get the urine to the laboratory as quickly as possible.

23/09/2013

;)

22/09/2013

Alhamdulillah camp is end and we are received 567patient for screening of hepatitis b and c

22/09/2013

Today on 22-September-2013 organized the Free Medical Camp with Dr. Nasir Habib at Khayaban-e-Sir Syed. We are perform the Hepatitis B & C, Sugar, Complete Blood Picture, ALT on the Camp

19/09/2013

INR Test

The INR is a test of blood clotting, which is primarily used to monitor warfarin therapy, where the aim is to maintain an elevated INR in a certain range eg, 2.0 to 3.0. It is initially checked frequently, but as treatment is stabilised it may be done less often, eg fortnightly. Changes in the warfarin dose take several days to affect the INR result.
How the Test is Performed

The INR Test is a blood test and requires a small tube of blood from a vein – approximately 4 millilitres. It is important that the tube is filled to the correct level, otherwise false results may occur.
Medical Conditions and Symptoms

The INR is usually monitored as part of warfarin therapy, but it may also be checked by your doctor in relation to Liver Function Tests, because liver dysfunction can lead to decreased production of certain clotting factors.
The commoner reasons for warfarin therapy are:

Deep Venous Thrombosis (DVT) – a clot in a deep vein, commonly of the leg
Pulmonary Embolism (PE) – a clot in the lung, that has travelled through the veins (“embolised”) from a DVT formed elsewhere, such as the deep veins of the leg or pelvis
Atrial Fibrillation (AF) – an irregular heartbeat, sometimes accompanied by an enlarged left atrium – both of which predispose to the formation of blood clots in the heart, which may embolise to the blood vessels of the brain causing a cerebral infarction, a stroke – also known as a CerebroVascular Accident (CVA)
Some cases of Heart failure (LVF =Left Ventricular Failure or CCF =Congestive Cardiac Failure), especially when the heart is enlarged as in some forms of cardiomyopathy.
Artificial heart valves of the mechanical type – because of the risk of a clot forming on the valve and causing a blockage in the heart.

Test Results Explained

The INR test result is given as a number. There are no units of measurement because the number is a ratio: the ratio of the sample’s Prothrombin Time (PT – a measure of clotting), to the Prothrombin Time of a normal sample of blood. A result of 1.0, up to 1.5, is therefore normal.
People on warfarin treatment will have different target INR ranges to aim for with warfarin treatment, depending on the reason for anticoagulation (blood-thinning treatment). One example is a range of 2.0 to 3.0 for DVT.
An INR lower than the desired range means the blood is “not thin enough” or clots too easily. An INR result higher than the desired range means the blood is “too thin”.
Warfarin doses are adjusted, initially every few days, aiming for the desired target range of INR. As treatment is stabilised it may be done less often, eg fortnightly. Changes in the warfarin dose take several days to affect the INR result. Patients on warfarin treatment will usually be advised by telephone by their doctor, or by the laboratory doing the INR test, on whether to change their warfarin dose, or exactly what dose to take, based on the INR result. The result needs to be taken in context of recent INR measurements and dose changes. There are many medications that can affect the INR, and even a change in diet can result in changes to the INR – either raising or lowering it.
Related Specialists

General Practitioner (GP)
Haematologist
Cardiologist
General Physician
Cardiothoracic Surgeon
Vascular Surgeon
Neurologist
Hepatologist
Intensivist
Emergency Physician
Oncologist
Respiratory Physician

Related Procedures

Blood Test (venesection)

Related Tests

PT
APTT
Coagulation Profile
Blood Group or Crossmatch
D-Dimer
Full Blood Count
Liver Function Tests
Platelet Count
CT Pulmonary Angiogram (CTPA)
Carotid Doppler Ultrasound Scan
Echocardiogram (Echo) (Ultrasound)
Legs Doppler Ultrasound Scan
Chest X-Ray (CXR)
Electrocardiogram (ECG)
VQ Scan (Ventilation-Perfusion Scan)

Also Known As

Prothrombin Time (PT)
PT ratio

Links

Wikipedia – Prothrombin Time
ClotCare Online Resource – FAQs about Warfarin
Lab Tests Online – PT and INR

29/08/2013

Gout
Definition
Gout is a form of acute arthritis that causes severe pain and swelling in the joints. It most commonly affects the big toe, but may also affect the heel, ankle, hand, wrist, or elbow. It affects the spine often enough to be a factor in back pain. Gout usually comes on suddenly, goes away after 5-10 days, and can keep recurring. Gout is different from other forms of arthritis because it occurs when there are high levels of uric acid circulating in the blood, which can cause urate crystals to settle in the tissues of the joints.
Description
Uric acid, which is found naturally in the blood stream, is formed as the body breaks down waste products, mainly those containing purine, a substance that is produced by the body and is also found in high concentrations in some foods, including brains, liver, sardines, anchovies, and dried peas and beans. Normally, the kidneys filter uric acid out of the blood and excrete it in the urine. Sometimes, however, the body produces too much uric acid or the kidneys aren't efficient enough at filtering it from the blood, and it builds up in the blood stream, a condition known as hyperuricemia. A person's susceptibility to gout may increase because of the inheritance of certain genes or from being overweight and eating a rich diet. In some cases, another disease (such as lymphoma, leukemia, or hemolytic anemia) may be the underlying cause of the uric acid buildup that results in gout. An additional factor is occupational or environmental; it is now known that chronic exposure to high levels of lead decreases the body's excretion of urates, allowing uric acid to accumulate in the blood.
Hyperuricemia doesn't always cause gout. Over the course of years, however, sharp urate crystals build up in the synovial fluid of the joints. Often, some precipitating event, such as an infection, surgery, the stress of hospitalization, a stubbed toe, or even a heavy drinking binge can cause inflammation. White blood cells, mistaking the urate crystals for a foreign invader, flood into the joint and surround the crystals, causing inflammation—in other words, the redness, swelling, and pain that are the hallmarks of a gout attack.
Causes and symptoms
As a result of high levels of uric acid in the blood, needle-like urate crystals gradually accumulate in the joints. Urate crystals may be present in the joint for a long time without causing symptoms. Infection, injury to the joint, surgery, drinking too much, or eating the wrong kinds of foods may suddenly bring on the symptoms, which include pain, tenderness, redness, warmth, and swelling of the joint. In many cases, the gout attack begins in the middle of the night. The pain is often so excruciating that the sufferer cannot bear weight on the joint or tolerate the pressure of bedcovers. The inflamed skin over the joint may be red, shiny, and dry, and the inflammation may be accompanied by a mild fever. These symptoms may go away in about a week and disappear for months or years at a time. However, over the course of time, attacks of gout recur more and more frequently, last longer, and affect more joints. Eventually, stone-like deposits known as tophi may build up in the joints, ligaments, and tendons, leading to permanent joint deformity and decreased motion. (In addition to causing the tophi associated with gout, hyperuricemia can also cause kidney stones, also called renal calculi or uroliths.)
Gout affects an estimated one million Americans; according to the National Institutes of Health, it accounts for about 5% of all cases of arthritis. It occurs more often in men than in women; the s*x ratio is about 4:1. Uric-acid levels tend to increase in men at puberty, and, because it takes 20 years of hyperuricemia to cause gout symptoms, men commonly develop gout in their late 30s or early 40s. Women more typically develop gout later in life, starting in their 60s. According to some medical experts, estrogen protects against hyperuricemia, and when estrogen levels fall during menopause, urate crystals can begin to build up in the joints. Excess body weight, regular excessive alcohol intake, the use of blood pressure medications called diuretics, and high levels of certain fatty substances in the blood (serum triglycerides) associated with an increased risk of heart disease can all increase a person's risk of developing gout.
Gout appears to be on the increase in the American population. According to a study published in November 2002, there was a twofold increase in the incidence of gout over the 20 years between 1977 and 1997. It is not yet known whether this increase is the result of improved diagnosis or whether it is associated with risk factors that have not yet been identified.
Diagnosis
Usually, physicians can diagnose gout based on the physical examination and medical history (the patient's description of symptoms and other information). Doctors can also administer a test that measures the level of uric acid in the blood. While normal uric acid levels don't necessarily rule out gout and high levels don't confirm it, the presence of hyperuricemia increases the likelihood of gout. The development of a tophus can confirm the diagnosis of gout. The most definitive way to diagnose gout is
Gout, a form of acute arthritis, most commonly occurs in the big toe. It is caused by high levels of uric acid in the blood, in which urate crystals settle in the tissues of the joints and produce severe pain and swelling.
Gout, a form of acute arthritis, most commonly occurs in the big toe. It is caused by high levels of uric acid in the blood, in which urate crystals settle in the tissues of the joints and produce severe pain and swelling.
(Illustration by Electronic Illustrators Group.)
to take a sample of fluid from the joint and test it for urate crystals.
Treatment
The goals of treatment for gout consist of alleviating pain, avoiding severe attacks in the future, and preventing long-term joint damage. In addition to taking pain medications as prescribed by their doctors, people having gout attacks are encouraged to rest and to increase the amount of fluids that they drink.
Acute attacks of gout can be treated with nonaspirin, nonsteroidal anti-inflammatory drugs (NSAIDs) such as naproxen sodium (Aleve), ibuprofen (Advil), or indomethacin (Indocin). In some cases, these drugs can aggravate a peptic ulcer or existing kidney disease and cannot be used. Doctors sometimes also use colchicine (Colbenemid), especially in cases where nonsteroidal anti-inflammatory drugs cannot be used. Colchicine may cause diarrhea, which tends to go away once the patient stops taking it. Corticosteroids such as prednisone (Deltasone) and adrenocorticotropic hormone (Acthar) may be given orally or may be injected directly into the joint for a more concentrated effect. While all of these drugs have the potential to cause side effects, they are used for only about 48 hours and are not likely to cause major problems. However, aspirin and closely related drugs (salicylates) should be avoided because they can ultimately worsen gout.
Once an acute attack has been successfully treated, doctors try to prevent future attacks of gout and long-term joint damage by lowering uric acid levels in the blood. There are two types of drugs for correcting hyperuricemia. Such uricosuric drugs as probenecid (Benemid) and sulfinpyrazone (Anturane) lower the levels of urate in the blood by increasing its removal from the body (excretion) through the urine. These drugs may promote the formation of kidney stones, however, and they may not work for all patients, especially those with kidney disease. Allopurinol (Zyloprim), a type of drug called a xanthine-oxidase inhibitor, blocks the production of urate in the body, and can dissolve kidney stones as well as treating gout. The potential side effects of allopurinol include rash, a skin condition known as dermatitis, and liver dysfunction. In 2004, the FDA was seeking trial data on a new drug called oxypurinol (Oxyprim) for treating chronic gout. These medications may have to be taken for life to prevent further gout attacks.
New quality of care indicators were released in 2004 to improve care for patients with gout. The aim of the guidelines was to prevent repeat gout attacks and to reduce medication errors associated with intravenous colchicine in hospitals.
Alternative treatment
Alternative approaches to gout focus on correcting hyperuricemia by encouraging weigt loss and limiting the intake of alcohol and purine-rich foods. In addition, consuming garlic (Allium sativum) has been recommended to help prevent gout. Increasing fluid intake, especially by drinking water, is also recommended. During an acute attack, contrast hydrotherapy (alternating three-minute hot compresses with 30-second cold compresses) can help dissolve the crystals and resolve the pain faster.
Prognosis
Gout cannot be cured but usually it can be managed successfully. As tophi dissolve, joint mobility generally improves. (In some cases, however, medicines alone do not dissolve the tophi and they must be removed surgically.) Lowering uric acid in the blood also helps to prevent or improve the kidney problems that may accompany gout.
Prevention
For centuries, gout has been known as a "rich man's disease" or a disease caused by overindulgence in food and drink. While this view is perhaps a little overstated and oversimplified, lifestyle factors clearly influence a person's risk of developing gout. Since obesity and excessive alcohol intake are associated with hyperuricemia and gout, losing weight and limiting alcohol intake can help ward off gout. Dehydration may also promote the formation of urate crystals, so people taking diuretics or "water pills" may be better off switching to another type of blood pressure medication. Everyone should be sure to drink at least six to eight glasses of water each day. Since purine is broken down in the body into urate, it may also be helpful to avoid foods high in purine, such as organ meats, sardines, anchovies, red meat, gravies, beans, beer, and wine. A 2004 study revealed that eating more low-fat dairy products could reduce risk of developing gout.
Key terms
Allopurinol — A drug that corrects hyperuricemia by inhibiting urate production.
Colchicine — A drug used to treat painful flare-ups of gout.
Corticosteroids — Medications related to a natural body hormone called hydrocortisone, which are used to treat inflammation.
Hyperuricemia — High levels of a waste product called uric acid in the blood.
Probenecid — A drug that corrects hyperuricemia by increasing the urinary excretion of urate.
Purine — A substance found in foods that is broken down into urate and may contribute to hyperuricemia and gout.
Sulfinpyrazone — A drug that corrects hyperuricemia by increasing the urinary excretion of urate.
Synovial fluid — Fluid surrounding the joints which acts as a lubricant, reducing the friction between the joints.
Tophus (plural, tophi) — A chalky deposit of a uric acid compound found in gout. Tophi occur most frequently around joints and in the external ear.
Urate crystals — Crystals formed by high levels of uric acid in the blood.
Resources
Books
Parker, James N., M.D., and Philip M. Parker, Ph. D. The 2002 Official Patient's Sourcebook on Gout. San Diego, CA: ICON Health Publications, 2002.
Periodicals
Arromdee, E., C. J. Michet, C. S. Crowson, et al. "Epidemiology of Gout: Is the Incidence Rising?" Journal of Rheumatology 29 (November 2002): 2403-2406.
Coghill, Kim. "FDA Panel Discusses Endpoints for Approval of Gout Products." Bioworld Today (June 3, 2004).
"Dairy-rich Diet May Help Prevent Gout." Tufts University Health & Nutrition Letter (June 2004): 2.
Hsu, C. Y., T. T. Shih, K. M. Huang, et al. "Tophaceous Gout of the Spine: MR Imaging Features." Clinical Radiology 57 (October 2002): 919-925.
Lin, J. L., D. T. Tan, H. H. Ho, and C. C. Yu. "Environmental Lead Exposure and Urate Excretion in the General Population." American Journal of Medicine 113 (November 2002): 563-568.
MacReady, Norma. "New Gout Quality-of-care Standards Take Aim at Medication-related Errors." Internal Medicine News (June 1, 2004): 18.
Perez-Ruiz, F., M. Calabozo, G. G. Erauskin, et al. "Renal Underexcretion of Uric Acid is Present in Patients with Apparent High Urinary Uric Acid Output." Arthritis and Rheumatism 47 (December 15, 2002): 610-613.
Raj, J. M., S. Sudhakar, K. Sems, and R. W. Carlson. "Arthritis in the Intensive Care Unit." Critical Care Clinics 18 (October 2002): 767-780.
Shekarriz, B., and M. L. Stoller. "Uric Acid Nephrolithiasis: Current Concepts and Controversies." Journal of Urology 168, no. 4, Part 1 (October 2002): 1307-1314.
Organizations
Arthritis Foundation.1300 W. Peachtree St., Atlanta, GA 30309. (800) 283-7800. http://www.arthritis.org.
National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS). National Institutes of Health (NIH), 1 AMS Circle, Bethesda, MD 20892-3675. 〈www.niams.nih/gov〉.
Other
National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS). Questions and Answers About Gout. Bethesda, MD: NIAMS, 2002. NIH Publication No. 02-5027. 〈www.niams.nih.gov/hi/topics/gout/gout/htm〉.
Gale Encyclopedia of Medicine. Copyright 2008 The Gale Group, Inc. All rights reserved.
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gout (gout) a group of disorders of purine and pyrimidine metabolism, characterized by typhi causing recurrent paroxysmal attacks of acute inflammatory arthritis usually affecting a single peripheral joint, usually responsive to colchicine, and usually followed by complete remission; hyperuricemia and uric acid urolithiasis are also present in fully developed cases.gout´y
latent gout , masked gout lithemia without the typical features of gout.

Dorland's Medical Dictionary for Health Consumers. © 2007 by Saunders, an imprint of Elsevier, Inc. All rights reserved.
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gout (gout)
n.
An inherited disorder of uric-acid metabolism occurring predominantly in men, characterized by painful inflammation of the joints, especially of the feet and hands, and arthritic attacks resulting from elevated levels of uric acid in the blood and the deposition of urate crystals around the joints. The condition can become chronic and result in deformity.
gouty adj.
The American Heritage® Medical Dictionary Copyright © 2007, 2004 by Houghton Mifflin Company. Published by Houghton Mifflin Company. All rights reserved.
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gout
Etymology: L, gutta, drop
a disease associated with an inborn error of uric acid metabolism that increases production or interferes with excretion of uric acid. Excess uric acid is converted to sodium urate crystals that precipitate from the blood and become deposited in joints and other tissues. Men are more often affected than premenopausal women. The great toe is a common site for the accumulation of urate crystals. The condition can cause exceedingly painful swelling of a joint, accompanied by chills and fever. The symptoms are recurrent. Episodes become longer each year. The disorder is disabling and, if untreated, can progress to the development of destructive joint changes, such as tophi. Treatment usually includes administration of colchicine, phenylbutazone, indomethacin, or glucocorticoid drugs and a diet that excludes purine-rich foods such as organ meats. It may include surgical removal of ulcerated tophi. Chronically, probenecid, allopurinol, or cholchicine may be used to decrease uric acid levels. Acquired gout is a condition having the signs and symptoms of gout but resulting from another disorder or treatment for a different condition. Diuretic drugs can alter the concentration of uric acid so that uric acid salts precipitate from the blood and are carried to the joints. See also chondrocalcinosis, Lesch-Nyhan syndrome, tophus.
Mosby's Medical Dictionary, 8th edition. © 2009, Elsevier.
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gout [gowt]
a form of arthritis in which uric acid appears in excessive quantities in the blood and may be deposited in the joints and other tissues. During an acute attack there is swelling, inflammation, and extreme pain in a joint, frequently that of the big toe. After several years of attacks, the chronic form of the disease may set in, permanently damaging and deforming joints and destroying cells of the kidney. Most cases occur in men and the first attack rarely occurs before the age of 30.
Causes. The causes of gout include excessive production of uric acid, as an inherited condition or as a side effect of chemotherapy for tumors, and impairment of clearance due to the antihypertensive agenthydrochlorothiazide or to low-dose aspirin.
Acute Gout. This form usually strikes without warning. The affected joint, which in 70 per cent of cases is that of the big toe, becomes swollen, inflamed, and very painful. The first attack may follow an operation, infection, or minor irritation such as tight shoes, or it may have no apparent cause. The patient may have a headache or fever, and often cannot walk because of the pain.

Without treatment, acute attacks of gout usually last a few days or weeks. The symptoms then disappear completely until the next attack. As the disease progresses, the attacks tend to last longer and the intervals between attacks become shorter.

A definite diagnosis of gout is made by identifying needle-shaped sodium urate crystals in the synovial fluid aspirated from an affected joint. The crystals may be seen inside polymorphonuclear leukocytes. Acute gouty arthritis is an example of an acute inflammatory process. Serial serum uric acid levels are also monitored; levels consistently above 8 mg/100 ml are an abnormal finding.
Treatment. An acute attack of gout can be treated successfully with any of several medicines. colchicine has long been used; in most cases it relieves the pain and swelling in 72 hours or less, although it does not affect the high concentration of uric acid. indomethacin is a nonsteroidal antiinflammatory drug that is particularly effective against acute gout and has become the treatment of choice. Aspirin should be avoided during acute attacks. The dietary management of gout is a subject of disagreement among researchers.
Chronic Gout. After a number of acute attacks of gout, the patient who goes without medical treatment may develop symptoms of chronic gout. This seldom occurs less than 10 years after the first acute attack. Joints affected by chronic gout degenerate in the same way as those affected by rheumatoid arthritis and may eventually lose their ability to move.
Treatment. Chronic gout is treated with probenecid, allopurinol, or other medicines that promote urinary excretion of uric acid. Other treatment may also be necessary if the kidney is involved. With appropriate treatment, gout should be well controlled.
Management Between Attacks. If acute gout is recognized at an early stage and treated correctly, the development of the chronic form can generally be prevented. Weight should be kept within normal limits, and increasing daily intake of liquids is beneficial because it encourages urine production.

Arthritis Foundation