Dr.Mohammed Salauddin,1 Dr. Manju Bijarnia,2Dr. Junaid Ahmad,3Dr. Shivangi Jain,2Dr. Sandhya Rathore2
- Professor &Head of Department of Anatomy Dr. M.P.K. Homoeopathic Medical College, Hospital & Research Centre, Saipura, Jaipur.
- MD scholar, Department of Paediatrics, HOMOEOPATHIC UNIVERSITY, JAIPUR.
- MD scholar, Department of Homoeopathic pharmacy, HOMOEOPATHIC UNIVERSITY, JAIPUR.
Gout is principally a disease of men and to some extent post-menopausal women. The prevalence of gout is directly related to the degree of hyperuricemia. Levels in men and women increase with age.Overall, gout occurs in 2% to 3% of the adult male population.(1) In the general population, the prevalence of Hyperuricemia ranges between 2.0 and 13.2%, andthe prevalence of gout is between 1.3 and 3.7%. The higher the serum level, the more likely anindividual is to develop gout. Incidence of gout in India is not very clear. The prevalence is 0.12% as per International League of Nations Against Rheumatism, Community Oriented Program for Control of Rheumatic Disease (ILAR COPCORD) study in Bhigwan village of India. Urban Indian population is involved more than rural population.(2)
Keywords:Gout, Homoeopathy,Colchicum, Lycopodium.
The word “gout” was initially used by Randolphus of Bocking, around 1200 AD. It is derived
from the Latin word gutta, meaning “a drop” (of liquid). According to the Oxford English
Dictionary, this is derived from humorism and “the notion of the ‘dropping of a morbid
material from the blood in and around the joints”.(3)Gout is true crystal deposition disease. It can be defined as the pathological reaction of the jointor periarticular tissues to the presence of monosodium urate monohydrate (MSUM) crystal.The deposition of crystals in the joints and periarticular soft tissue can lead to arthritis andbone destruction. Initially favouring lower rather the upper limbs and especially targeting thefirst metatarsophlangeal and small joints of the feet and hands. As the crystal deposits slowlyincrease and enlarge there is progressive involvement of more proximal sites and the potentialfor cartilage and bone damage, development of secondary OA.(4)
FACTORS RESPONSIBLE FOR GOUT:
- Heredity– An inherited tendency on the part of some, derived especially through goutyparents, the transmission by the male side being more common.(5)
- Mode of living– A sedentary, inactive life as tending to lower the vitality of the system,too much confinement indoors, insufficient fresh air act as risk factor.
- Climate– In spring and especially in summer a larger excretion occurs as heat increasesthe alkalinity of the blood. Decreasing in autumn and winter.(6)
- Diet– A high protein &caloric intake cause increases uric acid. The output of uric acidmay rise to lgm daily on a high purine diet (meat, liver, fish etc)
- Ph of blood– All substances which increases the solubility of uric acid in the bloodaugment also its excretion in urine, while all those which diminish its solubility bycausing acidity or lowered alkalinity lessen, also its amount in the urine.(6)
- Alcohol- Alcohol promotes Hyperuricemia because of increased urate production & decreased uric acid excretion. It has long been recognized that certain persons are prone to repeated attack of gout after ingestion of alcoholic beverages.(7)
- Obesities and co-morbidites- Higher adiposity & weight gain are strong risk factors for gout in men, while weight loss is protective.(8)
PATHO-PHYSIOLOGY OF GOUT:
- Increased urate production-
- Purines, which are later metabolized to uric acid, enter a common metabolicpathway by which either nucleic acid or uric acid is produced. Normalproduction of uric acid is considered to be 600 mg per day in men with normalrenal function on a purine-free diet. 4 Overproduction of uric acid may occurbecause of an abnormality in the enzymes that regulate purine metabolism. Twosuch abnormalities have been documented. An increase in the activity of phosphoribosylpyrophosphate synthetase results in increased uric acid synthesis. A deficiency of hypoxanthine-guanine phosphoribosyltransferase also increases serum uric acid levels.
- Accelerated purine nucleotide degradation can also cause Hyperuricemia, i.e.
with conditions like rapid cell turnover, proliferation or cell death. Increased activity of the enzyme increase purine synthesis & associated with sever gout.(9)
- Decreased uric acid excretion:
- Over 90% of individuals with sustained Hyperuricemia have a defect in therenal handling of uric acid. Gouty individuals excrete 40% less uric acid thannon gouty individuals for any given plasma urate concentration. Altered uricacid excretion could theoretically result from decreased glomerular filtration,decreased tubular secretion or enhance tubular reabsorption. Decreased uratefiltration does not appear to cause primary hyperuricemia but does contribute tothe Hyperuricemia of renal insufficiency.(10)
- About two thirds to three fourths of all uric acid produced daily are excreted bythe kidneys. The gastrointestinal tract eliminates the other one third to onefourth. Under normal conditions, uric acid is filtered in the glomeruli of thekidney, reabsorbed in the proximal tubule and secreted distally. Tubularsecretion is almost entirely responsible for the excretion of uric acid. Renalmanagement of uric acid is defective in approximately 98 percent of patientswith primary hyperuricemia and gout
GOUT is a disorder of purine metabolism and occurs when its final metabolite uric acid,
crystallizes in the form of monosodium urate precipiting and forming deposits in joints on
tendons and in the surrounding tissues. When tophi breach, they trigger a local immunemediated inflammatory reaction, with one of the key protines in the inflammatory cascade
being interlukin 1β.
COMPLICATION OF HYPERURICEMIA:
- Asymptomatic Hyperuricemia– it is characterized by an increased serum uric acidlevel in the absence of clinical evidence of disposition disease (i.e. arthritis, tophi,nephropathyor nephrolithiasis).(11) The normal plasma uric acid is 0.1-0.4 moml/1. The normal excretion ranges from 250-600 mg.(12)
- Acute gouty arthritis– Acute gout is a sodium urate monohydrate induced crystalinflammation of joints, bursas and tendon sheaths. Clinically, the affected structuresclassically, the first metatarsophalangcal joint is the first joint affected.(12)
- Chronic Tophaceous Gout- large deposit containing monosodium urate monohydratecrystal produce firm nodules over affected joints on the extensor surface of the finger,
hands, olecranon bursas, extensor surface of forearm.(13)
- Renal complications– May arise at any stage of gout but nephrolitiasis is the onlycommon clinical presentation of renal involvement. Several renal problem causes by
Hyperuricemia: 1. nephrolitiasis, 2. urate nephropathy, a rare cause of renal
insufficiency attributed to monosodium urate crystal deposition in the renal interstitium,
3. Uric acid nephropathy, a reversible cause acute renal failure.(14)
CLINICAL FEATURE OF GOUTY ARTHRITIS:
- Acute gouty arthritis- is characterized by a rapid crescendo onset. Typically, thepatient goes to sleep without symptoms & awakened by severe pain, erythema &swelling in the affected joint.
The signs and symptoms of gout almost always occur suddenly-often at night &without warning. They include:
- Intense joint pain– usually affects the large joints of toe [First metatarsal jointmost commonly affected termed PODOGRA], but it can occur in also feet,ankles, knees, hands and wrists. The pain is likely to be most severe within thefirst four to 12 hrs after it begins.
- Lingering discomfort-after the most severe pain subsides, some joint discomfortmay last from a few days to a few weeks.
- Inflammation and redness– the affected joint or joints become swollen, tender,warm and red.
- Limited range of motion– decreased joint mobility may occur as gout progress.
- Chronic gouty arthritis– when uric acid levels in the bloodstream remain too high,more crystal is deposited. Gout becomes chronic condition.
- More frequent and longer-lasting flare-ups of gouty arthritis- as chronic goutgets worse, flare-ups occur more often and last longer. Overtime, theinflammations cause permanent damage to bone and cartilage.
- Flare-ups in other parts of the body- in about half of all patients with gout, thefirst attack occurs in the joint at the base of the big toe. When chronic goutoccurs, others joints may be affected, including the ankle and knee.
- Nodule from under the skin-uric acid crystal may begin to be deposited in softtissue, forming nodules called tophi. Chronic gout sometimes referred to astophaceous gout.
- Kidney problem- chronic gout associated with kidney problems. May beassociated with kidney stones or kidney failure.
LABORATORY INVESTIGATIONS- (15,16)
- Hematologic findings: Acute gout is usually accompanied by leukocytosis andelevation of the erythrocyte sedimentation rate & other acute phase reactants.
- Hyperuricemia: in the adult clinically significant hyperuricemia exists when serumurate levels are ≥ 7mg/dl, with the normal level in women 1mg/dl lower than in men.Although hyperurecimia is a cardinal feature of primary and secondary gout, it doesnot establish a diagnosis of gout it often found in asymptomatic individual.
- Analysis of synovial fluid: The synovial fluid in acute gout is typical ofinflammation reactions, showing decreased viscosity, poor mucin clot &polymorphonuclear leukocystosis (5000 to 50000/ul).
- Radiologic findings: There are no radiographic findings in early gout exceptpossible soft tissue swelling. With continued urate deposition, punched out,radiolucent areas of varying size develop in the bone to involved joints.
- Dual-energy CT:Can quantitatively identify monosodium urate crystal depositswith high sensitivity and specificity within joints, tendons, and periarticular softtissues.(17)
The American college of rheumatology have criteria for the clinical diagnosis of acute gout.The presence of 6 of the 11 criteria has a total 95% specificity in differentiating gout frompseudogout.
|More than one attack of acute arthritis|
|Maximum inflammation developing within 1 day|
|Redness over the affected part|
|The first metatarsophalangeal joint painful & swollen|
|Unilateral first metatarsophalangeal joint involved|
|Tophus (proven or suspected)|
|Asymmetrical swelling within a joint on radiology|
|Subcortical cysts without erosion seen on radiology|
|Unilateral tarsal joint attack|
|Joint fluid culture negative for micro-organism during an attack|
|Criteria for the clinical diagnosis of acute gout(13)|
|BURSITIS||Bursitis is a painful inflammatory condition that affects the small fluid-filled sacs (bursac).|
|CELLULITIS||Acute bacterial infection of skin & subcutaneous tissue, with sever
inflammation & possible spreading. It is characterised by redness,
swelling, tenderness or pain & warmth.
|OESTOARTHRITIS||It is results from mechanical abnormalities of the joint which cause degradation of joint cartilage and subchondrial bone. Most oftenaffects the joints of the finger, hip, knee, big toes and cervical joints.|
|RHEUMATOID ARTHRITIS||It is a chronic, inflammatory multisystem autoimmune disease. Peripheral joints such as the wrists, knees, shoulders, hands & feet are mostly affected. It is characterised by pain, stiffness, swelling, redness & heat around the affected joints.|
|PSORIATIC ARTHRITIS||Psoriatic arthritis is an immune-mediated connective tissue disease,
associated with skin disorder marked by bumps & scaling (psoriasis).
HLA-B27, HLA-DRm-DR7 antigen associated with this disease.
|TENDINITIS||It is a very common condition especially among individuals engaged
in heavy labor or sports. Common sites of tendinitis including shoulder, elbow, knee, Achilles tendon at the heel.
|OSTEMYELITIS||Acute inflammatory process within bone, bone marrow & surrounding soft tissue that develops secondary to infection with bacterial
HOMOEOPATHIC MANAGEMENT OF GOUT:(18,19,20,21)
LYCOPODIUM: This is a drug for chronic gout, with chalky deposits in the joints. It is suited to persons who are mentally keen, but of weak muscular power. These patientssuffer from gastric ailments especially lower abdomen flatulence. There is a pain in theheels as if treading on a pebble. One foot feels hot and the other feels cold. Tophi formation with nocturnal pains > by heat, muscular contractions. Drawing, tearing inthe limbs at night & on alternate days < rest. Muscles & joints rigid, painful, withnumbness. Finger-joints inflamed also with arthritic nodes. Swelling of the dorsum ofthe feet > warmth. Lithic acid deposit in urine. Toe or other joint dark red in spots.Pain: aching-pressure, drawing, chiefly right-sided < 4-8pm. Affects right side, or painsgoes from it to If. Associated with abdominal complaints with bowel trouble.
COLCHICUM: This drug has a specific power of relieving the gouty paroxysms but itseems to be more beneficial in chronic affections of these parts. The parts are red, hot,swollen with tearing pains felt more in the night. The parts are sensitive to touch. Thepatient complains of tearing pains in the joints in hot weather, and stinging during cold.Gout settles in the great toe or in the heel. With the gout the patient also has disordersof the stomach. The smell of food, especially fish, causes nausea and may even causefainting. There may be an icy coldness felt in the stomach. The urine is dark, brown,black- looks like ink. Gout attacking many joints; shifting from one to another, withburning & tearing pains, from external impression, noise, touch. Affected part verysensitive to contact & motion. Arthritic pains in joints; patient screams with pain ontouching a joint or stubbing a toe. The joint becomes inflamed, dark red, hot &intensely painful. Patient nearly beside himself with agony, gout in persons of vigorousconstitution. Uric acid diathesis.
URTICA URENS: This helps in the elimination of uric acid from the body. The patienthas a tendency to gout and stone formations especially in kidneys. The joint symptomsare associated with urticaria or alternate with it. The shoulders (deltoid region), wristsand ankles are commonly affected. Skin symptom with itch, wheals & urticaria areassociated symptoms. The patient cannot tolerate touch, water or exposure of theaffected parts to cool, moist air and snow air.
LITHIUM CARB: There is a swelling and tenderness of the finger and toe joints, betterby hot water application. Gout in knees, sides of feet and soles, ankle-joints pain onwalking; profuse urine, with uric acid deposit; painful urination; pain in heart beforeand at time of urinating; valvular deficiencies; aggr. from mental agitation, whichcauses a fluttering and trembling of heart, general puffiness of body and limbs; increaseof bulk and weight; clumsiness in walking at night and weariness in standing; swelling.tenderness, sometimes redness of last joints of fingers; intense itching of feet and handsat night from no apparent cause; uric acid deposits in urine.
LEDUM: When gout is the result of alcoholism, Ledum should be thought of. Theinflammation of the joints begins in the lower limbs and ascends upwards. The ball ofthe great toe is swollen. It is red, sometimes bluish, and cold to touch. It is generally worse from getting warm in bed. The patient is sensitive to the cold, yet the heat of the bed is intolerable. Low, asthenic cases (maltreated by large doses of colchi); lancinating, tearing pains <by motion than by touch & at midnight. Pains are sticking, tearing, throbbing; rheumatic pains are <by motion: at night, by warmth of bed & bed covering; > only when holding feet in ice-water. Gout begins in lower limbs & ascends. Joint becomes the seat of nodosities & “gout stone”, which are painful; acute & chronic arthritis. Oedematous swelling of the joint, which may feel cold to touch; habitual gout in the articulations of hands & feet. Ball of great toe swollen & painful.
BENZOIC ACID: Tearing in joints with nearly clear urine; old nodes become painful,and as the pains abate palpitation sets in, ceasing only when pains increase; gout goingfrom left to right or commencing in right great toe; urine of offensive odour, depositingreddish cloudy sediment. Chronic rheum arthritis, wandering pains.
NATRUM MURIATICUM: Big toe red, with tearing & stinging on walking or standing.Tarsal joints feel bruised, veins of feet distended. Cracking of joints, which feel stiff onmoving them. Lame bruised sensation in small of back, as if a portion of the spine weretaken out. Can’t bear sun heat, complaints aggravate in sun heat. Sadness mood withweeping disposition. Joints pain < full moon, new moon.
SABINA: Red & shining swelling of big toe, with excessive pains < by the least touchor slightest motion. Heaviness of the affected limbs. Wandering pains, burning,affecting one joint after another, especially the big toe & hand > cold application. Shechange her position to get some relief.
STAPHISAGRIS: Arthritic nodes from deposition of urates of soda. Chronic gout ofmen advanced in life, corpulent with feeble pulse, palpitation, dyspnoea on exertion.Pains in smaller joints of hands & feet with much swelling & hardness. Aftersuppressed grief, onanism, sexsual excesses. Suppressive in nature with sensitiveness.
SULPHUR: Habitual gout, especially of drunkards & those who indulge in rich food &take but little exercise. Uric acid urine; dull aching, pressive pain in joints. Hot patientwith desire for cold food. Desire for sweet. Can’t tolerate hunger, morning diarrhoea.Constipation with hard stool & burning in anus after stool. Burning sensation in generalfeature. Skin affection with or history of suppressed skin affection. When other remedyfails to act.
Discussion And Conclusion:
Homoeopathy offers a wider range of option than conventional medicine. Constitutional homoeopathic treatment with the management is an excellent choice for gout. Homoeopathic medicine not only give relive to the patient suffering from acute pain, but also help to preventing the recurrence of such episodes. The constitutional approach of homoeopathy, which considers mind and body together as one part, believes that emotional factors are vital inthe development of most of the disease, including gout.
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