| REVIEW OF LITERATURE: Historical Concept- Egyptians were the first to recognize gout as a disease in 2640 BC. Hippocrates recognized its debilitating nature by the fifth century BC, calling it the “unwalkable disease.†Galen was also first to description of tophus as chalk like structure. Podagra, a manifestation of gout, was first used by a Dominican monk named Randolphus of Bocking in 1200 AD. In Greek, pod means “foot†while Agra translates to “seizure†or “to take.†The term also has Latin roots, with the word gutta translating to “drop.’ (4) Alexander of Tralles (525 – 605 A.D.), a Byzantine physician, and his contemporary, Aetius, were the first to indicate the usefulness of colchicum in the treatment of gout. (4) In 1683 English physician Sydenham distinguished gout from other form of arthritis and differentiated an acute and advanced [chronic] form (5) .Anton van Leeuwenhoek (1632–1723), the Dutch biologist who became the father of microscopy, discovered that the gouty tophus was made up of crystals, but the actual nature of the crystal remained unknown. In 1776 the chemical identity of uric acid was first established as a constituent of a renal calculus by the Swedish chemist Scheele, and the English chemist Woolaston demonstrated urate in a tophus from his own ear in 1797 (4) It was not until 1763 that the Viennese physician Baron von Storck began to use colchicum extract specifically for terminating acute gouty attacks. In the mid-1800s, Sir Alfred B. Garrod published identification of increased levels of uric acid published his identification of increased levels of uric acid in the blood of gouty patient’s investigations that characterize many of the aspects of clinical gout as clinicians know it today. In the late 1800s, it was discovered that high-dose salicylates were an efficacious remedy for acute gout (6). McCarty and hollander publish experiments which demonstrate that synovial fluid contain monosodium urate crystals which would serve as basis for diagnosis of gout (4) DEFINATION – Gout is the term used to describe the constellation of clinical features that result from deposition of microcrystals of sodium urate monohydrate or uric acid from hyperuricaemic body fluids. These include acute arthritis, tenosynovitis, bursitis or cellulitis, tophaceous deposits ,renal disease and urolithasis (7) EPIDEMIOLOGY: - • The incidence of gout varies in population from 0.2 to 3.5 per 1000, with an overall prevalence of 2-26 per 1000. • Gout is found to have increased prevalence in recent years. • It is rare in children and premenopausal females. • The risk of developing gout increases with age and with serum uric acid (SUA) levels. • Serum uric acid levels are higher in men, increase with age and are positively associated with body weight. (8) • Prevalence rises up to 10% in men and 6% in women more than 80 years old age. • It occurs in men 2–6 folds more than women. (9) ETIOLOGY :- Gout happens when urate, a substance in your body, builds up and forms needle-shaped crystals in your joints. This leads to:- Pain, Swelling, Redness, Changes in how you move and use the affected joint. . The other factor to develop gout :-- High urate levels and a family history of gout .Mostly seen in men than female [postmenopausal] with increasing age. Drinking alcohol and sugar-sweetened beverages, such as soda. Having an unhealthy diet and eating foods that are rich in purines (usually from animal sources), a substance that breaks down into urate. A group of conditions that include high blood pressure, high blood sugar, abnormal cholesterol levels and obesity. Chronic kidney disease, psoriasis, cancer. Rare genetic conditions that lead to increased urate. Diuretics, Low-dose aspirin, fructose syrup and some other medications. (10) PATHOGENSIS- About one-third of the body uric acid pool is derived from dietary sources and two -thirds from endogenous purine metabolism. The concentration of uric acid in body fluids depends on the balance between endogenous synthesis and elimination by the kidneys (two-thirds) and Gut (one-third). Purine nucleotide synthesis and degradation are regulated by a network of enzyme pathways, but xanthine oxidase plays a pivotal role in catalysing the conversion of hypoxanthine to xanthine and Xanthine to uric acid (8) CLINICAL FEATURES:- The classical presentation is with an acute monoarthritis , which affects the first metatarsophalangeal joint in over 50% of cases. Other common sites are the ankle, mid foot, and knee, small joints of hands, wrist and elbow. Large proximal joints are rarely involved. Typical features include: rapid onset, reaching maximum severity in 2–6 hours, worse in the early morning. Severe pain, often described as the ‘worst pain ever’. Extreme tenderness, so the patient is unable to wear a sock or to let bedding rest on the joint .Marked swelling with overlying red, shiny skin. Self-limiting over 5–14 days, with complete resolution. During the attack, the joint shows signs of marked synovitis, swelling, erythema. There may be accompanying fever, malaise and even delirium, especially if a large joint such as the knee is involved. As the attack subsides, desquamation of overlying skin are common .In old age may be atypical, with painful tophi and chronic symptoms, rather than acute attacks. In old age may be atypical, with painful tophi and chronic symptoms, Rather than acute attacks. Joints of the upper limbs are more frequently affected Some people never have a second episode and in others several years may elapse before a second attack occurs. Patients with repeated attacks may progress to chronic gout, with chronic pain, joint damage, deformity and functional impairment. Patients with uncontrolled hyperuricaemia who suffer multiple attacks of acute gout may also progress to chronic gout .Crystals may be deposited in the joints and soft tissues to produce irregular firm nodules called tophi. Tophi have a white color, differentiating them from rheumatoid nodules (8). CLINICAL CLASSIFICATION Gout can occur in four phases – ASYMPTOMATIC HYPERURICEMIA:- Majority of patients with asymptomatic hyperuricemia never develop gout. The risk of acute gout attack increases with the level of serum urate. This stage ends with the first gout attack. (1) ACUTE GOUTY ARTHRITIS :- The big toe (first metatarsophalangeal joint) is the classic site for gout. One-third of patients may get their first attack at another site such as the in-step of the foot, ankle, knee, or hand, joints. The attack is acute, it starts in the night, the joint and surrounding tissues the signs are swollen, hot, red, shiny and extremely painful. There is a mild fever with chills. (11)Left untreated, the attack will start to improve in a week or two and the skin over the involved joint may desquamate as the episode subsides. Atypical manifestations include bursitis, cellulitis or mild pain and discomfort without swelling, lasting a day or two. The erythema over affected joint during an attack is characteristic of gouty synovitis .Acute gout in one joint may provoke migratory attacks affecting other joints over subsequent days. Acute gout can precipitate by dietary excess, trauma, surgery and many other medical illness Polyarticular gout attacks are more common in women, especially with diuretic use. First attacks are seldom associated with residual disability, but recurrent attacks are followed by progressive cartilage and bone erosion, deposition of tophi, secondary osteoarthritis and disability associated with permanent restriction of joint function. (7) INTERCRITICAL GOUT :- After an acute attack, some people never have a second episode, in others next episode occurs after years. In most a second attack may occur within one year and the frequency of attacks gradually increases with time. After resolution of the acute attack, the patient is in the inter-critical stage. (11) Although the disease seems to be inactive, hyperuricemia persists, and subclinical inflammation may be present in the joints (1). Monosodium urate crystal deposit continues. CHRONIC TOPHACEOUS GOUT:-. Although patients may present with tophi as their initial symptom, chronic tophaceous gout usually develops ten or more years after an acute attack. However, microtophi are documented early in the disease in patients with hyperuricemia. (1) Tophi appear as firm, nodular or fusiform swellings. In inflamed tophi, the overlying skin may be erythematous. In ulcerated tophi, white chalky material, the urate crystals, may exude. (11)Tophi may be intra articular, per articular, or extra-articular, the most common sites being the digits of hands and feet, knees, and the olecranon bursa. They lead to destructive deforming arthritis with extensive bone destruction. (1) Tophi may develop rapidly in feet or hands of post-menopausal women with heart failure and renal insufficiency who develop acute or sub-acute gouty arthritis following prolonged diuretic administration. Crystal deposits appear in cartilage, synovial membranes, tendons and soft tissues. The classic location of a tophus is the helix and antihelix of the ear. (12) After gouty arthritis, renal disease is the most frequent complication of hyperuricaemia. Urate nephropathy is attributed to the disposition of monosodium urate crystals in the renal interstitial tissue. Other manifestations include uric acid calculi (11). PROGNOSIS :- The prognosis of gout depends on the comorbidity of each individual. Mortality is higher in individual with cardiovascular comorbidity. When gout receives proper treatment, most patients will live a normal life with mild sequelae. Patients whose symptoms appear earlier in life will usually have a more severe disease at presentation. For those who do not modify their lifestyle, recurrent flare-ups are common. (1) DIFFERINCIAL DIAGNOSIS:- 1. Rheumatic arthritis 2. Osteoarthritis 3. Septic arthritis 4. Crystalline-associated arthropathies Calcium pyro-phosphatase deposition disease (CPPD) 5. Psoriatic arthritis (1) INVESTIGATIONS:- 1. Synovial fluid analysis 2. Serum uric acid level 3. Urine analysis 4. Renal function test 5. X-ray of affected part 6 CRP 7 ESR 8 CT scan (1) COMPLICATION:- Tophi, joint deformity, osteoarthritis, bone loss. Urate nephropathy and nephrolithiasis.Gout might also cause ocular complications, such as conjunctivitis, uveitis from the urate crystal precipitation. (1) TREATMENT:- Acute gout NSAIDs, Colchicine Local or systemic corticosteroids Long term treatment = Uricosuric drug – allopurinol, febuxostat, probencid. Treat associated problems, e.g. obesity, hyperlipidemia, hypertension (13) MANAGEMENT:- Dietary changes – Avoiding Purine rich food such as asparagus, spinach , red meat, organ meat, sea food, food rich in fructose –sugary drinks, alcohol- especially beer and hard liquor. Stress relief – Yoga and Meditation Physical activity – Exercise, Controlled weight reduction in obese patients. Avoiding use of thiazides or loop diuretics, niacin and other medications. (12) HOMOEOPATHY VIEW – Homoeopathy is based upon the easily comprehensible principle, law of nature, individualization and restores the sick to health gently. In gout, homoeopathy can give cure in acute as well as chronic cases. Certain homoeopathic medicines work directly on the "uric acid diathesis," but the constitutional method of taking a holistic approach to case taking, analyzing symptoms, and then choosing a similimum for a chronic case will lead to a cure. The totality of symptoms in the mental and physical plane and peculiar characteristic symptoms help in finding the similimum. Homoeopathy has a holistic approach to patients, homoeopathic medicines help and improve the general health of person, because it treats the person as whole and not only the disease. One of the three principles of homeopathy is the law of similars: ‘similia similibus curantur’, which means ‘like cures like.’ Put simply, a disease is cured with a substance that causes similar symptoms/disease in a healthy human being.Individualization in Homoeopathy includes its unique holistic consultation process, means two persons having the same complaints will vary in their symptoms,presentation, modalities, physical makeup and mental expressions which will be known by a proper case taking. Homoeopathy is the science dealing with the deranged vital force and functional changes in the individual patient, irrespective of the name of the disease. “Gout and Its cure by J. Compton Burnett†“In a given case of gout the symptoms are not those of the individual himself, but of its material presence in the individual : the pain, the swelling, the redness, the tenderness, the fever, the restlessness- these are produced by the gouty material, which we see from the fact that they disappear as soon as this material is washed out ; so that what we require are remedies that are homeopathic to the state of the patient which preceded the gouty deposit into the tissue, inclusive of these deposits.In fact ,the pathology of gout must be considered, in prescribing adequately ,Homeopathically.†(14) In aphorism 259, Dr Hahnemann advises for consider minuteness of dose necessary and proper in homoeopathic treatment everything must be removed from diet and regimen which can have any medicinal action , in order that the small dose may not be overwhelmed and extinguished or distributed by any foreign medical irritant. (15) Hahnemann in aphorism 153 states that more importance is given to the characteristics which is defined as the more striking, singular, uncommon, peculiar, signs and symptoms which help in finding out a similimum cure and ‘supply where necessary. (15) In 261 Aphorism, Dr Hahnemann gives an idea about the most appropriate regimen, removal of obstacles for cure and ‘supply where necessary. (16) Some of homoeopathic remedy which are much important for treatment of gout from source book like. Homoeopathic Therapeutics by , Lilienthal, Phatak, and Robert [The Rheumatic Remedies], Boericke’s new manual of homoeopathic materia medica. Are as under – 1] ANTIMONIUM CRUDUM - Weakness and shaking of hands in writing, followed by offensive flatus. Twitching in muscles. Jerks in arms. Pain in the joints of fingers. Pain in feet. (17) Worse in evening, better open air. (18) 2] ABROTANUM: Pain in shoulders, arms, wrists, and ankles. Pricking and coldness in fingers and feet. Contraction of limbs worse cold air (17) , better motion. (18) 3] BELLADONNA – Shifting rheumatic pain; jerking limbs, agg touch (18). 4] BENZOICUM ACIDUM – Nodes and gouty concretions on the joints of upper and lower limb; cracking in the joints on motion (urates of soda); urine very deep red, strong-smelling, and of high specific gravity (19) , worse open air. (18) 5] BRYOINA ALBA – joints red, swollen hot. Pins and needles in soles, preventing walking. Constant motion of left arm and leg, with sighing. Swelling of elbow. Knees totter and bend under him when walking. (17) worse touch better pressure (18) 6] COLCHICUM AUTUMNALE- where the gout attacks many joints, with burning and tearing pains, aggravated by the touch, and at night muscular pains, swelling, and coldness of legs and feet, with the pain, weariness, heaviness, and inability to move ; feeling of muscular weakness. (19) 7] GUAIACUM -Gouty inflammation and abscess of the knee ; followed by contraction of limbs ; immovable stiffness of the contracted limbs ; can bear no heat, with pain in joints (19),worse motion (18) 8] LEDUM - (maltreated by large doses of Colchicum); lancinating, tearing pains; worse by motion and at midnight, when joints feel so hot that he throws off’ all covering; ball of great toe swollen and painful, gouty nodosities in joints; fine tearing pain in toes. (19) 9] LYCOPODUM CLAVATUM – Tophi , ameliorated by heat ; muscular contractions ; drawing, tearing in the limbs at night and on alternate days ; worse at rest ; muscles and joints rigid, painful, with numbness ; better in warmth (19); alternation of heat and cold in gout . (20) 10] RHODODENDRON CHRYSANTHUM - Arthritic node; paralytic weakness of the limbs, aggravated in rough weather, and rest; sensation in lower legs and feet as if asleep. (19) 11] SULPHUR –For gout; urine charged with uric acid; stiffness in the knee or ankle-joints; better by dry warm weather. (19) 12] URTICA URENS- Continuous Pain in deltoid [right]; agg rotating arm inwards; could not put on the coat; acute gout (17) worse from touch. (18) Many more of medicine are present for gout. |