Gout: Diagnosis and management.

Gout is a heterogeneous group of diseases resulting from monosodium urate (MSU) crystal deposition in tissues or from supersaturation of uric acid in extracellular fluids. Clinical manifestations include 1) Recurrent attacks of articular and periarticular inflammation, also called gouty arthritis; 2) Accumulation of articular, osseous, soft tissue, and cartilaginous crystalline deposits, called tophi; 3) Uric acid calculi in the urinary tract; and 4) Interstitial nephropathy with renal function impairment, called gouty nephropathy. Gout predominantly is a disease of adult men, with a peak incidence in the fifth decade. In women usually found after menopause. The metabolic disorder underlying gout is hyperuricaemia. The duration and magnitude of hyperuricemia directly correlate with the likelihood of developing gouty arthritis and uric acid urolithiasis, and with age at onset of initial clinical gouty manifestations. The urate crystals induce phagocytes and synovial cells to generate and release such mediators as cyclooxygenase and lipoxygenase metabolites of arachidonic acid, phospholipase A2-activating protein, lysosomal proteases, tumor necrosis factor (TNF)-α, interleukin (IL)-1, IL-6, and IL-8. Definitive diagnosis of gout needs the demonstration of MSU crystals in synovial fluid or tophus. Gout is frequently associated with comorbidity such as obesity, hypertension, renal disease and dyslipidaemia. Therapeutic goals include terminating acute attacks; providing rapid, safe relief of pain and inflammation; averting future attacks; and preventing such complications as formation of tophi, kidney stones, and destructive arthropathy. Colchicine, nonsteroidal anti-inflammatory drugs and corticosteroid are drugs used for treating acute gouty arthritis. Colchicine is also used for prophylaxis. Urate lowering drugs also play a role in prophylactic management of gout. With early intervention, careful monitoring, and patient education, the prognosis is excellent.

Is there a relationship between serum C-reactive protein level and dyslipidaemia in systemic lupus erythematosus?

AIM: to look for the association between CRP and dyslipidaemia in SLE. METHODS: seventy six patients fulfilled the American College of Rheumatology criteria for classification of Systemic Lupus Erythematosus (SLE) (revised in 1997) were enrolled in our study. Clinical and laboratory measures included complete history and physical examination, determination of serum CRP level by latex agglutination test and lipid profile. Statistical significance of association was analysed by X2 test. T-test were used to compare values of each lipid component between positive and negative CRP group. All analyses were performed using the SPSS 10.0 computer software. RESULTS: the study was done in 76 (73 female and 3 male) SLE patients. Dyslipidaemia was found in 57 patients (75.0%). Hypercholesterolemia was found in 31 patients (40.8%), hypertriglyceridemia in 33 patients (43.4%), low HDL cholesterol in 19 patients (25%) and high LDL cholesterol in 28 patients (36.8%). Patients with positive CRP (66 patients) demonstrated dyslipidaemia in 49 patients (74.2%) and patients with negative CRP (10 patients) showed dyslipidaemia in 8 patients (80.0%)(P 1.0). There was no association between CRP and abnormal values of each lipid component (cholesterol, triglyceride, HDL and LDL cholesterol)(P value 0.30, 0.74, 0.43, 0.15 respectively). There was also no association between CRP and dyslipidaemia as a whole (P 1.00). The difference between serum level of each lipid component between positive and negative CRP group was also non significant (P value 0.68, 0.90, 0.96, 0.59 respectively). CONCLUSION: there was no association between CRP and dyslipidaemia in SLE patients. In the development of dyslipidaemia in SLE, factors other than inflammation should be put into consideration.

Iron deposit state and risk factors for anemia in the elderly.

AIM: To determine the type of anemia, iron deposit and risk factors for anemia in the elderly. METHODS: A cross-sectional study was conducted among 84 patients admitted to the geriatric inpatient ward of dr. Cipto Mangunkusumo Hospital. The patients underwent anamnesis, administration of a dietary questionnaire which included SQFF and food recording, physical examination, laboratory investigations (blood, urine and benzidine test), chest x-ray, ECG and spirometry. Anemic elderly patients also underwent iron store measurements, including serum iron (SI), total iron binding capacity (TIBC) and serum ferritin (SF). RESULTS: The proportion of anemia was 54.76%. Increased anemia was inversely correlated with increased body mass index (OR 0.870; 95% CI 0.762-0.994), serum albumin (OR 0.285; 95% CI 0.090-0.907) and calorie intake (OR 0.998; 95% CI 0.996-0.999), and positively correlated with renal impairment (OR 2.647; 95% CI 1.084-6.467). Anemia due to chronic disease (ACD) accounted for 21 subjects, 5 subjects with iron deficiency coexisting with ACD, 1 subject with megaloblastic anemia, and the cause of anemia in 19 patients could not be identified due to diagnostic procedural limitation. Most of the anemic elderly subjects had normal iron deposits. As many as 42.1% of the men and 44.4% of the women had elevated iron deposits. The level of hemoglobin, SI, TIBC in ACD patients were lower than in non-ACD patients (Hb 10.4 vs 10.8 g/dl, SI 58.71 vs. 92.38 ug/dl, TIBC 283.11 vs. 288.95 microg/dl). In contrast, serum ferritin levels in ACD patients were higher than in non-ACD (178.26 vs. 111.35 ng/ml). CONCLUSION: Body mass index, serum albumin, calorie intake and renal impairment are risk factors for anemia in the elderly. Normal iron deposits accounted for 57.9% and 55.6% of anemic elderly men and women with elevated iron deposits.