Silica publicity has been implicated with the development of various connective tissue diseases. 1 year progressing to chronic type 1 respiratory failure. This was followed by development of full blown MCTD with combined features of rheumatoid arthritis scleroderma and systemic lupus erythematosus with severe arthritis myositis and joint contractures. CASE Statement This was a case report of a 32-year-old stone crusher presented with gradually progressive breathlessness in the beginning on exertion and later also at rest for 1 year. At the same time he also noticed Raynaud’s phenomenon involving the fingers and toes. Over the next 6 months he developed a gradual binding down of the skin over the dorsa of hands forearms face and leg. There was history of recurrent non-painful oral ulcers. There was no history of prolonged fever dysphagia excess weight loss or photosensitivity. The patient also had severe joint pains predominantly involving all joints of the hands including the wrist joint and the legs bilaterally. Patient have been working being a rock crusher for days gone by 6 years. On evaluation the patient acquired diffuse hyperpigmentation noticeable respiratory distress using a respiratory price of 34/min with minor pallor. Study of the the respiratory system uncovered extensive bilateral great crepitations. Cutaneous evaluation demonstrated binding down of epidermis of the facial skin and all limbs. Both hands had sclerodactyly. Laboratory investigations exposed a microcytic hypochromic anemia (Hb – 8 g%). Liver and renal PCDH8 function test had been within the standard limitations. The erythrocyte sedimentation price grew up (80 mm/1st h by Westergren technique). Arterial bloodstream gas analysis uncovered type 1 respiratory system failing with PaO2- 54 mmHg pH – 7.38 PaCO2- 38 mmHg. Examining for immune system markers uncovered antinuclear antibody (ANA) positive-9 (IF assay) anti-double stranded-deoxyribonucleic acidity positive anti-Scl70 IgG antibody positive – 86 U/L anti-U1 ribonucleoprotein (RNP) antibodies positive in high titers anti-cyclic citrullinated peptide and rheumatoid aspect positive. Epidermis biopsy in the trunk was appropriate for systemic sclerosis. The upper body X-ray uncovered diffuse reticulo nodular shadows regarding both lungs. Comparison improved computed tomography from the upper body was suggestive of diffuse intra and interlobular septal thickening with fibrosis and arbitrarily located nodules [Amount 1]. X-ray of hands demonstrated osteo acrolysis. Top gastrointestinal endoscopy was regular. The individual was struggling to execute pulmonary function lab tests. Mantoux check was detrimental. Fiberoptic 3-Methyladenine bronchoscopy uncovered regular airways. Bronchoalveolar lavage uncovered several neutrophils. Acidity and Gram fast bacilli assessment from the sputum were detrimental. Transbronchial lung biopsy was appropriate for silicosis and uncovered focal interstitial fibrosis interspersed with pigment laden macrophages and refractile materials. He satisfied the Alarcon Kusukawa and Segovia diagnostic criteria for the diagnosis of MCTD. Individual 3-Methyladenine was treated with air. Low dosage prednisonolone (20 mg OD) was presented with in view from the arthritis. Methotrexate in a dosage of 25 mg regular was started along with proton pump inhibitors and physiotherapy also. The patient taken care of immediately the procedure 3-Methyladenine and his joint aches have regressed significantly. His hypoxia in addition has improved on therapy but he is still on supplemental air. Figure 1 High res computed tomography lung screen showing arbitrarily distributed nodules and fibrosis Debate Some patients have got features of several rheumatic disease and therefore do not match traditional classification. Sufferers with mix of scientific finding comparable to those of systemic lupus erythematosus intensifying systemic sclerosis polymyositis arthritis rheumatoid and with unusually high titers of circulating ANA with specificity for nuclear RNP are believed to possess 3-Methyladenine MCTD.[1] Hypotheses implicating modified self-antigens and/or infectious agents in the pathogenesis of MCTD have already been advanced [2] but non-e have already been proven yet. Silica publicity continues to be implicated just as one trigger.[3] Crystalline silica (quartz) contaminants significantly less than 1 μ will be the many pathogenic in silicosis. These contaminants are phagocytosed by macrophages and so are transported towards the local lymph nodes. Though silica is inert chemically.