Among rare neuromuscular junction conditions, autoimmune myasthenia gravis remains the most common cause. Its prevalence is between 45 and 142 per 1000 000 inhabitants, while its incidence varies from 2.5 to 20. case / million / year depending on the populations studied 2. SAS is part of a heterogeneous group of primary inflammatory myopathies. This syndrome is characterized by the association of inflammatory myopathy, interstitial lung disease, characteristic cutaneous abnormalities such as "mechanic's hands", Raynaud's syndrome, inflammatory arthritis, and Biological, anti autoantibodies specific anti-nuclear called "anti synthetases" which gave their name to the syndrome. The frequency of clinical signs is variable: 94% for inflammatory arthritis, 62% for the phenomenon of Raynaud, 71% for the sign of the mechanic's hand 5. There are currently eight different SASs. It is exceptional to be in the presence of two SAS simultaneously. Depending on the antibody present, the clinical expression of the disease is different 6. Our patient was positive for PL7 antibody. Hervier B et al noted by reporting 17 cases that anti-PL7 positive patients have in 60 to 100% of pulmonary manifestations. This is the case of our patient who had for several years as main symptom a dyspnea of ​​effort. In all cases according to some authors 6, it is necessary to think of looking for an anti-synthetase antibody in an interstitial pneumopathy. Prognosis depends to a great extent on pulmonary involvement. Patients positive for PL12 had skin, vascular (Raynaud's syndrome), pulmonary and esophageal 6. The aforementioned extra pulmonary signs are absent in our patient concordant with the negativity of anti PL12 in the latter. The physiopathology of SAS remains unknown to the present day. Only hypotheses have been suggested, indexing a genetic susceptibility and environmental factors (viral and bacterial infections) that can be an immunologically triggering factor. The mechanism of immune response and antibody production remains unclear 7. The diagnosis of myasthenia gravis was mentioned in our patient before the pharmacological test, the dosage of anti anti RACH. From a therapeutic point of view, anticholinestherases represent the first-line treatment of the symptomatic strand. The background treatment is done with corticosteroids and immunosuppressants. Plasma exchanges and immunoglobulin administration are reserved for severe relapses or myasthenia gravis 2. There are currently no randomized controlled trials in the treatment of SAS 6. However, treatment lines are proposed. In the first line, corticosteroids (CS) at 1 mg / kg / day over a period of 4 to 8 weeks followed by a progressive reduction. In the absence of a response after 12 weeks, immunosuppressive therapy should be combined. Azathioprine is the most widely used drug, as several studies have shown its efficacy in the range of 57-75% at 2 to 3 mg / kg / day. Second-line therapy is the administration of intravenous immunoglobulin (Ig IV), cyclosporine or plasma exchange. However, a randomized, placebo-controlled study showed no benefit to plasma exchange 7. The treatment of myasthenia gravis and SAS containing to some extent the same molecules, we put our patient under anticholinestherasics (Pyridostigmine), corticosteroid (Prednisolone) and immunosuppressant (Azathioprine).We are waiting for a specialist immunological advice that we lack in Togo.