Kounis syndrome is associated with mast cell activation resulting in acute coronary syndrome secondary to an allergic insult. Various drugs such as antibiotics, analgesics, and environmental exposures such as bee, wasp sting, and poison ivy are known to induce Kounis syndrome. A 68-year-old man admitted with a cobra bite on both hands to emergency care unit and sustained cardiorespiratory arrest. Electrocardiogram, taken 6 hours after the cardiac arrest, showed ST elevations in leads V2 to V5 suggestive of anterior ST elevation myocardial Infarction (STEMI). Serum Troponin was 10 ng/ml (control= <0.5). Serum IgE levels were significantly high (19155IU/ml, baseline 100). 2-Dimensional echocardiogram showed anterior and apical-septal hypokinesia with left ventricular ejection fraction of 30-35%. Coronary angiogram was normal. He remained hypotensive requiring inotropic and vasopressor support during ICU stay. This was a case of Kounis syndrome leading to cardiogenic shock secondary to Cobra (naja naja) bite. This is the only reported case of cobra bite causing Kounis syndrome and cardiogenic shock. Identification of the cause of myocardial infarction in snake envenomation is useful in the management as some of the drugs like adrenaline, morphine, and beta blockers may worsen the clinical syndrome if it is due to Kounis syndrome.

Background Acquired Gitelman syndrome is a very rare disorder reported in association with autoimmune disorders, mostly Sjögren syndrome. It is characterized by the presence of hypokalaemic metabolic alkalosis, hypocalciuria, hypomagnesaemia and hyper-reninaemia, in the absence of typical genetic mutations associated with inherited Gitelman syndrome. Case presentation A 20 year old woman who was previously diagnosed with primary Sjögren syndrome and autoimmune thyroiditis presented with two week history of lower limb weakness and salt craving. Examination revealed upper limb and lower limb muscle weakness with muscle power of 3/5 on MRC scale and diminished deep tendon reflexes. On evaluation, she had hypokalaemia with high trans-tubular potassium gradient, metabolic alkalosis and hypocalciuria, features suggestive of Gitelman syndrome. New onset hypokalaemic alkalosis in a previously normokalaemic patient with Sjögren syndrome strongly favored a diagnosis of acquired Gitelman syndrome. Daily potassium supplementation and spironolactone resulted in complete clinical recovery. Conclusions Acquired Gitelman syndrome associated with Sjögren syndrome is rare. It should be considered as a differential diagnosis during evaluation of acute paralysis and hypokalaemic metabolic alkalosis in patients with autoimmune disorders, especially Sjögren syndrome.

Hoffman syndrome is a rare clinical presentation characterized by the presence of proximal weakness and muscle pseudo-hypertrophy in a hypothyroid patient. 50-year-old male presented with gradual onset muscle stiffness and weakness involving both bilateral upper and lower limbs for 3-months duration. Examination revealed generalized hypertrophy of the muscles, mainly involving the Gastrocnemius with proximal muscle weakness and slow relaxing deep tendon reflexes. His Thyroid Stimulating Hormone and creatinine kinase were elevated. Anti-Thyroid peroxidase antibodies were positive. Electromyogram (EMG) and muscle biopsy was suggestive of a myopathic disorder and a diagnosis of Hoffmann syndrome was made. Complete resolution of weakness was observed following thyroxine therapy. Hoffmann syndrome is a rare, myopathic disorder seen in long standing, untreated hypothyroidism and it has a favourable response to thyroid hormone replacement in majority of patients.

We describe a case of a 70 years old female patient in whom an initial diagnosis of acute coronary syndrome (ACS) revealed to be finally an acute aortic dissection. This case report emphasizes the importance to maintain a high grade of suspicion of aortic dissection as a possible alternative in presence of electrocardiographic myocardial ischemic changes. In many medical centers where thrombolytic therapy, antiplatelet receptor blockers, heparin or percutaneous coronary angioplasty is the first line therapy for ACS the outcome may be catastrophic in situation such as in aortic dissection.

M. pneumoniae infection usually causes self-limiting disease. Rarely, it could lead to severe life-threatening pneumonia or refractory infection. Excessive cell mediated immune response to infection is thought to be the mechanism of refractory and severe mycoplasma pneumonia. IL-8 is thought to play a part in severe and refractory mycoplasma infections. Furthermore, serum LDH has been shown to be a marker of severe and refractory disease. However, the relationship and the mechanism of raised LDH and IL-18 are not clearly explained in the literature. There were several case studies showing the benefit of steroids amongst children with severe and refractory mycoplasma pneumonia. We report a case of a young man who developed severe and refractory mycoplasma pneumonia who showed a dramatic response to steroids.