Changes in microRNA expression have been detected in vitro in influenza infected cells, yet little is known about them in patients. microRNA profiling was performed on whole blood of H1N1 patients to identify signature microRNAs to better understand the gene regulation involved and possibly improve diagnosis. Total RNA extracted from blood samples of influenza infected patients and healthy controls were subjected to microRNA microarray. Expression profiles of circulating microRNAs were altered and distinctly different in influenza patients. Expression of highly dysregulated microRNAs were validated using quantitative PCR. Fourteen highly dysregulated miRNAs, identified from the blood of influenza infected patients, provided a clear distinction between infected and healthy individuals. Of these, expression of miR-1260, -26a, -335*, -576-3p, -628-3p and -664 were consistently dysregulated in both whole blood and H1N1 infected cells. Potential host and viral gene targets were identified and the impact of microRNA dysregulation on the host proteome was studied. Consequences of their altered expression were extrapolated to changes in the host proteome expression. These highly dysregulated microRNAs may have crucial roles in influenza pathogenesis and are potential biomarkers of influenza.
In this covid 19 pandemic,there were increased incidence of Mucormycosis and thereby increase in usage of antifungals especially oral posaconazole which is more recently available in tablet form.There are already enough case reports of the incidence of new onset hypertension and hypokalemia with supressed renin and aldosterone which is termed as “Posaconazole induced pseudohyperaldosteronism”.We describe here about a similar case that presented with hypertensive urgency as Acute pulmonary edema with an associated primary adrenal insufciency.The potential mechanism include inhibition of 11 β HSD which degrades cortisol to cortisone,thereby increasing the levels of cortisol that stimulates Mineralocorticoid receptor.Also there is inhibition of steroidogenesis at the level of adrenal which in our patient presented with features of Acute adrenal insufciency.
Hemophagocytic lymphohistiocytosis is a hyper-inammatory condition that is either Familial (Primary) or Secondary to autoimmune diseases , infection, malignancy or other triggers.It is a cytokine storm syndrome where there inefcient antigen removal that leads to sustained cytokine release.It is a rare phenomenon occuring in adults that has got a specic trigger which is less documented and have a good response to steroids where as Familial form is a childhood disease due to genetic defects, both of which are life threatening and may need Allogenic bone marrow transplant. Macrophage activation syndrome is also a subtype of this entity that occurs in the treatment phase of SLE and Still's disease.We describe here 8 cases of secondary HLH, their primary triggers and treatment response.
Melioidosis or Whitmore's disease is an infection of humans and animals caused by aerobic gram negative bacillus Burkholderia pseudomallei. This infection with a wide clinical spectrum is predominantly present in tropical climates, mainly Southeast Asia and Northern Australia. The clinical manifestations include pneumonia, skin ulcers or abscesses, osteomyelitis, prostatitis, encephalomyelitis and fulminant septic shock. The denitive diagnosis is made by a positive culture of Burkholderia pseudomallei. The bacteria is innately resistant to 6 classes of commonly used antibiotics. CDC recommends an intensive phase of intravenous antibiotics for 10 to 14 days followed by eradication therapy with oral antibiotics for 3 – 6 months. The intravenous agents effective against the bacteria are meropenem and ceftazidime. Trimethoprim sulfamethoxazole and amoxicillin/clavulanic acid are the oral antimicrobial agents used. Here we present two cases of Melioidosis, at opposite ends of the spectrum with varying antibiotic response. One patient is a young non immunocompromised female and the second an elderly immunocompromised (T2DM) male, both presented with skeletal melioidosis.
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