Vancomycin-induced neutropenia is an uncommon but potentially serious side effect of prolonged vancomycin therapy. We present a case of a 19 year old male with disseminated methicillin-resistant Staphylococcus aureus (MRSA) Infection who was treated with IV vancomycin and developed fever and neutropenia. After discontinuation of IV vancomycin and substitution with clindamycin, both fever and neutropenia resolved within 72 h. Diagnosis of vancomycin-induced neutropenia and fever was considered as there was no alternative cause of this. In addition, quick resolution of fever and neutropenia upon removal of causative drug further supported the diagnosis. Since vancomycin is widely used in clinical practice, this adverse effect should be monitored carefully. Many studies report immune mediated mechanism to be the cause of this adverse effect. However, further studies need to be done in this regard to establish the exact mechanism.

The coexistence of Moyamoya syndrome (MMS) and Graves’ disease (GD) is uncommon. Here, we report a case of a 41-year-old Filipino female, who presented with thyrotoxicosis and acute ischemic stroke. Based on her clinical presentation, cerebral computed tomography angiography, and thyroid function tests, she was diagnosed with MMS and GD. Her Burch-Wartofsky point scale score was 30, suggesting an impending thyroid storm. Antithyroid therapy was started with her neurological status deterioration initially, but after controlling the thyroid storm, the patient’s neurological status stabilized. She remained stable till she travelled to her country. We hypothesized that MMS in a patient with GD is mediated through anti-dsDNA antibodies, by altering key biological mechanisms, that is, inflammation, neutrophil extracellular traps, and apoptosis that drive a distinctive and coordinated immune and vascular activation. To the best of our knowledge, this is the first case of MMS associated with GD reported in Qatar.

Original Article introduCtionSepsis, severe sepsis, and septic shock are the spectra of the deleterious host response to infection. Even with optimal treatment, mortality due to severe sepsis or septic shock is approximately 40% and can exceed 50% in the sickest patients. [1] Patients with systemic infection and organ dysfunction or shock are often difficult to distinguish from patients with similar clinical signs and laboratory finding but without infection.Serum procalcitonin (PCT), normally produced in the C-cells of the thyroid gland, is the precursor of calcitonin. A specific protease cleaves serum PCT to calcitonin, catacalcin, and an N-terminal residue. Normally, PCT is not released into the blood as it is all cleaved, and hence, they are undetectable in healthy individuals and its level increases in severe infections. In these conditions, serum PCT is probably produced by extra-thyroid tissues as high levels of PCT are found even in those patients who have undergone total thyroidectomy. Parenchymal cells (including the kidney, liver, lung, muscles, and adipocytes) provide the main source of circulating PCT in sepsis. [2] PCT is detectable 3-4 h after an inflammatory stimulus and peaks at 14 h and the remaining elevated for 24 h, with a half-life in the serum of 22-35 h. [3] The pathophysiological role of serum PCT during sepsis is not clear. [4,5] PCT has been studied extensively, and its efficacy as a marker of bacterial infection and critical illness has been proved. As positive bacteriological results may be caused by Objective: The objective of the study was to compare the diagnostic value of serum procalcitonin (PCT), C-reactive protein (CRP), lactic acid, and white blood cells (WBC) as markers of sepsis in critically ill patients in the main tertiary hospital in Qatar. Materials and Methods: The PCT levels and other inflammatory markers (CRP, lactic acid, and WBC) were retrospectively reviewed in 137 consecutive adult patients with a suspected diagnosis of sepsis who admitted to the Internal Medicine inpatient service (i.e., Medical Wards and Medical Intensive Care Unit) at Hamad General Hospital, Qatar. The serum PCT was measured by chemiluminescence immunoassay and the results were compared with commonly used inflammatory markers between the patients with and without proven sepsis. Results: A significantly higher PCT level was observed among patients with severe sepsis and septic shock compared to those without sepsis (19.34 ± 50 and 25.91 ± 61.3 vs. 4.72 ± 10, respectively; P = 0.011). No significant differences were found in CRP and WBC between these groups. Nonsurvivors of both septic and nonseptic groups had a mean PCT level of 22.48 ± 8.26 significantly higher than that measured in survivors of both the groups (P = 0.01), a difference not evident in other inflammatory parameters. Conclusions: PCT is a highly efficient inflammatory laboratory parameter for the diagnosis of severe sepsis and septic shock, but WBC and CRP levels were of little value. PCT value assists in the diagnosis of septic ...

Background/objective: Several inflammatory biomarkers of infection including procalcitonin (PCT) and C – reactive protein (CRP) have been shown to be useful in diagnosis of infection in different clinical settings. The purpose of this study was to determine the diagnostic value of serum PCT, CRP and White Blood Cells (WBC) as markers of sepsis in critically ill patients in Qatar. Materials and methods: The PCT levels and other related inflammatory markers (CRP and WBC) were measured in 137 adult patients with a suspected diagnosis of sepsis and admitted to Internal Medicine inpatient service (i.e., Medical Wards and Medical Intensive Care Unit) at Hamad General Hospital, Hamad Medical Corporation-Qatar during the period from January 2011 to December 2013. Results: The serum PCT was measured by chemoluminiscence immunoassay and the results were compared with other inflammatory markers between the patients with and without proven sepsis. A significantly higher PCT level was observed among patients with severe sepsis and septic shock compared to those without sepsis (19.34 ± 50 and 25.91 ± 61.3 vs. 4.72 ± 10, respectively; (p = 0.011). No significant differences were found in CRP and WBC between these groups. Non-survivors of both septic and non-septic groups had a mean PCT level of 22.48 ± 8.26 significantly higher than that measured in survivors of both groups (p = 0.01), a difference not evident in other inflammatory parameters. Conclusion: PCT is a highly efficient inflammatory laboratory parameter for the diagnosis of severe sepsis and septic shock but WBC and CRP levels were of little value. PCT value assists in diagnosis of septic shock hence supporting appropriate disposition of patients. Levels of PCT also have prognostic implications with regards to mortality suggesting intensification of antibiotic therapy and supportive measures including appropriate family counseling.