Creatinine Phosphokinase Levels Research Articles

SEVERE RHABDOMYOLYSIS AND ARDS SECONDARY TO ADENOVIRUS IN A MORBIDLY OBESE YOUNG PATIENT: A THERAPEUTIC DILEMMA

SESSION TITLE: Critical Care 1 SESSION TYPE: Med Student/Res Case Rep Postr PRESENTED ON: 10/09/2018 01:15 PM - 02:15 PM INTRODUCTION: Severe rhabdomyolysis due to adenovirus and acute respiratory distress syndrome due to adenovirus have been well reported in literature. However, there are no case reports presenting together in a single patient. CASE PRESENTATION: 50 years old morbidly obese male(>500 lbs) with past medical history of OSA (on CPAP qHS), diabetes who presented with progressively worsening shortness of breath, productive cough with yellowish sputum and fever 101 at home. In ED, he was febrile to 103F, tachycardic 107, RR 22, BP 130/80, SpO2 96% on non re-breather. CXR on admission was suggestive of pulmonary edema and initial labs were significant for acute renal failure with a progressively rising creatinine from 1.5 mg/dl to 5mg/dl within 6 hours and initial creatinine phosphokinase(CPK) levels of >200000 which progressively rose inspite of aggressive fluid resuscitation. He was placed on Bi-level non invasive ventilation without improvement and was subsequently intubated a few minutes later for refractory respiratory failure. He was later found to be positive for adenovirus. Further clinical course was complicated by progression to acute respiratory distress syndrome (ARDS), requirement of renal replacement therapy, and need for vasopressors. Although his PaO2/FiO2 ratios were <100 post intubation on maximal ventilatory support, given his morbid obesity, prone ventilation was not considered. We approached our ECMO team and the patient was placed on veno-venous ECMO within 24 hours of intubation. Afterwards, he showed slow improvement over the next few weeks and eventually underwent tracheostomy and percutaneous endogastric tube placement. He was eventually discharged from our hospital after a prolonged stay of almost 60 days. DISCUSSION: Rhabdomyolysis due to adenovirus is mainly due to viral myositis. CPK values can exceed >800,000. Most cases of ARDS due to adenovirus have been in morbidly obese patients who were not candidates for proning but received paralytics and ECMO. There are no specific recommendations for management of ARDS due to adenovirus, potential agents are cidofovir and brincidofovir, however, their use is limited due to severe nephrotoxicicty and myelosuppression. CONCLUSIONS: The lack of concrete recommendations or guidelines for management of adenovirus induced ARDS makes management difficult. When complicated by rhabdomyolysis which requires fluid resuscitation in the initial stages, maintaining euvolemic status for the management for ARDS complicates management even further. In the above case, the patient was successfully managed with early initiation of RRT and ECMO although we avoided use of antivirals in the absence of concrete literature to support their use. Reference #1: Tseytlin, D., & Maynard, S. (2016). Severe rhabdomyolysis secondary to adenovirus infection: case report and literature review. Clinical nephrology, 85(4), 245-250. Reference #2: Severe ARDS caused by adenovirus: early initiation of ECMO plus continuous renal replacement therapy Reference #3: Kam, M., Chai, H. Z., Goh, K. J., Tan, Q. L., Sewa, D. W., Tan, A. H., … & Phua, G. C. (2017). The Use of Extracorporeal Membrane Oxygenation in Severe Adenovirus Pneumonia Complicated by ARDS: A Single-Center Experience. Chest, 152(4), A350. DISCLOSURES: No relevant relationships by Animesh Gour, source=Web Response no disclosure on file for Anisha Kamath; No relevant relationships by Mangalore Amith Shenoy, source=Web Response

A ROCK AND A HARD PLACE: A CASE OF CLOZAPINE-INDUCED NEUROLEPTIC MALIGNANT SYNDROME

SESSION TITLE: Critical Care 4 SESSION TYPE: Med Student/Res Case Rep Postr PRESENTED ON: 10/09/2018 01:15 PM - 02:15 PM INTRODUCTION: Neuroleptic malignant syndrome (NMS) is a rare life-threatening neurologic emergency characterized by mental status changes, rigidity, fever, and dysautonomia. The incidence rate of NMS is 0.02-3% among patients taking typical or atypical neuroleptic agents; however, clozapine-induced NMS is a rarely-reported and unique entity as it doesn’t present with the four cardinal clinical features of NMS. We present a rare case of clozapine-induced NMS with the four cardinal features of NMS. CASE PRESENTATION: A 45-year-old man with history of schizoaffective disorder and catatonia was transferred from a local psychiatric hospital to the emergency department (ED) for evaluation of fever and altered mental status. Two days prior to the transfer, he was started on clozapine. In the ED, he had a temperature of 39.1° Celsius, blood pressure of 100/57 mmHg, respiratory rate of 24 breaths-per-minute, and heart rate of 118 beats-per-minute. The patient was diaphoretic, drooling, and shivering. He was lethargic with Glasgow Coma Scale of 8 and was therefore intubated. At that point, the rest of the examination was non-significant. Initial laboratory work-up including creatinine phosphokinase (CPK) was non-significant. Computed tomography (CT) scan of the head was normal. Lumbar puncture was performed and cerebrospinal fluid analysis was unremarkable. The patient was admitted to the intensive care unit (ICU) where he continued to develop fevers despite the use of antipyretics, cooling blankets, an d aggressive intravenous hydration. The fever spikes were associated with intermittent episodes of sinus tachycardia and fluctuations of his blood pressure. On day two, he developed rigidity, and blood work-up was significant for CPK level of 4419 U/L. He was started on benzodiazepines and dantrolene for a presumed diagnosis of NMS. However, his rigidity and fever didn’t improve. On day four, he developed ventilator-associated pneumonia. After a week in the ICU with no success in liberation of mechanical ventilation, family decided to shift care to comfort measures only. The patient perished a few hours later. DISCUSSION: Clozapine is considered among the most potent neuroleptic agents, with use reserved for treatment-resistant cases. Although it has many side effects, there are very few case reports about clozapine-induced-NMS. Risk factors for developing clozapine-induced NMS include young age, male gender, and history of catatonia. CONCLUSIONS: It is important to be aware of these risk factors for early recognition and treatment of NMS, given its high mortality rate of 10-30%. Reference #1: Clozapine-induced neuroleptic malignant syndrome: review and report of new cases.P. Sachdev, J. Kruk, M. Kneebone, D. KissaneJ Clin Psychopharmacol. 1995 Oct; 15(5): 365–371. DISCLOSURES: No relevant relationships by Abdullah Chahin, source=Web Response No relevant relationships by Faeq Kukhon, source=Web Response No relevant relationships by Mahmoud Mowafy, source=Web Response No relevant relationships by Magaly Sazani, source=Web Response No relevant relationships by Abraham Walusimbi, source=Web Response

Rhabdomyolysis and Acute Poisoning; a Brief Report.

Some studies have reported creatinine phosphokinase (CPK) as a new emerging way in predicting the outcomes of poisoned patients. This study aimed to evaluate the association of serum CPK level in the first 24 hours with outcomes of poisoned patients. This retrospective cross-sectional study was performed using the medical profiles of poisoned patients aged between 13 and 70 years old who were referred to the emergency department of a big referral medical toxicology center during 6 years and whose necessary data for this study was available. 318 patients with the mean age of 34.9±14.5 years were studied (77.1% male). The mean serum CPK level of patients was 4693.1 ± 10303.8 (35-89480) IU/L. There was no significant correlation between serum CPK level and cause of poisoning (r= 0.16; p=0.51), age (r = -0.021; p = 0.651), sex (r = 0.131; p = 0.281), seizure (r = -0.022; p = 0.193), level of consciences (r = -0.138; p = 0.167), and duration of hospital stay (r= 0.242, p = 0.437). The mean serum CPK level was significantly higher in ICU admitted (p<0.0001), AKI (p<0.0001), hyperkalemia (p<0.0001), hypophosphatemia (p=0.045), and hypocalcaemia (p=0.008) cases. The best cut off point of serum CPK level in predicting acute kidney injury (AKI) was estimated to be 10000 IU/L (sensitivity = 83.8% and specificity = 68.8%). It seems that CPK could be considered as a candidate tool for screening the intoxicated patients in need for ICU admission and at risk for AKI.

Prevalence of hyperuricemia in professional athletes and its role in the genesis of various pathological conditions and metabolic disturbances

In recent decades, the prevalence of hyperuricemia (HU) is increasing worldwide; the role of uric acid (UA) in the genesis of various metabolic disorders, cardiovascular diseases, and kidney disease is being discussed. There are very few investigations of the rate of HU and its role in the development of diseases in certain social groups, including in professional athletes.Objective:to estimate the prevalence of HU and its role in the genesis of various pathological conditions and metabolic disturbances in professional athletes.Patients and methods.A retrospective comparative one-stage study was conducted, for which 2148 athletes who met inclusion criteria were selected and examined in the Federal Research and Clinical Center for Sports Medicine and Rehabilitation, Federal Biomedical Agency, in 2015. A control group consisted of 99 ageand sex-matched healthy volunteers examined at the V.A. Nasonova Research Institute of Rheumatology in 2017. The analysis included a comparison of the rate of HU and other examined parameters in professional athletes and healthy volunteers. The examined parameters were separately compared in athletes with/without HU, followed by statistical processing of results.Results.HU was detected in 306 (14.2%) of the 2148 athletes, more often in men (n=253 (20%) than in women (n=53 (6%); (p&lt;0.001). The rate of HU in the athletes was comparable with that in the healthy population (12.1%). The athletes with HU (n=306) compared with the other athletes (n=1842) had the following statistically higher indicators: the mean serum levels of creatinine, triglycerides, aspartate aminotransferase, alanine aminotransferase, gamma-glutamyltranspeptidase, creatinine phosphokinase, and myoglobin, glomerular filtration rate, and body mass index (BMI) (p&lt;0.00001 for all cases).Conclusion.HU is detected quite often in professional athletes (14.2%), which is comparable with the indicators seen in healthy volunteers (12.1%). The high prevalence of HU and its association with indicators reflecting kidney function, lipid metabolic disturbances, and BMI necessitate further investigations aimed at searching the causes of HU and methods of its prevention and treatment in professional athletes.

Importance of biochemical parameters in order to predict clinical severity in patients diagnosed with Crimean-Congo haemorrhagic fever

Abstract Objective We aimed to investigate new biochemical indicators to predict the clinical course of patients following the diagnosis of Crimean-Congo haemorrhagic fever (CCHF). Material and methods We retrospectively evaluated patients diagnosed with CCHF. They were divided into three groups based on a scoring system known as severity grading score in order to predict severity. Red cell distribution width (RDW), mean platelet volume (MPV), creatinine phosphokinase (CPK), alkaline phosphatase (ALP), glutamyl transferase (GGT) and C-reactive protein (CRP) levels were evaluated on the first day of admission. These biochemical parameters may predict the clinical course of our three patient groups. Results In our study, there were 38 (70.4%) male and 16 (29.6%) female patients, and the mean age was 44.33±16.94 years. Based on our scoring system, 17 (31.4%), 30 (55.5%) and 7 (12.9%) patients were in group 1, 2 and 3, respectively. Statistically significant difference was observed between groups 1–3 and groups 2–3 for ALP values; however, a statistically significant difference was observed among all three groups for GGT values. Significant differences were not observed among the groups for RDW, MPW, CPK and CRP levels (p&gt;0.05). Conclusion ALP and GGT values can be used as auxiliary indicators to predict the clinical course for patients with CCHF. However, CPK, CRP, MPV and RDW values were not observed to be important for prognosis.

Ileus as a Sign of Neuroleptic Malignant Syndrome: A Case Report and Review of the Literature

Introduction: Neuroleptic malignant syndrome (NMS) is a rare and unpredictable adverse reaction associated with the use of first-generation and second-generation antipsychotics. Atypical antipsychotics may create atypical forms of NMS due to their different pharmacological characteristics. Decreased dopaminergic tone in the brain is coincided with a dysregulation of autonomic nervous system in this syndrome. This paper reports on an NMS case, in which current views and symptoms that occurred during the course of the disease were rare symptoms that are not usually found in NMS. Case Presentation: The patient was a 43-year-old male with schizoaffective disorder under treatment with clozapine and risperidone. He had lead pipe muscle rigidity, stupor, fever and autonomic dysfunction, increased levels of creatinine phosphokinase, leukocytosis, and microglobulina. Levenson’s criteria is widely accepted for diagnosis of NMS. Six days after admission to the psychosomatic ward, the patient had ileus. Due to lack of response to neomycin and GI rest and embedding NG tube, the patient underwent therapeutic sigmoidoscopy and colonoscopy for decompression. Conclusions: Diagnosis of NMS is largely based on clinical history and the presence of specific clinical symptoms. Antipsychotics polypharmacy increases the NMS risk. Mechanisms underlying the development of ileus in the patient are speculative and multifactorial. Paralytic ileus can be one of the autonomic dysfunctions in NMS. Furthermore, NMS is categorized in differential diagnosis of acute abdomen caused by the pseudo-obstruction. All physicians should be aware of this possibility when faced with patients under treatment with neuroleptics.

Risk factors for delayed-onset rhabdomyolysis in doxylamine succinate intoxication patients

Background and Objectives: Patients who overdose on doxylamine, hypnotic agent, usually exhibit good outcomes, but some experience serious complications. Some patients who present with normal creatinine phosphokinase levels in the emergency department later develop rhabdomyolysis during observation. We investigated factors associated with delayed-onset rhabdomyolysis in patients with doxylamine overdoses. Methods: Our investigation period was between 1 January 2011 and 29 February 2016. The initial blood samples were obtained for arterial blood gas analysis and measurements of the levels of electrolytes, creatinine phosphokinase, blood urea nitrogen, creatinine, aspartate aminotransferase, alanine aminotransferase, and lactate dehydrogenase. Urine analyses including pH and occult blood analyses were performed. Follow-up samples were obtained at 6 and 12 h after admission. Delayed-onset rhabdomyolysis was defined by a follow-up serum creatinine phosphokinase level greater than fivefold the upper limit of normal (&gt;1000 IU/L). Comparisons of categorical variables between groups were performed using either the χ2 or Fisher exact tests. Continuous variables were compared between groups using the Mann–Whitney U test. Results: A total of 337 patients were enrolled. The large amount of ingested doxylamine (odds ratio = 7.002), tachycardia (odds ratio = 2.809), low arterial blood gas analysis pH (odds ratio = 2.267), and presence of occult blood in the urine (odds ratio = 2.048) were significant associated with delayed-onset rhabdomyolysis. Conclusion: Laboratory follow-up examinations were required for patients, ingested more than 18 mg/kg doxylamine poisoning, who had pulses exceeding 120 beats/min, had arterial blood gas analysis pH values below 7.3 on blood and urine testing, and/or exhibited the presence of occult blood in the urine, even if the initial creatinine phosphokinase level was normal.

Establishment of a drug-induced rhabdomyolysis mouse model by co-administration of ciprofloxacin and atorvastatin

Rhabdomyolysis is one of the serious side effects of ciprofloxacin (CPFX), a widely used antibacterial drug; and occasionally, acute kidney injury (AKI) occurs. Often, rhabdomyolysis has occurred in patients taking CPFX co-administered with statins. The purpose of this study is to establish a mouse model of drug-induced rhabdomyolysis by co-administration of CPFX and atorvastatin (ATV) and to clarify the mechanisms of its pathogenesis. C57BL/6J mice treated with L-buthionine-(S,R)-sulfoximine (BSO), a glutathione synthesis inhibitor, were orally administered with CPFX and ATV for 4 days. Plasma levels of creatinine phosphokinase (CPK) and aspartate aminotransferase (AST) were significantly increased in the CPFX and ATV-co-administered group. Histopathological examination of skeletal muscle observed degeneration in gastrocnemius muscle and an increased number of the satellite cells. Expressions of skeletal muscle-specific microRNA and mRNA in plasma and skeletal muscle, respectively, were significantly increased. The area under the curve (AUC) of plasma CPFX was significantly increased in the CPFX and ATV-co-administered group. Furthermore, cytoplasmic vacuolization and a positively myoglobin-stained region in kidney tissue and high content of myoglobin in urine were observed. These results indicated that AKI was induced by myoglobin that leaked from skeletal muscle. The established mouse model in the present study would be useful for predicting potential rhabdomyolysis risks in preclinical drug development.

PET/CTA detection of muscle inflammation related to cholesterol crystal emboli without arterial obstruction

BackgroundPET/CTA was used to evaluate the effect of cholesterol crystal emboli (CCE) on muscle injury. Cholesterol crystals (CCs) released during plaque rupture travel downstream and lodge in muscle triggering inflammation and tissue injury. MethodsThigh muscles in three groups of rabbits (n = 22) were studied after intra-arterial injection of CCs, Group I (n = 10); polystyrene microspheres, Group II (n = 5); or normal saline, Group III (n = 7). After 48 hours, muscle inflammation and injury were measured by fluorodeoxy-glucose uptake using PET/CTA, serum tissue factor (TF), and creatinine phosphokinase (CPK). Macrophages were stained with RAM11 and CCs with Bodipy. ResultsSUVmax of thigh muscles was greater for Group I vs Group II and III (0.40 ± 0.16 vs 0.21 ± 0.11, P = .038 and 0.23 ± 0.06, P = .036). CPK levels rose significantly in Group I vs Group II and III (6.7 ± 6.0 vs 0.6 ± 0.4, P = .007 and 0.9 ± 0.4 mg·dL−1, P = .023). No arterial thrombosis was detected by CTA or histology of embolized arteries and TF did not rise significantly. There were extensive macrophage infiltrates surrounding muscle necrosis in Group I only. ConclusionsCholesterol crystal emboli triggered muscle inflammation and necrosis with an intact circulation. PET/CTA may help in the early detection of inflammation caused by CCs.

Clinical Signs and Blood Test Results Among Humans Infected With Zoonotic Simian Foamy Virus: A Case-Control Study.

A spillover of simian foamy virus (SFV) to humans, following bites from infected nonhuman primates (NHPs), is ongoing in exposed populations. These retroviruses establish persistent infections of unknown physiological consequences to the human host. We performed a case-control study to compare 24 Cameroonian hunters infected with gorilla SFV and 24 controls matched for age and ethnicity. A complete physical examination and blood test were performed for all participants. Logistic regression and Wilcoxon signed rank tests were used to compare cases and controls. The cases had significantly lower levels of hemoglobin than the controls (median, 12.7 vs 14.4 g/dL; P = .01). Basophil levels were also significantly lower in cases than controls, with no differences for other leukocyte subsets. Cases had significantly higher urea, creatinine, protein, creatinine phosphokinase, and lactate dehydrogenase levels and lower bilirubin levels than controls. Cases and controls had similar frequencies of general, cutaneous, gastrointestinal, neurological, and cardiorespiratory signs. The first case-control study of apparently healthy SFV-infected Cameroonian hunters showed the presence of hematological abnormalities. A thorough clinical and laboratory workup is now needed to establish the medical relevance of these observations because more than half of cases had mild or moderate anemia. NCT03225794.

The Use of Statins in Patients With Chronic Liver Disease and Cirrhosis.

Statins are drugs developed to treat hypercholesterolemia. Its use in patients with liver disease has been limited because one of its potential and most feared side effects is hepatotoxicity. However, there is robust evidence that supports the safety of statins in this population in the absence of severe liver dysfunction. In this review, we will summarize the efficacy and safety of statins in cirrhosis. Statins are effective in the treatment of dyslipidemia in patients with liver disease, because of their pleiotropic properties. These properties are independent of their effect on cholesterol levels, such as improving endothelial dysfunction or having antioxidant, antifibrotic, anti-inflammatory, antiproliferative, antiangiogenic, proapoptotic, or immunomodulation properties. Statins have been studied in other areas such as in treatment of portal hypertension, prevention of hepatocellular carcinoma, and/or protection against ischemia/reperfusion injury. Approved indications for statins in patients with cirrhosis are those of the general population, including dyslipidemia and increased cardiovascular risk. Compensated cirrhosis is not a contraindication. In patients with decompensated cirrhosis, statins should be prescribed with extreme caution at low doses, and with frequent monitoring of creatinine phosphokinase levels in order to detect adverse events in a timely fashion.

L-carnitine on myocardial function after coronary artery bypass grafting.

This study aims to evaluate the effect of L-carnitine on postoperative cardiac performance and morbidity and complications in patients undergoing coronary artery bypass grafting. Between April 2005 and June 2008, a total of 60 patients (36 males, 24 females; mean age 60.6 years; range 57 to 65) who were scheduled for coronary artery bypass grafting were prospectively randomized to receive one of three different strategies of myocardial preservation. Group A (n=20) received antegrade crystalloid cardioplegia, Group B (n=20) received antegrade blood cardioplegia, and Group C (n=20) received antegrade blood cardioplegia with carnitine. Samples for lactate dehydrogenase (LDH), creatinine phosphokinase (CPK), creatinine phosphokinasemyocardial band (CK-MB), and Troponin-I were taken from coronary sinus during the operation and from peripheral venous line postoperatively. Blood samples were obtained before CPB, just after CPB and postoperative 1, 6, 12, 24 and 48 hours. Levels of CPK, CK-MB and Troponin-T levels were studied by immunoassay method. The patients who received carnitine had significantly improved cardiac output, cardiac index, and right and left ventricular stroke work immediately after cardiopulmonary bypass and at the first postoperative hour (p=0.01). Troponin-T levels decreased in all patients after 12 hours postoperatively, and this change was most prominent in Group C (p=0.001). Intravenous supplementation of carnitine during cardioplegia provides better results on the recovery of cardiac function and metabolic parameters after coronary artery bypass grafting.

Necrotizing Autoimmune Myopathy: Clinicopathologic Study from a Single Tertiary Care Centre.

Background:Idiopathic inflammatory myopathies (IIMs) are a group of chronic, autoimmune disorders which include a new entity, necrotizing autoimmune myopathy (NAM). NAM lacks inflammation and presents with markedly elevated creatinine phosphokinase (CPK) levels. It is associated with connective tissue diseases (CTDs), statin use, malignancies, and most cases are idiopathic.Objectives:The objectives of this study are to describe the clinicopathologic features in muscle biopsy-proven cases of NAM. To emphasize the role of laboratory parameters such as CPK levels and myositis profile in the diagnosis of NAM.Materials and Methods:This is a retrospective study including 15 patients of NAM diagnosed on muscle biopsy over a period of 2 years. The slides of the biopsies were reviewed, and clinical data, electromyography findings, and CPK levels were obtained. Myositis profile was done.Results:Necrotizing myopathy accounted for 13.63% (15 cases) of total inflammatory myopathies (110 cases) in the study. These were grouped into CTD-associated NAM, statin-associated NAM, paraneoplastic NAM and idiopathic NAM which was the common type. All cases presented with progressive proximal muscle weakness and had markedly elevated CPK levels. Anti-3-hydroxy-3-methyl-glutaryl-coenzyme A reductase and antisignal recognition particle antibodies were seen to be positive in six patients. Muscle biopsies showed predominant fiber necrosis with significant fiber degeneration and regeneration in the absence of inflammation. All patients received immunotherapy with significant improvement was seen in six patients with two mortalities.Conclusion:Necrotizing myopathy is a new addition to the spectrum of IIM. Clinicopathologic correlation is important for appropriate diagnosis. It is found to be refractory to corticosteroids monotherapy. The course of illness is not uniform, and in some patients, there can be rapid worsening with mortality.

Significance of Diagnostic Paracentesis in the Preoperative Diagnosis of Strangulated Small Bowel Obstruction

Objective: This study aimed to clarify the significance of diagnostic paracentesis (DPC) and ascites analysis in the preoperative diagnosis of strangulated small bowel obstruction (SBO). Methods: Between June 2008 and May 2018, 38 patients underwent DPC and ascites analysis based on a preoperative diagnosis of strangulated SBO. The patients were divided into two groups based on the intraoperative macroscopic bowel condition: the strangulated (26 patients) and simple (12 patients) groups. The following factors were investigated and compared between the two groups: patient characteristics, preoperative vital signs, blood test results, ascites analysis results white blood cell [WBC] and red blood cell [RBC] counts, and lactate dehydrogenase and creatinine phosphokinase levels), and computed tomography (CT) findings. Results: No procedure-related complications were noted. The vital signs did not differ significantly between the two groups. The arterial base excess (BE) level was significantly lower in the strangulated group than in the simple group, and a BE level of ≤ -1.1 mmol/L had a sensitivity of 65%, specificity of 92%, and overall accuracy of 74% for differentiating the two groups. The ascites RBC count was significantly higher in the strangulated group than in the simple group, and an ascites RBC count of ≥ 20,000/mm3 had a sensitivity of 81%, specificity of 83%, and overall accuracy of 82% for differentiating the two groups. Regarding the distribution of the patients, 24 (92%) patients of the strangulated group were present in the area of BE level of ≤ -1.1 mmol/L or ascites RBC count of ≥ 20,000/mm3. Strangulation sign on CT, besides accumulation of ascites, was more frequently and significantly detected in the strangulated group than in the simple group. Conclusion: Our results suggest that DPC and ascites analysis, particularly ascites RBC count, are significant in the preoperative diagnosis of strangulated SBO when combined with CT findings and BE level.

A case report and literature review of daptomycin-induced liver injury

Daptomycin is a lipopeptide antimicrobial used to treat gram positive organisms including multi-drug resistant infections. It has been shown to occasionally cause abnormalities in liver function but more commonly is associated with elevations in serum creatinine phosphokinase (CK) (Hair and Keam, 2007) [1]. We describe a case where a patient being treated for methicillin-resistant Staphylococcus aureus (MRSA) bacteremia with daptomycin developed asymptomatic elevated transaminases without evidence of multiorgan failure, hyperbilirubinemia or elevation of CK levels. Other etiologies for liver injury were considered and ruled out, and after daptomycin was discontinued, the transaminases returned to normal levels. We also provide a review of other cases to date documenting possible cases of daptomycin-induced liver injury.

Evaluation of cardiac functions in children with Duchenne Muscular Dystrophy: A prospective case-control study.

BackgroundDuchenne muscular dystrophy (DMD) is the most common childhood form of muscular dystrophy. The incidence of cardiomyopathy in DMD increases with age, so its early detection is important because institution of cardioprotective medical therapies may slow adverse remodeling and attenuate heart failure symptoms in these patients.ObjectiveTo assess the cardiac functions in children clinically suspected to have DMD.MethodsOver a one-year period, 28 male children aged from 3 to 18 years old, who met the criteria for diagnosis of DMD compared to 47 healthy controls children, were approached to participate in the study. The included children were subjected to full clinical examination, and blood samples were collected to determine creatinine phosphokinase (CPK), troponin I enzyme, myoglobin and lactate dehydrogenase (LDH) enzyme level. Echocardiography and 12-leads electrocardiogram (ECG) were also done for children in both groups. Data were analyzed using Independent-samples t-test, Mann-Whitney U, Chi square, and Fisher’s exact test.ResultsThe mean age of the cases group was 7.29±3.24 years versus 8.06±2.86 years for controls. In DMD group, 25% had positive family history of DMD while 35.7% of them had positive consanguinity. All cases had elevated CPK level while CPK level in controls was normal (p<0.0001). LDH level was elevated in 19 cases (67.86%) of DMD while all controls children had normal LDH level (p<0.0001). Furthermore, the mean serum myoglobin level of DMD patients was higher relative to that of healthy controls (39.39±7.25 versus 33.68 ±12.38 ng/ml respectively) (p=0.01). Echocardiography of our patients revealed that seven cases (25%) had low ejection fraction (EF) and fraction shortening (FS). In addition, all controls children had normal EF (p<0.0001) and normal FS (p<0.0001). Interestingly, ECG showed that 28.57% of cases had sinus tachycardia vs. 6.88% for controls (p=0.0001). Prolonged QTc interval was present in 39.29% of cases (mean 431.39±43.60) while all controls had normal QTc duration for age (mean of 415.17±25.2) (p<0.0001).ConclusionECG manifestations in children with DMD in the form of sinus tachycardia and prolonged QTc interval are an early alarm for developing cardiomyopathy before overt echocardiographic findings appear.

Patients experiencing statin-induced myalgia exhibit a unique program of skeletal muscle gene expression following statin re-challenge.

Statins, the 3-hydroxy-3-methyl-glutaryl (HMG)-CoA reductase inhibitors, are widely prescribed for treatment of hypercholesterolemia. Although statins are generally well tolerated, up to ten percent of statin-treated patients experience myalgia symptoms, defined as muscle pain without elevated creatinine phosphokinase (CPK) levels. Myalgia is the most frequent reason for discontinuation of statin therapy. The mechanisms underlying statin myalgia are not clearly understood. To elucidate changes in gene expression associated with statin myalgia, we compared profiles of gene expression in skeletal muscle biopsies from patients with statin myalgia who were undergoing statin re-challenge (cases) versus those of statin-tolerant controls. A robust separation of case and control cohorts was revealed by Principal Component Analysis of differentially expressed genes (DEGs). To identify putative gene expression and metabolic pathways that may be perturbed in skeletal muscles of patients with statin myalgia, we subjected DEGs to Ingenuity Pathways (IPA) and DAVID (Database for Annotation, Visualization and Integrated Discovery) analyses. The most prominent pathways altered by statins included cellular stress, apoptosis, cell senescence and DNA repair (TP53, BARD1, Mre11 and RAD51); activation of pro-inflammatory immune response (CXCL12, CST5, POU2F1); protein catabolism, cholesterol biosynthesis, protein prenylation and RAS-GTPase activation (FDFT1, LSS, TP53, UBD, ATF2, H-ras). Based on these data we tentatively conclude that persistent myalgia in response to statins may emanate from cellular stress underpinned by mechanisms of post-inflammatory repair and regeneration. We also posit that this subset of individuals is genetically predisposed to eliciting altered statin metabolism and/or increased end-organ susceptibility that lead to a range of statin-induced myopathies. This mechanistic scenario is further bolstered by the discovery that a number of single nucleotide polymorphisms (e.g., SLCO1B1, SLCO2B1 and RYR2) associated with statin myalgia and myositis were observed with increased frequency among patients with statin myalgia.

Pseudohypertrophic myopathy in a child with hypothyroidism (Kocher—Debre—Semelaigne syndrome)

The Kocher-Debre-Semelaigne syndrome (KDSS) is a rare disease that clinically manifests as hypothyroidism and muscle pseudohypertrophy of the trunk and extremities. KDSS occurs mainly in countries where there is no screening for congenital hypothyroidism; however, this syndrome can develop when there is acquired hypothyroidism. In this syndrome, muscle hypertrophy is false (pseudohypertrophy); it is not accompanied by an increase in muscle strength but, on the contrary, leads to a decrease in muscle strength and the development of muscle hypotension. Increased levels of creatinine phosphokinase (CPK) and lactate dehydrogenase (LDH) are the characteristic laboratory sign of myopathy in this syndrome. The signs of hypothyroidism and muscle pseudohypertrophy are reduced by levothyroxine therapy. Indicators of the final height in the case of delayed treatment may remain poor. The clinical signs characteristic of the disease, especially in the presence of a nonspecific clinical picture of hypothyroidism, enable an early diagnosis and timely treatment, which emphasizes the importance of doctors’ awareness of this syndrome.

Molecular Characterization, Hematological and Biochemical Studies on Foot and Mouth Disease Virus Serotype O in Buffaloes and Cows in Dakahlia Governorate, Egypt

The present study aimed to evaluate the hematological and serum biochemical parameters in buffaloes and cows infected with foot and mouth disease (FMD) virus. Forty buffaloes and cows (6 months - 2 years old) were used. Twenty buffaloes and cows clinically healthy and were used as control, the other twenty buffaloes and cows showed characteristic clinical signs of FMD. Blood samples were collected and serum was separated from both groups to measure the hematological and biochemical parameters. Infected buffaloes and cows showed fever, anroxia, excessive foamy salivation and ulcer formation in the mouth. Compared to the control buffaloes, erythrocytic count (RBCs), hemoglobin (Hb) and packed cell volume (PCV) in the FMD infected buffaloes were significantly decreased, while mean corpascular hemoglobin (MCH) was significantly increased. In addition, significant increase in toltal leukocyte count (TLC), neutrophils, with a significant decrease in eosinophil and lymphocyte counts were observed. Moreover, cows infected with FMD virus showed no significant changes in the erythrogram, while, significant increases in TLC and neutrophils, with a significant decrease in eosinophil and lymphocyte counts were observed when compared with the control group. There were significant decreases in the levels of serum total proteins, albumin and globulin, while serum asprtate transferase (AST), creatinine phospho-kinase (CPK), glucose and cortisol levels were significantly increased in the infected animals. Tissue and saliva specimens were collected and analyzed by using universal primer using reverse-transcription polymerase chain reaction (RT-PCR). All the identified viruses were of serotype ‘O’. It is concluded that FMDV serotype ‘O’ is circulating among cows and buffaloes in the study area.

Acute rhabdomyolysis associated with levetiracetam therapy in a child

Objective: Levetiracetam (LEV) is a new antiepileptic drug that is effective in adults and children with partial-onset seizures or idiopathic or symptomatic generalized seizures. Side effects include fatigue, somnolence, infection, headache, behavioral changes and skin rashes. Methods: A 13-year-old girl presented with a history of myalgia since last 2–3 days to our hospital. On medical history, she had partial onset of secondarily generalized seizures during sleep since 2 months. The patient was administered LEV monotherapy. One week after starting LEV therapy, she experienced mild myalgia. The physical and neurological examinations were normal. Results: On laboratory examination, creatinine phospho kinase (CPK) was 986 U/L (normal range 27–168). Rhabdomyolysis was diagnosed with clinical and biochemical findings. After stopping LEV, serum CPK level gradually decreased and returned into normal values. Conclusion: We conclude that LEV may cause rhabdomyolysis. Children treated with LEV should be warned regarding these potential adverse effects, to facilitate early withdrawal of drug.