Clinical Features of Rhabdomyolysis After Open and Laparoscopic Roux-en-Y Gastric Bypass

Background Rhabdomyolysis (RML) is caused by muscle injury, this may cause kidneys overload and lead to acute renal failure (ARF). The risk factors for RML in bariatric surgery (BS) are operative time (OT) >4 h and high BMI. The frequency of RML in BS varies from 12.9 to 37.8%. This study has the objective of describing the characteristics associated with RML and ARF in BS. Methods We studied retrospectively 114 patients submitted to BS. Criteria for RML were CPK level >950 IU/l (five times the normal value). The variables were BMI, OT, age, intraoperative hydration and diuresis, CPK, creatinine, arterial hypertension, peripheric vascular disease, diabetes, open and laparoscopic techniques—inclusion criteria: patients submitted to gastric bypass; exclusion: renal failure and statins use. Results RML incidence was 7%. The factors associated with RML in the bivariate analysis were hepatic steatosis, high BMI, high weight, higher excess weight, and prolonged OT. The risk factor for RML in the multivariate analysis was BMI ≥ 50 kg/m². When the OT was below 2 h the incidence of RML was zero, but this was not significant in the multivariate analysis. The factors associated with a higher risk of CPK elevation (multivariate analysis) were hypertension and open technique. Conclusion BS is safe, with low incidence of RML/ARF. High BMI is associated with a higher risk of RML. Probably a longer OT is associated with a higher risk of RML not statistically demonstrated in this study. The factors associated with a higher risk of CPK elevation were hypertension and open technique.     

Acute renal failure due to rhabdomyolysis after proximal humerus fracture associated with axillary artery rupture

The anatomical proximity of axillary artery to the humeral head makes it quite vulnerable to blunt trauma during shoulder injury. Axillary artery rupture and prolonged ischemia may lead to rhabdomyolysis and acute renal failure. Herein we present a case of a patient who sustained proximal humerus fracture associated with axillary artery rupture and acute renal failure due to rhabdomyolysis.     

Clinical and laboratory features of hyponatremia-induced myopathy

Background The present study was undertaken to determine the clinical and laboratory features of hyponatremia-induced myopathy. Methods We collected 14 hyponatremic subjects (six men and eight women) with serum creatine kinase (CK) levels of more than 500 IU/ml during the 5-year period between 2001 and 2005. The mean ± SD patients’ age was 66.5 ± 16.7 years (range, 37 to 88 years). Results The causes of the hyponatremia were: syndrome of inappropriate secretion of antidiuretic hormone (SIADH; n = 4), mineralocorticoid-responsive hyponatremia of the elderly (MRHE; n = 2), hypopituitarism (n = 1), psychogenic polydipsia (n = 3), congestive heart failure (n = 3), and unknown cause (n = 1). The subjects were subgrouped into two groups: acute onset of myopathy and slowly progressive onset. The age at onset was 62.0 ± 5.7 years (mean ± SEM) in the subjects with acute onset, and 77.8 ± 1.5 years in those with slowly progressive onset (P = 0.02). At the onset, there was no difference in serum Na levels between the acute onset and the slowly progressive onset groups, but there was a significant difference in maximal serum CK levels between the groups (7072 ± 2317 vs 722 ± 104 IU/ml; P = 0.02). Maximal serum CK levels were widely distributed among the ages in the subjects with acute onset, whereas maximal serum CK levels were mildly elevated in the elderly subjects with slowly progressive onset. The elevated serum CK levels were normalized at a maximum of 14 days after the onset in all the subjects. Conclusions The present findings indicate that hyponatremia infrequently causes skeletal muscle disruption, and that there are two types of hyponatremia-induced myopathy, acute onset and slowly progressive onset.     

Deep vein thrombosis complicating severe hypernatremia,rhabdomyolysis, and acute renal failure in a patient with untreated seizure disorder

We report a 22-year-old male patient with untreated seizure disorder, presenting with increased frequency of seizures followed by encephalopathy. Laboratory evaluation showed severe hypernatremia (175 meq/l sodium), rhabdomyolysis, and acute renal failure (ARF). Excessive insensible water loss in hot and humid weather, associated with an inability to obtain adequate water replacement, led to a hyperosmolar state (plasma osmolality, 398 mOsm/kg). He was vigorously treated with hypotonic fluid supplement and, further, needed dialysis therapy (peritoneal dialysis followed by hemodialysis) for acute renal insufficiency. The patient survived without any neurological sequelae, but the clinical course was complicated by acute deep vein thrombosis. This case represents what we believe is a unique report in the literature of severe hypernatremia developing via the pathogenic mechanism outlined above and the complication of acute peripheral venous thrombosis, which has not been reported in adults. The purpose of this report is to emphasize hyperosmolarity as a newly described cause of rhabdomyolysis, ARF, and a hypercoagulable state.     

Influenza B‐associated rhabdomyolysis in Taiwanese children

Aim: Influenza B‐associated rhabdomyolysis (IBAR) is an infrequent and little‐known complication of influenza B virus infection in children. Diagnosis is usually made based on clinical history, the presence of influenza in the community and detection of virus in nasopharyngeal specimens. The aim of this study was to describe the clinical and laboratory manifestations, complications and outcomes of IBAR in Taiwanese children. Methods: A retrospective analysis was conducted in patients aged <17 years who had been diagnosed with IBAR at a university children’s hospital in North Taiwan during 2000–2007. All children enrolled in the study had presented with rhabdomyolysis associated with laboratory‐confirmed influenza B infections. Demographic data, clinical manifestations, complications and outcomes were included in the analysis. Results: Overall, 24 IBAR cases were analysed. IBAR typically occurred in school‐aged children with a 7:3 male:female ratio. The mean age was 7.2 ± 1.9 years. Nearly 63% of cases occurred between the ages of 6 and 9 years. The median interval between the onset of influenza and onset of IBAR was 3.4 days (range, 1–14). The calf muscles were involved in all cases. Laboratory tests indicated a mean initial blood creatine kinase of 4212 U/L. The median time to clinical recovery was 5 days (range 1–24). No patient had renal failure. IBAR tends to occur mainly in winter and spring during influenza B outbreaks. IBAR sometimes induces some complications, and early detection and careful medical treatment are necessary. Conclusion: The results of this study indicate that outcomes of IBAR are good with proper medical care.     

Myoglobin‐Induced Apoptosis: Two Pathways Related to Endoplasmic Reticulum Stress

Myoglobin plays an important role in rhabdomyolysis‐induced acute kidney injury (AKI), but the underlying mechanisms are still unclear. The present study investigates myoglobin‐induced apoptosis in HK‐2 cells (human renal proximal tubule cells) to discover some of the mechanisms involved in rhabdomyolysis related AKI. Metmyoglobin is reduced to ferrous myoglobin by ascorbic acid, and then the HK‐2 cells are incubated with ferrous myoglobin. Cell viability is measured by 3‐(4,5)‐dimethylthiahiazo(‐z‐y1)‐3,5‐di‐phenytetrazoliumromide (MTT) assay, and cell injury is tested by supernatant lactose dehydrogenase (LDH). Cell apoptosis is evaluated by fluorescent microscopy of Hoechst staining and by flow cytometry of Annexin V/PI double staining. The apoptosis related protein expression is determined by Western blot. HK‐2 cells were incubated with 200 µM ferrous myoglobin for 24 h, the cell viability decreased and supernatant LDH release increased. Hoechst staining indicated more apoptosis after incubation. Molecular chaperone glucose‐related protein 78 (GRP78), cytochrome C, caspase‐9 started to increase within 3 h after incubation while caspase‐4, caspase‐8 showed no significant change. (iii) When the inositol triphosphate receptor (IP3R) calcium channel was blocked by 2‐aminoethoxydiphenyl‐borinate (2‐APB), caspase‐9 was completely inhibited, GRP78 and caspase‐4 increased dramatically, and caspase‐3 expression was not affected. The apoptosis in HK‐2 cells showed no significant change. Apoptosis in HK‐2 cells incubated with ferrous myoglobin is an endoplasmic reticulum stress induced, IP3R calcium channel mediated, caspase‐9 dependent intrinsic pathway. When the intrinsic pathway was inhibited using an IP3R calcium channel blocker, endoplasmic reticulum stress increased, resulting in the activation of caspase‐4 that cleaved caspase‐3 and generated a substitutive pathway of apoptosis.     

Myositis as an adverse event of immune checkpoint blockade for cancer therapy

Objectives

Immune checkpoint inhibitors (ICIs) can successfully treat cancer, but their use can be hindered by serious immune-related adverse events. We report six patients receiving ICIs who presented with de novo myositis.

A rare but potentially lethal complication of dengue

Severe rhabdomyolysis is an uncommon but potentially fatal complication of dengue fever that is not well characterised and may be underreported. With the resurgence and continued rise of dengue cases worldwide, physicians must be aware of the less common but serious complications of dengue. Here, we report a patient who presented with severe rhabdomyolysis secondary to dengue fever with a serum creatine kinase of 742 900 U/L.     

Effect of Alcohol and Electrical Stimulation on Leakage of Creatine Kinase from Isolated Fast and Slow Muscles of Rat

Binge drinking of alcohol may lead to acute alcoholic myopathy with rhabdomyolysis, which is characterized by skeletal muscle damage, elevated serum creatine kinase (CK), and myoglobinuria. This study was undertaken to test whether alcohol acts directly on the skeletal muscles to enhance the leakage of CK, and to assess the influence of fiber-type composition and repetitive contractions of the muscle on the effect of alcohol. After 4 hr of incubation in normal physiological solution at 37°C, mean leakage of CK was 0.7 units/mg from isolated rat extensor digitorum longus (EDL), which has more fast-twitch glycolytic muscle fibers, and 1.2 units/mg from the soleus, which has more slow-twitch oxidative muscle fibers. Ethanol at 0.1, 0.2, and 0.5% concentrations caused significantly greater increase in leakage of CK from soleus than from EDL. In normal physiological solution, electrical stimulation at 1 Hz for 4 hr increased the leakage of CK by about the same degree in both EDL and soleus. In the presence of 0.1 and 0.2% ethanol, electrical stimulation markedly potentiated the alcohol-induced leakage of CK from both soleus and EDL. These results indicate that alcohol increases the leakage of CK by acting directly on skeletal muscle fibers, especially of the slow-twitch oxidative type, and that repeated muscle contractions potentiate the alcohol effect. These studies suggest that exercise may increase the chances of rhabdomyolysis in the alcoholics.