- [Muscle Cramps: Superficial Knowledge Versus Evidence]. [Journal Article]
- SSSportverletz Sportschaden 2018 Nov 13
- CONCLUSIONS: It is necessary to spread current scientific knowledge among the population, especially via coaches and doctors acting as multipliers.
- A 49-Year-Old Man with Debilitating Aches and Pains and a Mysterious Culprit. [Journal Article]
- ACArthritis Care Res (Hoboken) 2018 Nov 10
- The patient reported pain that started insidiously in his feet and gradually progressed proximally from the lower extremities to the pelvis, spine and chest. He described it as dull and aching, const...
The patient reported pain that started insidiously in his feet and gradually progressed proximally from the lower extremities to the pelvis, spine and chest. He described it as dull and aching, constant and exacerbated by minimal movement and even inspiration. He complained of frequent severe muscle spasms, cramps, progressive weakness and difficulty with ambulation leading to the use of a wheelchair. He also reported being diagnosed with multiple non-traumatic rib fractures. He had seen multiple physicians in the past for his condition and was given a multitude of treatments without effect. Non-steroidal anti-inflammatory medications provided minimal relief. He had been treated with sulfasalazine 2 gm po daily, golimumab 50 mg subcutaneously once monthly for 6 months then etanercept 50 mg subcutaneously once weekly for 6 months for "presumed spondyloarthritis" with no effect. He was diagnosed with fibromyalgia by other physicians and was prescribed pregabalin without improvement. He denied using any other medications. This article is protected by copyright. All rights reserved.
- Physiological, biochemical and histopathological changes associated with heatstroke in the Galah (Eolophus roseicapilla) and Rock Dove (Columba livia). [Journal Article]
- APAvian Pathol 2018 Nov 09; :1-49
- The pathophysiology of heat illnesses in birds has not been well characterised. In this study, we describe the changes in heart rate, respiratory rate, blood biochemistry and histopathological findin...
The pathophysiology of heat illnesses in birds has not been well characterised. In this study, we describe the changes in heart rate, respiratory rate, blood biochemistry and histopathological findings in galahs and rock doves after heat exposure under standardized conditions designed to induce heatstroke. Birds in the heat exposed group were exposed to environmental heat stress and compared to control birds. Both groups of birds were under general anaesthesia throughout the experiment and serial blood collections were performed for biochemical analyses, while organs were collected at the end of the experiment for histopathology. No electromyography traces consistent with the onset of heat cramps were observed in any of the birds. Biochemical changes suggestive of skeletal muscle and hepatocellular injury, including hyperkalaemia and increased serum muscle and hepatic enzyme activities, were often observed in heat exposed galahs and rock doves at the onset of heatstroke. Microscopic analyses did not reveal any significant cardiac changes, although some lungs had signs of acute congestion. Some heat exposed rock doves had microscopic changes indicative of necrosis in the pectoral muscle. There were significant hepatic changes in some heat exposed galahs, but not in rock doves. This suggests that there may be species differences amongst birds in the organs most affected by heatstroke. The observed species differences in the physiological, biochemical and histopathological changes indicate that bird species should be studied separately for clinical syndromes such as heatstroke.
- Myopathies Related to Glycogen Metabolism Disorders. [Review]
- NNeurotherapeutics 2018 Nov 05
- Most of the glycogen metabolism disorders that affect skeletal muscle involve enzymes in glycogenolysis (myophosphorylase (PYGM), glycogen debranching enzyme (AGL), phosphorylase b kinase (PHKB)) and...
Most of the glycogen metabolism disorders that affect skeletal muscle involve enzymes in glycogenolysis (myophosphorylase (PYGM), glycogen debranching enzyme (AGL), phosphorylase b kinase (PHKB)) and glycolysis (phosphofructokinase (PFK), phosphoglycerate mutase (PGAM2), aldolase A (ALDOA), β-enolase (ENO3)); however, 3 involve glycogen synthesis (glycogenin-1 (GYG1), glycogen synthase (GSE), and branching enzyme (GBE1)). Many present with exercise-induced cramps and rhabdomyolysis with higher-intensity exercise (i.e., PYGM, PFK, PGAM2), yet others present with muscle atrophy and weakness (GYG1, AGL, GBE1). A failure of serum lactate to rise with exercise with an exaggerated ammonia response is a common, but not invariant, finding. The serum creatine kinase (CK) is often elevated in the myopathic forms and in PYGM deficiency, but can be normal and increase only with rhabdomyolysis (PGAM2, PFK, ENO3). Therapy for glycogen storage diseases that result in exercise-induced symptoms includes lifestyle adaptation and carefully titrated exercise. Immediate pre-exercise carbohydrate improves symptoms in the glycogenolytic defects (i.e., PYGM), but can exacerbate symptoms in glycolytic defects (i.e., PFK). Creatine monohydrate in low dose may provide a mild benefit in PYGM mutations.
- Fostering Innovation in Symptom Management among Hemodialysis Patients: Paths Forward for Insomnia, Muscle Cramps, and Fatigue. [Journal Article]
- CJClin J Am Soc Nephrol 2018 Nov 05
- Individuals receiving in-center maintenance hemodialysis bear a high burden of both physical and mood symptoms. More than half of patients on hemodialysis report sleep disturbance, muscle cramps, and...
Individuals receiving in-center maintenance hemodialysis bear a high burden of both physical and mood symptoms. More than half of patients on hemodialysis report sleep disturbance, muscle cramps, and fatigue. Patients describe symptoms as having a deleterious effect on their quality of life, suggesting that symptom alleviation may meaningfully improve patient-reported outcomes. Moreover, patients on hemodialysis have identified symptom management as a key area for research and innovation, prioritizing symptom alleviation over other health outcomes such as mortality and biochemical indices. Despite the importance of symptoms to patients, there has been little research explicitly geared toward improving patient symptoms, and therefore minimal innovation in symptom management. In general, the physiologic underpinnings of symptoms are poorly understood, hampering the development of targeted therapies. In fact, there have been few drugs or devices approved by the US Food and Drug Administration for the indication of improving any patient-reported outcomes for patients on hemodialysis. Recognizing this gap in innovation, the Kidney Health Initiative, a public-private partnership between the American Society of Nephrology and US Food and Drug Administration, convened a workgroup to first prioritize symptoms for the development of therapeutic interventions, and then identify near-term actionable research goals for the prioritized physical symptoms of insomnia, muscle cramps, and fatigue. This paper summarizes the pathophysiology of the three prioritized symptoms, identifies key knowledge gaps, acknowledges factors that challenge development of new therapies, and offers the nephrology community actionable research goals for insomnia, muscle cramps, and fatigue.
- Hypoparathyroidism and the Kidney. [Review]
- EMEndocrinol Metab Clin North Am 2018; 47(4):839-853
- Hypocalcemia and hyperphosphatemia are the pathognomonic biochemical features of hypoparathyroidism, and result directly from lack of parathyroid hormone (PTH) action on the kidney. In the absence of...
Hypocalcemia and hyperphosphatemia are the pathognomonic biochemical features of hypoparathyroidism, and result directly from lack of parathyroid hormone (PTH) action on the kidney. In the absence of PTH action, the renal mechanisms transporting calcium and phosphate reabsorption deregulate, resulting in hypocalcemia and hyperphosphatemia. Circulating calcium negatively regulates PTH secretion. Hypocalcemia causes neuromuscular disturbances ranging from epilepsy and tetany to mild paresthesia. Circulating phosphate concentration does not directly regulate PTH secretion. Hyperphosphatemia is subclinical, but chronically promotes ectopic mineralization disease. Vitamin D-thiazide treatment leads to ectopic mineralization and renal damage. PTH treatment has the potential for fewer side effects.
- Early postoperative carbamazepine-induced tetany in a patient with trigeminal neuralgia. [Journal Article]
- JAJ Anaesthesiol Clin Pharmacol 2018 Jul-Sep; 34(3):405-406
- Points & Pearls: Electrical injuries in the emergency department: an evidence-based review [Journal Article]
- EMEmerg Med Pract 2018 Nov 01; 20(Suppl 11):1-2
- Electrical injuries can be caused by exposure to current from low-voltage and high-voltage sources as well as lightning strikes, and the circumstances of the exposure will dictate management strategi...
Electrical injuries can be caused by exposure to current from low-voltage and high-voltage sources as well as lightning strikes, and the circumstances of the exposure will dictate management strategies. Human tissues have varying resistance characteristics and susceptibility to damage, so injuries maybe thermal, electrical, and/or mechanical, potentially causing burns, thrombosis, tetany, falls, and blast injury. This issue reviews the types of trauma seen with electrical injury and how body systems can be affected by occult or delayed effects, and the optimal evidence-based resuscitation and management strategies associated with each. [Points & Pearls is a digest of Emergency Medicine Practice.]
- GeneReviews® [BOOK]
- BOOKUniversity of Washington, Seattle: Seattle (WA)
- Phosphorylase kinase (PhK) deficiency causing glycogen storage disease type IX (GSD IX) results from deficiency of the enzyme phosphorylase b kinase, which has a major regulatory role in the breakdow...
Phosphorylase kinase (PhK) deficiency causing glycogen storage disease type IX (GSD IX) results from deficiency of the enzyme phosphorylase b kinase, which has a major regulatory role in the breakdown of glycogen. The two types of PhK deficiency are liver PhK deficiency (characterized by early childhood onset of hepatomegaly and growth restriction, and often, but not always, fasting ketosis and hypoglycemia) and muscle PhK deficiency, which is considerably rarer (characterized by any of the following: exercise intolerance, myalgia, muscle cramps, myoglobinuria, and progressive muscle weakness). While symptoms and biochemical abnormalities of liver PhK deficiency were thought to improve with age, it is becoming evident that patients need to be monitored for long-term complications such as liver fibrosis and cirrhosis.
New Search Next
- Effects of Coenzyme Q10 on Statin-Induced Myopathy: An Updated Meta-Analysis of Randomized Controlled Trials. [Journal Article]
- JAJ Am Heart Assoc 2018 Oct 02; 7(19):e009835
- Background Previous studies have demonstrated a possible association between the induction of coenzyme Q10 (CoQ10) after statin treatment and statin-induced myopathy. However, whether CoQ10 supplemen...
Background Previous studies have demonstrated a possible association between the induction of coenzyme Q10 (CoQ10) after statin treatment and statin-induced myopathy. However, whether CoQ10 supplementation ameliorates statin-induced myopathy remains unclear. Methods and Results PubMed, EMBASE , and Cochrane Library were searched to identify randomized controlled trials investigating the effect of CoQ10 on statin-induced myopathy. We calculated the pooled weighted mean difference ( WMD ) using a fixed-effect model and a random-effect model to assess the effects of CoQ10 supplementation on statin-associated muscle symptoms and plasma creatine kinase. The methodological quality of the studies was determined, according to the Cochrane Handbook. Publication bias was evaluated by a funnel plot, Egger regression test, and the Begg-Mazumdar correlation test. Twelve randomized controlled trials with a total of 575 patients were enrolled; of them, 294 patients were in the CoQ10 supplementation group and 281 were in the placebo group. Compared with placebo, CoQ10 supplementation ameliorated statin-associated muscle symptoms, such as muscle pain ( WMD , -1.60; 95% confidence interval [ CI ], -1.75 to -1.44; P<0.001), muscle weakness ( WMD , -2.28; 95% CI , -2.79 to -1.77; P=0.006), muscle cramp ( WMD , -1.78; 95% CI , -2.31 to -1.24; P<0.001), and muscle tiredness ( WMD , -1.75; 95% CI , -2.31 to -1.19; P<0.001), whereas no reduction in the plasma creatine kinase level was observed after CoQ10 supplementation ( WMD , 0.09; 95% CI , -0.06 to 0.24; P=0.23). Conclusions CoQ10 supplementation ameliorated statin-associated muscle symptoms, implying that CoQ10 supplementation may be a complementary approach to manage statin-induced myopathy.