Showing posts with label creatine kinase. Show all posts
Showing posts with label creatine kinase. Show all posts

Thursday, June 30, 2016

Why is my CPK so high - Revisited

Over the years, the post with the greatest activity has been “Why is my CPK so high?” Readers have posted more comments and asked more questions on this subject than any other post. For this reason, I thought it might be appropriate to review creatine kinase (CPK) and provide links to other posts on the topic.

The Johns Hopkins Arthritis Center provides a good explanation of creatinine kinase (CPK).

CPK also called creatine kinase (CK) is an enzyme (chemical) found specifically in muscle cells. One form of CPK is found in heart muscle cells, another in the skeletal muscle cells. CPK is also found in brain cells. When these cells are damaged for any reason, the CPK is released into the blood and can be measured by a blood test. If the heart CPK (CPK-MB) is elevated it can mean that the heart is damaged which can occur in a heart attack or in conditions in which the heart muscle is inflamed such as viral myocarditis. Skeletal muscle can be damaged in trauma such as in severe injury to the muscles, or after intense exercise causing an increase in the skeletal muscle form of CPK (CPK-MM). Certain drugs such as cholesterol lowering drugs (statins) can damage muscle and elevate CPK. Other causes are alcohol, viruses, hereditary conditions. Finally CPK can be elevated in certain autoimmune diseases that cause inflammation in the muscle such as polymyositis or dermatomyositis.

In the post on “Why is my CPK so high,” Terry Blytheway does a good job of explaining CPK.

“Going back to basics, there are three types of creatine kinase or isoenzymes in the body: CK-BB is mainly produced by the brain and the smooth muscle; CK-MB is primarily produced by the heart muscle; and most of CK-MM is produced by the skeletal muscle.”

He goes on to explain what higher than normal CPK might indicate.

“…if the test reveals that the level of creatine kinase circulating in the blood is higher than it should be in normal conditions, then chances are that the human body in question has suffered damage either to the muscle or the brain. In fact, astronomical levels of creatine kinase are indicative of injuries, rhabdodomyolysis, myocardial infarction, myocarditis, myositis, malignant hypethermia, McLeod syndrome, neuroleptic malignant syndrome, and hypothyroidism. If most of this sounds like gibberish to you, just remember that a heart attack, a muscle disease or a stroke may result in abnormally raised creatine kinase levels in the blood. Statin medications used to decrease serum cholesterol levels may also be the culprit.”

If you are interested, below are links to other posts on CPK.


Thursday, June 2, 2016

Non-neural phenotype of spinal and bulbar muscular atrophy



Below is an abstract of a research paper published last year. This study was focused on non-neurological characteristics in 73 patients with Kennedy’s Disease. 

“Non-neurological clinical features have not been extensively investigated in previous reports. The aim of the present study was a deep characterisation of the involvement of the main androgen-responsive tissues in a large collection of patients with SBMA. The findings highlight novel non-neural dysfunctions and a wide phenotypic spectrum, suggesting the need for a comprehensive, multidisciplinary approach to SBMA.

Abstract

Objective To carry out a deep characterisation of the main androgen-responsive tissues involved in spinal and bulbar muscular atrophy (SBMA).

Methods 73 consecutive Italian patients underwent a full clinical protocol including biochemical and hormonal analyses, genitourinary examination, bone metabolism and densitometry, cardiological evaluation and muscle pathology.

Results Creatine kinase levels were slightly to markedly elevated in almost all cases (68 of the 73; 94%). 30 (41%) patients had fasting glucose above the reference limit, and many patients had total cholesterol (40; 54.7%), low-density lipoproteins cholesterol (29; 39.7%) and triglyceride (35; 48%) levels above the recommended values. Although testosterone, luteinising hormone and follicle-stimulating hormone values were generally normal, in one-third of cases we calculated an increased Androgen Sensitivity Index reflecting the presence of androgen resistance in these patients. According to the International Prostate Symptom Score (IPSS), 7/70 (10%) patients reported severe lower urinal tract symptoms (IPSS score >19), and 21/73 (30%) patients were moderately symptomatic (IPSS score from 8 to 19). In addition, 3 patients were carriers of an indwelling bladder catheter. Videourodynamic evaluation indicated that 4 of the 7 patients reporting severe urinary symptoms had an overt prostate-unrelated bladder outlet obstruction. Dual-energy X-ray absorptiometry scan data were consistent with low bone mass in 25/61 (41%) patients. Low bone mass was more frequent at the femoral than at the lumbar level. Skeletal muscle biopsy was carried out in 20 patients and myogenic changes in addition to the neurogenic atrophy were mostly observed.

Conclusions Our study provides evidence of a wide non-neural clinical phenotype in SBMA, suggesting the need for comprehensive multidisciplinary protocols for these patients.”