Die Überlegung mit dem Methylamin ist eine theoretische, aber mögliche. Damit Formaldehyd in entsprechenden Mengen anfallen kann, muß auch eine entsprechende Menge an Methylamin vorliegen. Das Enzym, das hierfür verantwortlich ist, ist die Semikarbazid-empfindliche Amino Oxydase. Hängt aber von der Aktivität des Enzyms ab. Experimentelle Studien zeigen, daß die SSAO-Aktivität ein Parameter für Artherioklerose sein kann (Formaldehyd wirkt auch gefäßschädigend).
Mit dem Formaldehydanstieg wurde übrigens auch bei der krebserzeugenden Nebenwirkung argumentiert. (Nicht ganz schlüssig.)
Ja, die Ringer wären das eine. Die waren alle drei dehydriert, was aber auch auf die übliche Praktik des Gewichtmachens geschoben werden kann (anteilig zumindest).
Es gibt auch einen Bericht über einen BB´ler, der einen Schlaganfall erlitt. Der nahm aber auch Ma-Huang.
Zu dem Gewichtheber habe ich den Fall mal rausgesucht:
A 24-year-old previously healthy man came to the emergency department complaining of severe bilateral thigh pain on awakening, which gradually worsened during the day to the point that he could no longer walk. On the day before his visit, the patient participated in approximately 3 hours of lower extremity exercise. For the preceding 8 days, he had not exercised because of a minor muscle strain. The patient had been an avid body builder for approximately 5 years and reported that he had performed similar lower extremity exercise without any problems. For the past year he had been using oral creatine supplementation at five times the recommended maintenance dose (25 g/d). The remainder of his medical history was unremarkable except for occasional alcohol use (average of 4 drinks per month). The patient denied use of tobacco, anabolic steroids, illicit drugs, or other ergogenic supplements. Review of systems was only notable for onset of gross hematuria shortly after his arrival at the emergency department.
In the emergency department, his blood pressure, respirations, temperature, and heart rate were normal. Findings on his physical examination were normal except for bilaterally tense, edematous anterior thighs and severe pain with any degree of knee flexion. Initial laboratory studies were serum sodium 149 mEq/L, potassium 4.2 mEq/L, blood urea nitrogen 22 mg/dL, creatinine 1.0 mg/dL, creatine phosphokinase 131,000 U/L, and a calculated serum osmolality of 311 mOsm/L. Urinalysis showed proteinuria (3+), hematuria (4+), 10 to 15 red blood cells per high-power field and 80 to 100 red cell casts per high-power field. Of note, serum calcium and phosphorus and urine myoglobin were not measured. The patient had no previous laboratory reports on file for comparison. Acute compartment syndrome was suspected and confirmed by anterior, medial, and lateral quadriceps compartment pressures of 34, 34, and 32 mm Hg on the right and 17, 15, and 15 mm Hg on the left, respectively. The patient was admitted for treatment of acute quadriceps compartment syndrome and rhabdomyolysis and underwent emergency bilateral tri-compartment fasciotomies. Left fasciotomies were done despite normal compartment pressures because the patient had severe symptoms on the left. Perioperatively, the rhabdomyolysis was treated with aggressive hydration with crystalloid and urine alkalinization and then diuresis.
During the first several days of hospitalization, the patient's creatinine levels began to rise, and he developed edema of the lower extremities extending up to the flanks. On hospital day 6, he developed increasing dyspnea and hypoxia. The patient developed a new grade 2/6 systolic murmur at the left upper sternal border. A chest radiograph showed cardiomegaly, pulmonary venous congestion, and bilateral effusions. An electrocardiogram showed a left axis deviation of N38|SD and incomplete right bundle branch block. An echocardiogram showed an ejection fraction of 48%, concentric left ventricular hypertrophy, and mild mitral and tricuspid regurgitation. The pulmonary edema was believed to be secondary to iatrogenic fluid overload, although it was unclear whether the echocardiogram findings were preexisting or temporarily associated with the acute illness. During the remainder of the hospital course, his pulmonary edema gradually resolved with aggressive diuresis. The rhabdomyolysis and acute renal failure resolved with hydration and urine alkalinization with a maximum creatine kinase of g800,000 U/L and creatinine of 3.1 mg/dL. The patient required aggressive inpatient physical therapy until he was able to walk independently. After a 22-day hospital course, he was discharged for continued outpatient physical therapy.
At a 6-month follow-up visit, the patient had returned to work but was still undergoing aggressive physical therapy and had achieved approximately 60% of his premorbid quadriceps strength. At that time an echocardiogram showed high-normal left ventricular thickness, ejection fraction of 55%, and mild right ventricular enlargement without further evidence of mitral or tricuspid regurgitation. A follow-up echocardiogram at 12 months again showed mild increased left ventricular thickness, which was within normal limits when calculated with respect to body surface area. The patient is no longer taking creatine or any other performance-enhancing agents because he believes that use of creatine led to this condition.
Although a causal relation cannot be proved with respect to creatine and the patient described in this article, this case raises further suspicion regarding the safety of creatine with higher doses and long-term use.
Ein Kompartmentsyndrom entsteht durch Flüssigkeitansammlung (z. B. Wasser, Blut) im Muskelgewebe, z. B. nach einem Trauma. Jeder kennt solche Schwellungen. Normalerweise nicht schlimm. Gefährlich wird es erst dann, wenn so etwas an Armen oder Beinen ein größeres Ausmaß annimmt. Die Muskeln liegen hier in bindegewebig umhüllten Logen (Faszienlogen), die man auch als Kompartimente bezeichnet (daher Kompartmentsyndrom). Hier kann die Schwellung nicht wesentlich "ausweichen", da das umgebende Bindegewebe nicht sehr dehnbar ist. Dadurch steigt der Druck im betroffenen Kompartiment. Das führt zur Kompression der darin ligenden Strukturen -> Muskeln, Nerven, Gefäße. Es kommt somit zur Druckschädigung. Wenn man Gefäße über länger Zeit abdrückt kann man sich vorstellen, was passieren kann. Reduzierte Durchblutung -> Absterben des Gewebes. Nervenschädigung -> Gefühlsstörungen bis hin zu Lähmungen. Zerstörung des Muskelgewebes (-> Rhabdomyolyse).
Wenn das droht, hilft nur noch eine chirurgische Spaltung der Faszien, um Platz zu schaffen.
jeckyll