Hyperbaric Oxygen Therapy Does Not Have a Negative Impact on Bone Signaling Pathways in Humans.

INTRODUCTION: Oxygen is emerging as an important factor in the local regulation of bone remodeling. Some preclinical data suggest that hyperoxia may have deleterious effects on bone cells. However, its clinical relevance is unclear. Hence, we studied the effect of hyperbaric oxygen therapy (HBOT) on serum biomarkers reflecting the status of the Wnt and receptor activator of NF-κB ligand (RANKL) pathways, two core pathways for bone homeostasis. MATERIALS AND METHODS: This was a prospective study of 20 patients undergoing HBOT (mean age 58 yrs., range 35-82 yrs.) because of complications of radiotherapy or chronic anal fissure. Patients were subjected to HBOT (100% oxygen; 2.4 atmospheres absolute for 90 min). The average number of HBOT sessions was 20 ± 5 (range 8-31). Serum hypoxia-inducible factor 1-α (HIF1-α), osteoprotegerin (OPG), RANKL, and the Wnt inhibitors sclerostin and dickkopf-1 (DKK1) were measured at baseline and after HBOT by using specific immunoassays. RESULTS: HIF-1α in eight patients with measurable serum levels increased from 0.084 (0.098) ng/mL at baseline to 0.146 (0.130) ng/mL after HBOT (p = 0.028). However, HBOT did not induce any significant changes in the serum levels of OPG, RANKL, sclerostin or DKK1. This was independent of the patients' diagnosis, either neoplasia or benign. CONCLUSION: Despite the potential concerns about hyperoxia, we found no evidence that HBOT has any detrimental effect on bone homeostasis.

Influence of hyperbaric oxygen therapy on bone metabolism in patients with neoplasm.

BACKGROUND: Hyperbaric oxygen therapy (HBOT) is useful in the treatment of complications due to radiotherapy in patients with neoplasm. Its effects on bone metabolism are unclear. In our study, we analyzed the effects of HBOT on bone remodeling in oncological patients with radiotherapy. MATERIALS AND METHODS: Prospective clinical study in 23 patients with neoplasms undergoing treatment with HBOT due to complications of radiotherapy (hemorrhagic cystitis, proctitis or radionecrosis) and 25 patients with chronic anal fissure. The average number of HBOT sessions was 20 ± 5 (100% oxygen, 2.3 atmospheres and 90 min per day). Serum levels of aminoterminal propeptide of type I collagen (P1NP), C terminal telopeptide of type I collagen (CTX), alkaline phosphatase (AP), 25hydroxyvitamin D (25-OHD), parathyroid hormone (PTH), were measured at 3 time points: T0 (before beginning HBOT), T1 (at the end of HBOT) and T2 (6 months after HBOT). RESULTS: At baseline, the patients with neoplasm have higher bone turnover than those with anal fissure. These differences were 41% in CTX (0.238 ± 0.202 ng/mL in neoplasm and 0.141 ± 0.116 ng/mL in fissure; p = 0.04), 30% for PTH (46 ± 36 pg/mL in neoplasm and 32 ± 17 pg/mL in fissure; p = 0.04) and 15% for alkaline phosphatase (80 ± 24 U/L in neoplasm and 68 ± 16 U/L in fissure; p = 0.04). In the group with neoplasm, the values of P1NP decreased 6% after HBOT (T0: 49 ± 31 ng/mL, T2: 46 ± 12 ng/mL; p = 0.03). Also, there were non-significant decreases in PTH (-34%) and CTX (-30%). CONCLUSIONS: Patients with neoplasm and complications with radiotherapy have an increase in bone remodeling that may be diminished after HBOT.

Usefulness of bilateral bispectral index (BIS) monitoring in a comatose patient with myoclonic status epilepticus secondary to cefepime.

BACKGROUND: Status epilepticus, particularly non-convulsive status epilepticus (NCSE), is a frequent complication in patients with altered renal function receiving treatment with intravenous cefepime. To the best of our knowledge, we report the first case, illustrated by video-EEG, of a critically ill patient receiving treatment with cefepime who developed an episode of confirmed symptomatic myoclonic status epilepticus (MSE). METHODS: Case report and video-EEG. RESULTS: A 60-year-old man, who had received a liver transplant due to alcoholic cirrhosis one year ago, was admitted to our intensive care unit due to septic shock. Computed tomography revealed a prostatic abscess as cause of his sepsis. On Day 27, a respiratory infection due to Pseudomona aeruginosa was diagnosed, and treatment with intravenous cefepime (2 g/8 hours) was initiated. On Day 32, his mental status deteriorated and he developed inattention, a reduced level of consciousness, and multifocal and generalised continuous myoclonic jerks. A video-EEG study was compatible with the diagnosis of symptomatic MSE. On Day 35, cefepime was stopped and general anaesthesia with midazolam was started in order to achieve a faster clinical improvement. We used the BIS-Vista™ monitor to guide general anaesthesia and detect potential episodes of NCSE. On Day 40, an EEG confirmed the existence of moderate diffuse encephalopathy. Finally, the patient died as a consequence of severe heart failure. CONCLUSIONS: Cefepime may be a cause of MSE in non-anoxic comatose patients. Clinicians should be aware of this possibility when evaluating comatose patients on cephalosporin therapy in order to establish a correct diagnostic approach and accurate prognosis. [Published with video sequences].

A severe case of olanzapine overdose with analytical data.

INTRODUCTION: Olanzapine is a second-generation atypical antipsychotic agent approved for the treatment of psychotic disorders and mania. While olanzapine overdoses are common, cases with whole blood concentrations are less so. We describe here a well-documented case of a pure olanzapine overdose in which whole blood concentrations were determined, and compared with other concentrations in the literature. CASE REPORT: A 58-year-old woman with a 10-year history of paranoid schizophrenia and poor therapeutic compliance was found unconscious with two empty 28-tablet vials of Zyprexa (olanzapine) 10 mg tablets. Her initial vital signs were blood pressure 110/70 mmHg, pulse rate 82 beats/minute (sinus rhythm), respirations 20 breaths/minute, and the Glasgow Coma Scale score was 7. In the Intensive Care Unit, her pulse rate was 160 beats/minute, in sinus rhythm, and QTc 0.423 seconds (normal <0.4 seconds). Relevant analytical findings were metabolic acidosis, leukocytosis, creatine phosphokinase 1992 mg/dL, and glucose 207 mg/dL. Ten hours after being found, her blood sugar was 350 mg/dL and became normal at 25 hours. The patient needed intubation and insulin. RESULTS: Olanzapine was detected and quantitated by gas chromatography with nitrogen-phosphorus detector and confirmed by gas chromatography-mass spectrometry using a validated analytical method. At approximately 4, 8, and 12 hours post-ingestion, whole blood concentrations of olanzapine were 0.41, 0.34, and 0.38 mg/L, respectively. CONCLUSIONS: This study reports an acute olanzapine monointoxication with severe toxicity and high whole blood olanzapine concentrations. Clinical and analytical data of similar samples obtained in non-fatal life-threatening cases can be very useful when interpreting postmortem cases.

Cardiac contusion following blunt chest trauma.

Cardiac contusion following blunt chest trauma is not rare, and the works in the literature report incidence rates between 5 and 50%. Traffic accidents are the most frequent cause of cardiac contusion followed by violent fall impacts, aggressions and the practice of risky sports. The spectrum of post-traumatic cardiac lesions varies greatly, ranging from no symptoms to decrease in cardiac function. Cardiogenic shock is a rarely encountered manifestation of blunt cardiac contusion. We review our experience of cardiac contusion after blunt chest trauma, and we describe two very severe cases that manifested as cardiogenic shock. We emphasize an early diagnosis by continuous electrocardiographic monitoring, serial electrocardiograms, echocardiography, serum determination of biochemical cardiac markers, radionuclide imaging and coronary angiography. The treatment includes continuous monitoring of cardiac rhythm, use of inotropic drugs, insertion of a catheter in the pulmonary artery for continuous assessment of cardiac output and, in extreme cases, the insertion of a contrapulsation balloon to maintain haemodynamics until improvement of cardiac function.

Pneumonia due to Mycoplasma hominis in a healthy adult.

A case of pneumonia due to Mycoplasma hominis in a healthy adult is presented. The bacterium was diagnosed by a quantitative culture method and identification to the species level by sequence analysis of 16S rRNA gene. The objective of this presentation is to bring to attention the need to search for this opportunistic pathogen. Mycoplasma may be an important cause of bacterial pneumonia without microbiological diagnosis and its incidence may be underestimated.