Efficacy of anticytokine treatments added to corticosteroids in patients with COVID-19-associated pneumonia and hyperinflammation: a single center experience.

OBJECTIVE: Pneumonia and hyperinflammatory state related to COVID-19 infection are fatal clinical conditions without definite treatment modalities. Interleukin-6 and Interleukin-1 targeted therapies have been proposed as treatment options. This study was conducted to investigate the efficacy of anakinra and tocilizumab added to corticosteroids in patients with COVID-19-associated pneumonia and hyper-inflammatory syndrome in our tertiary clinical center. PATIENTS AND METHODS: Patients with COVID-19-associated pneumonia and hyperinflammatory state who did not respond to initial treatments, including corticosteroids, were included in the study. The patients' electronic records were reviewed retrospectively and recorded according to a standardized data table. Univariate and multivariate regression analyses were used to identify risk factors associated with intubation. RESULTS: 388 patients were included in the study. 197 patients were intubated and most of them died (n=194/197, 98%). 67 patients received tocilizumab, and 97 patients received anakinra. Anakinra [OR: 0.440, 95% CI=0.244-0.794, p=0.006] and tocilizumab [OR: 0.491, 95% CI=0.256-0.943, p=0.033] were both associated with a decreased risk for intubation. However, having a neutrophil/lymphocyte ratio ≥ 10 [OR: 2.035, 95% CI=1.143-3.623, p=0.016], serum lactate dehydrogenase (LDH) level ≥ 400 [OR: 3.160, 95% CI=1.937-5.156, p<0.001] and age ≥ 50 [OR: 4.048, 95% CI=2.037-8.043, p < 0.001] was associated with an increased risk for intubation. CONCLUSIONS: Both anakinra and tocilizumab, added to initial standard COVID-19 treatments (including glucocorticoids) reduced the need for intubation in patients with COVID-19-associated severe pneumonia and hyperinflammatory syndrome. Given the high mortality rate of intubated patients with COVID-19, both treatments may have added benefits on mortality.

Cerebrospinal fluid total tau protein levels in patients with multiple sclerosis.

BACKGROUND: Tau protein is present in the microtubules of axons. Markers of various types have been used to demonstrate multiple sclerosis (MS) activity and axonal damage. This study aimed to demonstrate the association between cerebrospinal fluid (CSF) tau protein concentrations and clinical prognosis in MS patients. METHODS: We included 45 patients that were diagnosed according to the McDonald's criteria. The control group was made up of 38 patients that had no signs or symptoms related to the primary central nervous system lesion correlated with the patient group. CSF total tau protein was measured using the ELISA method based on the sandwich method with Innogenetics Innotest hTau antigen kit in pg/ml type. RESULTS: In the patient group, the mean CSF total tau protein level was 238.66 +/- 237.44, whereas it was 93.65 +/- 82.14 in the control group. The mean total tau protein was higher in the three clinical forms when compared with the control group and it was statistically significant (P<0.05). CONCLUSIONS: High tau protein level may be an early marker of axonal damage and this marker may be used for monitoring axon preventing therapies in the follow-up.

The clinical and electrophysiological features of a delayed polyneuropathy developing subsequently after acute organophosphate poisoning and it's correlation with the serum acetylcholinesterase.

INTRODUCTION: Organophosphorus-induced delayed polyneuropathy (OPIDP) characterised with cramping pain, paresthesias in the lower extremities and occasionally in the hands, followed by weakness of the distal limb muscles, especially in the legs, and partial denervation of affected muscles often develops within first 3 weeks following acute poisoning. OBJECTIVES: To determine the incidence of development of subsequent polyneuropathy among patients with acute organophosphate poisoning (OPP), to assess whether there was a difference between patient groups with severe poisoning and mild poisoning for the development of polyneuropathy, to determine whether there was a correlation between the serum AChE levels and the development of OPIDP, and to define the clinical and electrophysiological features of OPIDP. METHODS: Forty-one patients with acute OPP admitted to the Emergency department were included in this retrospective study. On days 1, 2, 3, and 7, each patient was assessed clinically, with the measurement of serum AChE, and results were recorded on special forms. RESULTS: OPIDP was diagnosed clinically in 14 patients (34.15%) during the 14th to 22nd days after poisoning. Twelve (85.7%) of 14 patients had a severe clinical status on day 1 after poisoning. The frequency of development of OPIDP was higher in the patients with severe poisoning than the patients with mild poisoning (p = 0.041). There was no significant correlation between the serum AChE levels and the development of OPIDP. CONCLUSION: We conclude that the serum AChE levels measured on the first day and consecutive several days can not be the predictive of the development of subsequent OPIDP.

Adult metachromatic leukodystrophy: three cases with normal nerve conduction velocities in a family.

Here, we report three cases of late onset metachromatic leukodystrophy (MLD) within a family. The patients presented with psychiatric disturbances and dementia. The arylsulphatase A (ASA) level in leucocytes was zero in all the patients. The cranial magnetic resonance imaging (MRI) revealed bilateral symmetrical demyelination but the nerve conduction velocities were normal in all three cases. The clinical, biochemical, imaging and electrophysiological data of the family has been discussed.

The evaluation of mannitol therapy in acute ischemic stroke patients by serial somatosensory evoked potentials.

The effects of mannitol infusion therapy on acute ischemic stroke were investigated by serial median nerve somatosensory evoked potentials (SEP) in 31 patients with abnormal SEP recordings within 72 hours after onset. In 10 patients with missing N20 waves mannitol had no effect. In 12 patients mannitol improved N20 and central conduction time (CCT) latencies. In 9 patients absent N20 waves appeared after mannitol. As regard to the location of infarcts, CT revealed 7 hemispheric infarcts in patients with absent N20 waves in spite of mannitol infusion. The remaining patients' CTs revealed cortical and subcortical infarcts. This study concludes that mannitol treatment improved microcirculatory flow in the ischemic penumbra of acute ischemic stroke patients. We suggest that SEPs can be used in evaluating the effects of drugs to be used in the therapy of acute cerebrovascular accidents.

Evoked potentials and the effect of flumazenil in patients with liver cirrhosis.

The presence of increased amount of ligands for benzodiazepine receptors has been demonstrated in cirrhotic patients. Evoked potentials (EP) recordings are a simple, suitable, and objective method for comprehensive evaluation of hepatic encephalopathy (HE). We evaluated the visual EP, brain stem auditory EP, and somatosensory EP (SSEP) and the effect of benzodiazepine receptor antagonist flumazenil in patients with liver cirrhosis. EP of 38 patients with liver cirrhosis were recorded on the electrodiagnostic system Neuropack 8 (JB-441 B, Nihon Kohden). Eleven patients (nine males and two females; mean age 60 years; six with stage 0,4 with stage one, and one with stage 2 HE) showed impairment in SSEP N13-N19 interval. After baseline period, boluses of 1 mg, 2 mg, and 3 mg flumazenil were injected every thirty minutes and SSEP recordings were repeated after every dosage. We did not find any difference before and after flumazenil in SSEP N13-N19 interval (7.3 +/- 0.4, 7.1 +/- 0.5, 7.1 +/- 0.4, and 7.1 +/- 0.6 minutes, respectively) (p < 0.05). But four patients (36%) showed a clear SSEP improvement with flumazenil. Our results suggest that in a subset of cirrhotic patients, flumazenil may have a role.