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OBJECTIVE: This study evaluated the ability of mid-regional proadrenomedullin (MR-proADM) to identify disease severity in Coronavirus disease 2019 (COVID-19) patients in comparison to conventional inflammatory biomarkers and clinical scores. PATIENTS AND METHODS: In an observational trial, COVID-19 acute respiratory distress syndrome (ARDS) patients were enrolled. MR-proADM, C-reactive protein (CRP), procalcitonin (PCT) and lactic acid (LA) were measured in all patients at admission (T0), at 24 hours (T1) and in the third (T3) and fifth day (T5) of hospitalization. The aims of this study were to determine the role of MR-proADM to detect patients with high risk of mortality and compare the prognostic value of MR-proADM with commonly used clinical scores (Sequential Organ Failure Assessment score - SOFA score, Acute Physiologic Assessment and Chronic Health Evaluation II score - APACHE II score, and Simplified Acute Physiological score II - SAPS II score). RESULTS: Twenty-one COVID-19 ARDS patients admitted to the Intermediate Care Unit (IMCU) were enrolled. The median MR-proADM values were 2.28, 2.41, 1.96 and 1.89 nmol/L at T0, T1, T3 and T5, respectively. The 30-day all-cause mortality rate was 52.4%. Mean MR-proADM T0 value was significantly higher in non-survivors compared with survivors (3.5 vs. 1.1 nmol/L, p < 0.05). No significant differences were found for the other inflammatory biomarkers. In terms of the area under the receiver-operating characteristic curve (AUC), MR-proADM showed a similar discriminatory power compared with APACHE II, SOFA and SAPS II score (0.81, 0.91, 0.70 and 0.78, respectively). The optimal MR-proADM cut-point cut-off point was 1.07 nmol/L, which corresponds to a sensitivity of 91% and a specificity of 71%. CONCLUSIONS: MR-proADM, in addition to the clinical scores, could be useful to predict outcome in COVID-19 ARDS patients.

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OBJECTIVE: Patients with Covid-19 can have different symptoms, ranging from asymptomatic patients to various grades of respiratory failure, caused by typical interstitial pneumonia, cardiac involvement or neurological symptoms. PATIENTS AND METHODS: In April 2020, we focused our attention on a young woman with diffused purpura on her lower extremities, with no respiratory, cardiac or neurological symptoms. A complete blood analysis showed us a severe thrombocytopenia. We excluded other possible causes of thrombocytopenic purpura such as hematological (lymphocyte subsets), hepatological disease or splenomegaly. On autoimmune screening, we found Isolated immune thrombocytopenic purpura in a young adult Covid-19 patient positivity of anti-nuclear antibody (ANA) with a centrosome pattern and extractable nuclear antigens (ENA) and connective tissue disease screen resulted positive but none of the included specific antigens results positive, probably due to an aspecific antibody reaction. The wide variability of COVID disease presentation may be due to a personal different immune response to the virus. CONCLUSIONS: The immune response against the virus is crucial in the evolution and understanding of COVID-19 disease but it has still to be fully understood.

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Coronavirus disease 2019 (COVID-19) is a respiratory tract infection caused by a newly emergent coronavirus, SARS-CoV-2. The acute phase may be followed by a second phase actually not yet completely understood but probably associated to an autoimmune activation. At the moment is not possible to clearly define an association between immunological findings and pathological symptoms, however, this case report describes the case of a patient who following COVID-19 infection development autoimmune antibodies who persist in time longer than viral phase. Those antibodies can be responsible for the multi pathological clinical picture showed from our patient that, according to EULAR 2019 criteria, could be classified as systemic lupus erythematosus (SLE). SLE is probably one of the possible chronic rheumatologic diseases triggers by COVID-19 and this is the first case of SLE with vasculitis actually described in literature.

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OBJECTIVE: Coronavirus disease 2019 (COVID-19) related coagulopathy may be the first clinical manifestation even in non-vasculopathic patients and is often associated with worse clinical outcomes. CASE PRESENTATION: A 78 years old woman was admitted to the Emergency Unit with respiratory symptoms, confusion and cyanosis at the extremity, in particular at the nose area, hands and feet fingers. A nasal swab for COVID-19 was performed, which resulted positive, and so therapy with doxycycline, hydroxychloroquine and antiviral agents was started. At admission, the patient was hemodynamically unstable requiring circulatory support with liquids and norepinephrine; laboratory tests showed disseminated intravascular coagulation (DIC). During hospitalization, the clinical condition worsened and the cyanosis of the nose, fingers, and toes rapidly increased and became dried gangrene in three days. Subsequently, the neurological state deteriorated into a coma and the patient died. DISCUSSION: In severe cases, COVID-19 could be complicated by acute respiratory disease syndrome, septic shock, and multi-organ failure. This case report shows the quick development of dried gangrene in a non-vasculopathic patient, as a consequence of COVID-19's coagulopathy and DIC. CONCLUSIONS: In our patient, COVID-19 related coagulopathy was associated with poor prognosis.

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Chest pain is one of the most important reasons of Emergency Department arrivals (5% of total). As it is not possible to rule-in all patients claiming chest pain, it has been proposed to create new departments to monitor these patients during some hours, in order to exclude or confirm an acute coronary syndrome. These departments are named Chest Pain Units (CPUs). The Chest Pain Unit has been created since June 1998 in Alessandria Hospital "SS. Antonio e Biagio e C. Arrigo". Chest Pain Unit patients presenting in Emergency Department with an unclear defined chest pain are submitted to a continuous ECG monitoring of S-T trend for 24 h. Moreover, cardiac markers such as myoglobin, mass CK-MB and Troponin-I are tested at arrival and Troponin-I is tested again serially 3, 6, 9, 18 h after the first sampling. It is really important to be able to measure these markers of myocardial damage with robust and quick methods. A point-of-care analyzer is available in our chest pain unit and enables our department to obtain results in a very short time at low cost and with quality similar to that of clinical chemistry laboratories' instruments. This easy-to-use analyzer can be run by nurses without interfering in their normal activities. The presentation of our experience will be completed by describing all patients admitted in our Chest Pain Units from January to June 1998.

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