Duration of viral shedding in asymptomatic or mild cases of novel coronavirus disease 2019 (COVID-19) from a cruise ship: A single-hospital experience in Tokyo, Japan.

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), which is the cause of novel coronavirus disease 2019 (COVID-19), was first reported in Wuhan, China, and now has spread across the world as a global pandemic. The propagation from asymptomatic polymerase chain reaction (PCR)-positive individuals represents a complicating factor in the efforts to control the COVID-19 pandemic. We examined the course of PCR assays and the duration of viral shedding in 23 asymptomatic or mild COVID-19 patients from the cruise ship who were admitted to our hospital. Among these 23 cases, the median duration of viral shedding was 19 days (range, 6-37 days) from initial viral detection. Eight cases (35%) had another positive PCR result after testing negative once. Although the duration of viral shedding was approximately three weeks, the infectivity and transmissibility period from asymptomatic and mild COVID-19 cases is unclear. Further studies are needed to determine how long such asymptomatic and mild COVID-19 cases have infectivity.

The best time for surgery on a patient with recurrent pneumothorax and undetectable culprit lesions is at the exact time air leakage is discovered: a case report.

BACKGROUND: One cause of recurrent spontaneous pneumothorax includes overlooking bullae during a previous surgery for pneumothorax; and the identification of the culprit lesions is necessary for prevention of recurrence. CASE PRESENTATION: A 28-year-old man was referred to our hospital because of spontaneous right-sided pneumothorax. He underwent video-assisted thoracoscopic surgery, which did not reveal air leakage. The patient was subsequently seen at our hospital for 2 additional episodes of recurrent right-sided pneumothorax. At the third admission we observed intermittent air leakage while the patient was in the sitting position after chest drainage, and we performed surgery. An intraoperative submersion test showed air leakage dorsally from the pleural surface of S(6) and a minute culprit lesion, which were not seen at the first operation and confirmed the leakage site. The area was ligated and coated with regenerated oxidized cellulose mesh and autologous blood. CONCLUSION: In cases of pneumothorax with repeated recurrence, the best time to perform surgery on the patient with undetectable culprit lesion is the exact time that air leakage is observed.

Pure red cell aplasia caused by parvovirus B19 in two patients without chronic hemolysis.

Infection with human parvovirus B19 (PVB19) induces acquired pure red cell aplasia (PRCA). Chronic hemolytic anemia is well known as an underlying condition. However, additional factors have been recognized to accompany parvoviral PRCA; however, there are only limited reports on iron-deficiency anemia (IDA) and rituximab-induced B-cell dysfunction. We report two patients with PVB19-associated PRCA confirmed by positivity of viral DNA. Although they had no chronic hemolysis, patient 1 had IDA, and patient 2 had remitted small-lymphocytic lymphoma treated with rituximab-containing chemotherapy. Absence of reticulocytes in peripheral blood and marked depletion of erythroid precursors in bone marrow were observed both. Whereas patient 1 received only symptomatic therapy because anemia was not severe, patient 2 was treated with steroids, as PRCA etiology was at first uncertain, and immunological PRCA was not excluded. Both showed rapid increase of reticulocyte counts and recovery from anemia. Although immunoglobulin is considered effective for parvoviral PRCA, notable adverse reactions have been reported. When anemic symptom is not severe, reticulocyte observation only is recommended. The effects of steroids should also be re-evaluated. Optimal treatment according to disease severity remains to be established.

Simultaneous complication of multiple myeloma with Sjögren syndrome.

We report a 72-year-old female case of IgG-kappa type multiple myeloma (MM) simultaneously complicated with Sjögren syndrome (SS). She also presented marked hyperamylasemia of salivary-type isozyme. Although she had received sequential chemotherapy completed with high-dose therapy with autologous hematopoietic stem cell transplantation, she died of relapse fifteen months after the initial diagnosis. Various autoantibodies indicated that her sicca symptoms were due to true SS and not caused by MM cell infiltration to exocrine glands. MM cells appeared to produce amylase that fluctuated correspondingly to the disease status of MM. To our knowledge, this is the first English report of simultaneous complication of SS and MM referring to hyperamylasemia. Accumulation of this rare clinical manifestation is important to elucidate the pathogenesis of MM under condition of immunological disorder caused by SS.