Pneumothorax and Pneumatocoele Formation in a Patient with COVID-19: a Case Report.

Coronavirus disease 2019 (COVID-19) causes significant morbidity and mortality for a proportion of infected patients, and our knowledge and understanding of its clinical, radiological and histopathological features are still evolving. An association between COVID-19 and pneumothorax has been described in an increasing number of case reports and series in the literature, which have largely focused on clinical and imaging features. We report the case of a patient who developed COVID-19 complicated by pneumothorax, requiring surgical intervention. We describe the histopathological features seen in the thorascopically resected bullectomy specimen-this is, to our knowledge, the first reported description of the morphological features of pneumothorax in this important clinical setting.

Does Helicobacter pylori identification in the mucosa of the gallbladder correlate with cholesterol gallstone formation? / ¿Existe una correlación de la identificación de Helicobacter pylori en la mucosa de la vesícula biliar con la formación de cálculos biliares de colesterol?

OBJECTIVE: Helicobacter pylori (H pylori) represents a potential initiator of cholesterol crystallization and it has been proposed that it is related to gallstone formation. In this study, any possible association between the H pylori identification in the mucosa of gallbladder and cholesterol gallstone formation was evaluated. METHODS: Gallbladders containing pure or mixed cholesterol gallstones (cholelithiasis group, n = 89) and gallbladders without gallstones (control group, n = 42) were submitted to standard histopathological examination for H pylori detection, as well as to nested polymerase chain reaction amplification for H pylori DNA detection. RESULTS: Helicobacter pylori was identified in the gallbladder's epithelium in four patients with cholelithiasis and in two patients in the control group by histology. In all the cases which were found to be H pylori positive by histological examination, H pylori DNA were also detected. No correlation between gallstone formation and H pylori detection in the biliary epithelium was found. A higher incidence of acute inflammation in the cholelithiasis (22.5% vs 9.5%, p = not significant [ns]) and in the H pylori positive groups (33% vs 17.6%, p = ns) were histologically detected. A higher incidence (10% vs 0%), p = ns) of H pylori in gallbladders with gallstones and acute inflammation, compared to gallbladders with acute inflammation but without gallstones, was noticed. CONCLUSION: Helicobacter pylori is detectable in low frequency in the mucosa of the gallbladder and it does not seem to act as a lithogenic component for cholesterol gallstone formation. Its higher incidence in gallbladders with gallstones and acute inflammation, suggests a possible accessory role in a subset of patients with cholelithiasis.

OBJETIVO: Helicobacter pylori (H pylori) representa un iniciador potencial de la cristalización del colesterol, y se ha propuesto que guarda relación con la formación del cálculo biliar. En este estudio, se evaluó cualquier posible asociación entre la identificación de H pylori en la mucosa de la vesícula y la formación del cálculo biliar de colesterol. MÉTODOS: Las vesículas que contienen cálculos biliares de colesterol puros o mixtos (grupo de colelitiasis, n = 89) y vesículas sin cálculos biliares (grupo control, n = 42) fueron sometidos a un examen histopatológico estándar con el fin de detectar el H pylori descubrimiento, así como a la amplificación de la reacción en cadena de polimerasa para la detección de ADN H pilori. RESULTOS: El Helicobacter pylori fue identificado mediante histología en el epitelio de la vesícula en cuatro pacientes con el colelitiasis y en dos pacientes en el grupo de control. En todos los casos que resultaron ser H pylori positivo por el examen histológico, se halló también DNA H pylori. No se halló correlación ninguna entre la formación del cálculo biliar y la detección de H pylori en el epitelio biliar. Se detectó histológicamente una incidencia más alta de inflamación aguda en la colelitiasis (22.5% contra 9.5%, p = no significativo [ns]) y en los grupos H pylori positivos (33% contra 17.6%, p = ns). Se observó una incidencia más alta (10% contra 0%), p = ns) de H pylori en las vesículas con los cálculos biliares e inflamación aguda, en comparación con las vesículas con la inflamación aguda pero sin cálculos biliares. CONCLUSIÓN: Helicobacter pylori es detectable en baja frecuencia en la mucosa de la vesícula y no parece actuar como un componente litogénico en la formación del cálculo biliar de colesterol. Su mayor incidencia en las vesículas con cálculo biliar e inflamación aguda, hace pensar en un posible papel auxiliar en un subconjunto de pacientes con colelitiasis.

Does Helicobacter pylori identification in the mucosa of the gallbladder correlate with cholesterol gallstone formation?

OBJECTIVE: Helicobacter pylori (H pylori) represents a potential initiator of cholesterol crystallization and it has been proposed that it is related to gallstone formation. In this study, any possible association between the H pylori identification in the mucosa of gallbladder and cholesterol gallstone formation was evaluated METHODS: Gallbladders containing pure or mixed cholesterol gallstones (cholelithiasis group, n = 89) and gallbladders without gallstones (control group, n = 42) were submitted to standard histopathological examination for H pylori detection, as well as to nested polymerase chain reaction amplification for H pylori DNA detection. RESULTS: Helicobacter pylori was identified in the gallbladder's epithelium in four patients with cholelithiasis and in two patients in the control group by histology. In all the cases which were found to be H pylori positive by histological examination, H pylori DNA were also detected. No correlation between gallstone formation and H pylori detection in the biliary epithelium was found. A higher incidence of acute inflammation in the cholelithiasis (22.5% vs 9.5%, p = not significant [ns]) and in the H pylori positive groups (33% vs 17.6%, p = ns) were histologically detected. A higher incidence (10% vs 0%), p = ns) of H pylori in gallbladders with gallstones and acute inflammation, compared to gallbladders with acute inflammation but without gallstones, was noticed CONCLUSION: Helicobacter pylori is detectable in low frequency in the mucosa of the gallbladder and it does not seem to act as a lithogenic component for cholesterol gallstone formation. Its higher incidence in gallbladders with gallstones and acute inflammation, suggests a possible accessory role in a subset of patients with cholelithiasis.

Human herpesvirus type 8 genotypes in iatrogenic, classic and AIDS-associated Kaposi's sarcoma from Greece.

BACKGROUND: Kaposi's sarcoma-associated herpesvirus (KSHV)/human herpesvirus 8 (HHV-8) is consistently found in almost all observed Kaposi's sarcomas (KS), whether AIDS-associated, iatrogenic or classic. To our knowledge no data are available on the genetic polymorphism of HHV-8 from Greece. We report the study of 15 renal transplant recipients with KS, 5 with AIDS-associated KS, 11 with classic KS and 60 healthy individuals from Greece. MATERIALS AND METHODS: Polymerase chain reaction (PCR) was carried out on DNA extracted from peripheral-blood mononuclear cells (PBMC) or KS cutaneous biopsies, using specific primers for the HHV-8, KS330 fragment from ORF-26 (233 bp) and the highly variable region (VR1) from ORF-K1 (363 bp). RESULTS: HHV-8 DNA was detected in 30 out of 31 (97%) KS cases, regardless of their clinico-pathological subtype and in 10 out of 60 (16.7%) healthy individuals. Sequencing of the ORF26 fragment demonstrated that the 40 HHV-8 strains were of the A and C sub-types. Furthermore, sequencing of the ORF-K1 showed that these HHV-8 strains of Greek origin were of the A1, A4, C1 or C3 sub-type. CONCLUSION: Our findings imply a possible link of the C3 subtype of HHV-8 in renal transplant-related KS cases (iatrogenic KS) in Greece, a link of the A4 subtype in AIDS-associated KS cases and a potential involvement of the A1 subtype in Greek classic KS incidences, as HHV-8 strains among healthy individual tested belong to the C1, C3 or A1 subtypes.