COVID-19, Coronavirus Vaccines, and Possible Association with Lipschütz Vulvar Ulcer: A Systematic Review.

Lipschütz genital ulcer is a self-limited, non-sexually acquired disorder characterized by the sudden onset of a few ulcers. A primary Epstein-Barr virus infection is currently considered the most recognized cause. Recent reports document cases temporally related with coronavirus disease 2019 (COVID-19) or immunization against severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). We carried out a review of the literature to investigate the possible association between COVID-19 or the immunization against SARS-CoV-2 and genital ulcer. The pre-registered study (CRD42023376260) was undertaken following the Preferred Reporting Items for Systematic Reviews and Meta-Analyses methodology. Excerpta Medica, the National Library of Medicine, and Web of Sciences were searched. Inclusion criteria encompassed instances of acute Lipschütz ulcer episodes that were temporally linked to either COVID-19 or a vaccination against SARS-CoV-2. Eighteen articles were retained. They provided information on 33 patients 15 (14-24) years of age (median and interquartile range), who experienced a total of 39 episodes of Lipschütz ulcer temporally associated with COVID-19 (N = 18) or an immunization against SARS-CoV-2 (N = 21). The possible concomitant existence of an acute Epstein-Barr virus infection was excluded in 30 of the 39 episodes. The clinical presentation and the disease duration were similar in episodes temporally associated with COVID-19 and in those associated with an immunization against SARS-CoV-2. In conclusion, COVID-19 and immunization against SARS-CoV-2 add to Epstein-Barr virus as plausible triggers of Lipschütz genital ulcer.

Splenic rupture or infarction associated with Epstein-Barr virus infectious mononucleosis: a systematic literature review.

BACKGROUND: Epstein-Barr virus (EBV), also known as human herpesvirus 4, is one of the most common pathogenic viruses in humans. EBV mononucleosis always involves the spleen and as such it predisposes to splenic rupture, often without a trauma, and splenic infarction. Nowadays the goal of management is to preserve the spleen, thereby eliminating the risk of post-splenectomy infections. METHODS: To characterise these complications and their management, we performed a systematic review (PROSPERO CRD42022370268) following PRISMA guidelines in three databases: Excerpta Medica, the United States National Library of Medicine, and Web of Science. Articles listed in Google Scholar were also considered. Eligible articles were those describing splenic rupture or infarction in subjects with Epstein-Barr virus mononucleosis. RESULTS: In the literature, we found 171 articles published since 1970, documenting 186 cases with splenic rupture and 29 with infarction. Both conditions predominantly occurred in males, 60% and 70% respectively. Splenic rupture was preceded by a trauma in 17 (9.1%) cases. Approximately 80% (n = 139) of cases occurred within three weeks of the onset of mononucleosis symptoms. A correlation was found between the World Society of Emergency Surgery splenic rupture score, which was retrospectively calculated, and surgical management: splenectomy in 84% (n = 44) of cases with a severe score and in 58% (n = 70) of cases with a moderate or minor score (p = 0.001). The mortality rate of splenic rupture was 4.8% (n = 9). In splenic infarction, an underlying haematological condition was observed in 21% (n = 6) of cases. The treatment of splenic infarction was always conservative without any fatal outcomes. CONCLUSIONS: Similarly to traumatic splenic rupture, splenic preservation is increasingly common in the management of mononucleosis-associated cases as well. This complication is still occasionally fatal. Splenic infarction often occurs in subjects with a pre-existing haematological condition.

Interferences in the measurement of circulating phosphate: a literature review.

Background Inorganic phosphate in blood is currently determined by the reaction with molybdate. This report aims at reviewing conditions underlying spuriously altered levels of circulating inorganic phosphate. Content A systematic search of the Excerpta Medica, the National Library Database and the Web of Science database was conducted without language restriction from the earliest publication date available through January 31, 2020. Summary For the analysis, 80 reports published in English (n = 77), French (n = 1), German (n = 1) and Spanish (n = 1) were retained. Well-documented pseudohyperphosphatemia was observed in individuals exposed to liposomal amphotericin, in patients affected by a gammopathy, in patients with hyperlipidemia and in patients with hyperbilirubinemia. An unexplained elevated inorganic phosphate level sometimes provided a clue to the diagnosis of a gammopathy. Well-documented cases of pseudohypophosphatemia were observed in patients on large amounts of intravenous mannitol. Finally, pseudohypophosphatemia was occasionally observed on treatment with liposomal amphotericin and in patients with a gammopathy. Outlook In order to avoid unnecessary testing and treatment, the phenomenon of spuriously altered inorganic phosphate should be recognized. An unexplained hyperphosphatemia may provide a clue to the diagnosis of a gammopathy or a severe hyperlipidemia.

Hyponatremia in children with acute respiratory infections: A reappraisal.

Hyponatremia (<135 mmol/L), typically associated with an elevated anti-diuretic hormone level, is common among children admitted with bronchiolitis, pneumonia, or pulmonary exacerbation of cystic fibrosis. The main consequences of acute hyponatremia include cerebral edema and Ayus-Arieff pulmonary edema. A widespread belief is that, in children with pneumonia or bronchiolitis, hyponatremia results from inappropriate anti-diuresis. By contrast, the pathogenic role of extracellular fluid volume depletion or decreased effective circulating blood volume is underscored. Considering the prevalence of hyponatremia, sodium determination is advised on admission in children diagnosed with bronchiolitis, pneumonia, or pulmonary exacerbation of cystic fibrosis. There is no necessity to do anything beyond reassessing the appropriateness of fluid therapy in cases with mild (130-134 mmol/L) hyponatremia. In children with sodium <130 mmol/L, the underlying etiology is sometimes evident from history and physical findings. Given that clinical assessment of fluid volume status is difficult in hyponatremia, further laboratory evaluation is often required in these patients. An increase in sodium level ≤6 mmol/L per day is currently considered the therapeutic goal in all cases. Emergency correction with a 2 mL/kg body weight bolus of 3.0% saline over 10-15 min intravenously is advised in cases with severe symptoms due to hyponatremia and in cases with symptoms, even if mild, due to a rapid-onset (<48 h) of hyponatremia (two additional doses are administered if the patient's condition does not improve).

Renal salt-wasting syndrome in children with intracranial disorders.

Hypotonic hyponatremia, a serious and recognized complication of any intracranial disorder, results from extra-cellular fluid volume depletion, inappropriate anti-diuresis or renal salt-wasting. The putative mechanisms by which intracranial disorders might lead to renal salt-wasting are either a disrupted neural input to the kidney or the elaboration of a circulating natriuretic factor. The key to diagnosis of renal salt-wasting lies in the assessment of extra-cellular volume status: the central venous pressure is currently considered the yardstick for measuring fluid volume status in subjects with intracranial disorders and hyponatremia. Approximately 110 cases have been reported so far in subjects ≤18 years of age (male: 63%; female: 37%): intracranial surgery, meningo-encephalitis (most frequently tuberculous) or head injury were the most common underlying disorders. Volume and sodium repletion are the goals of treatment, and this can be performed using some combination of isotonic saline, hypertonic saline, and mineralocorticoids (fludrocortisone). It is worthy of a mention, however, that some authorities contend that cerebral salt wasting syndrome does not exist, since this diagnosis requires evidence of a reduced arterial blood volume, a concept but not a measurable variable.