scholarly journals Hoagland Sign as an Aid for Antimicrobial Stewardship—A Case Report

2022 ◽  
pp. 263394472110689
Author(s):  
Lakshmi J. Nair ◽  
Aravind Reghukumar ◽  
Athul Gurudas ◽  
Kirankumar V. Sasidharan ◽  
Kalyani Parvathy
Keyword(s):  
Antimicrobial Stewardship ◽  
Late Onset ◽  
Cervical Lymphadenopathy ◽  
Upper Eyelid ◽  
Inappropriate Use ◽  
Barr Virus ◽  
Eyelid Edema ◽  
Epstein Barr ◽  
Febrile Syndrome ◽  
Secondary Hemophagocytic Lymphohistiocytosis

Hoagland sign is an early and transient bilateral painless upper eyelid edema observed in patients with Epstein-Barr virus (EBV)-related infectious mononucleosis. This sign can predate the appearance of exudative pharyngitis and cervical lymphadenopathy. Usually, this sign disappears by first week of infection. Here, we describe the occurrence of late onset Hoagland sign in a 14-year old boy who presented to us on 10th day of fever. Hoagland sign appeared after 10 days from symptom onset in our patient. Despite persistence of fever, the presence of Hoagland sign which appeared prior to confirmation of EBV infection was a helpful indicator for stopping antibiotics. In view of tonsillar hypertrophy with potential airway compromise and biochemical parameters suggestive of possible secondary hemophagocytic lymphohistiocytosis, he was initiated on steroids with which defervescence and prompt resolution of symptoms occurred. EBV can present as acute undifferentiated febrile syndrome which might result in inappropriate use of antibiotics. This case highlights the importance of using clinical clues like Hoagland sign to optimize antimicrobial stewardship.

Epstein–Barr virus infection as a cause of cervical lymphadenopathy in children

2011 ◽  
Vol 75 (4) ◽  
pp. 564-567 ◽  
Author(s):  
Mosaad Abdel-Aziz ◽  
Hassan El-Hoshy ◽  
Mohammed Rashed ◽  
Mohamed Qotb ◽  
Seham Awad ◽  
...  
Keyword(s):  
Virus Infection ◽  
Epstein Barr Virus ◽  
Cervical Lymphadenopathy ◽  
Epstein Barr Virus Infection ◽  
Barr Virus ◽  
Epstein Barr ◽  
Barr Virus Infection

Molecular analysis of δ-aminolevulinate dehydratase deficiency in a patient with an unusual late-onset porphyria

Blood ◽  
2000 ◽  
Vol 96 (10) ◽  
pp. 3618-3623
Author(s):  
Reiko Akagi ◽  
Chiaki Nishitani ◽  
Hideo Harigae ◽  
Yutaka Horie ◽  
Luba Garbaczewski ◽  
...  
Keyword(s):  
Late Onset ◽  
Control Level ◽  
Rflp Analysis ◽  
Inherited Disease ◽  
Wild Type ◽  
Barr Virus ◽  
Alad Activity ◽  
Healthy Control ◽  
Aminolevulinate Dehydratase ◽  
Epstein Barr

Cloning, expression, and genotype studies of the defective gene for δ-aminolevulinate dehydratase (ALAD) in a patient with an unusual late onset of ALAD deficiency porphyria (ADP) were carried out. This patient was unique in that he developed the inherited disease, together with polycythemia, at the age of 63. ALAD activity in erythrocytes of the patient was less than 1% of the normal control level. ALAD complementary DNA (cDNA) isolated from the patient's Epstein-Barr virus (EBV)–transformed lymphoblastoid cells had 2 base transitions in the same allele, G177 to C and G397 to A, resulting in amino acid substitutions K59N and G133R, respectively. It has been verified that the patient had no other ALAD mutations in this and in the other allele. By restriction fragment length polymorphism (RFLP) analysis, all family members of the proband who had one-half ALAD activity compared with the ALAD activity of the healthy control were shown to have the same set of base transitions. Expression of ALAD cDNA in CHO cells revealed that K59N cDNA produced a protein with normal ALAD activity, while G133R and K59N/G133R cDNA produced proteins with 8% and 16% ALAD activity, respectively, compared with that expressed by the wild type cDNA. These findings indicate that while the proband was heterozygous for ALAD deficiency, the G397 to A transition resulting in the G133R substitution is responsible for ADP, and the clinical porphyria developed presumably due to an expansion of the polycythemic clone in erythrocytes that carried the mutant aladallele.

scholarly journals Late Onset Epstein Barr Virus Seropositive Posttransplant Lymphoproliferative Disorder in Two Renal Transplant Receivers

2013 ◽  
Vol 30 (3) ◽  
pp. 315-320 ◽  
Author(s):  
Saime Paydaş ◽  
Semra Paydaş ◽  
Mustafa Balal ◽  
Arbil Açıkalın ◽  
Melek Ergin ◽  
...  
Keyword(s):  
Renal Transplant ◽  
Lymphoproliferative Disorder ◽  
Epstein Barr Virus ◽  
Late Onset ◽  
Posttransplant Lymphoproliferative Disorder ◽  
Barr Virus ◽  
Epstein Barr
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