Chickenpox in childhood

Tarlow, M J; Walters, Sarah

doi:10.1016/s0163-4453(98)80154-0

Cited by 16 publications

(1 citation statement)

References 44 publications

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“…A large nationwide inpatient study showed a positive association between hospitalized patients with chronic inflammatory skin disease and the incidence of HZ, further supporting this link between HZ and the immune system [ 6 ]. Thus it is not surprising that bacterial superinfections with Staphylococcal or Streptococcal species are some of the most commonly reported complications of HZ [ 7 ].…”

Section: Discussionmentioning

confidence: 99%

Majocchi Granuloma Superinfected With Herpes Zoster

Lei,

Karatas,

Antohi

et al. 2024

Cureus

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Herpes zoster (HZ) infection is caused by the reactivation of the varicella-zoster virus (VZV) and has very rarely been reported at the site of a superficial fungal infection. Also, HZ occurring at the site of a deep fungal infection has not been reported in the literature. We discuss a unique case of a 45-year-old male patient presenting with a Majocchi granuloma (MG) superinfected with disseminated HZ.

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Section: Discussionmentioning

confidence: 99%

Majocchi Granuloma Superinfected With Herpes Zoster

Lei,

Karatas,

Antohi

et al. 2024

Cureus

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Noncutaneous varicella‐zoster virus (VZV) infection with fatal liver failure in a child with acute lymphoblastic leukemia (ALL)

Müller

Aepinus

Beck

et al. 2001

Med. Pediatr. Oncol.

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Here, we record our experience with a 5-year-old patient who died of a rapidly progressive VZV primary infection. This young patient presented with pre-B ALL and was treated in the medium-risk branch of the ALL-BFM 95 study protocol [1]. When the boy was only 2 weeks before the end of the last intensive chemotherapeutic protocol and in complete remission, he complained about back pain and intermittent abdominal pain. Physical examination revealed no cause for the pain and laboratory values were within expected limits. Consequently, we reasoned that recent administrations of vincristine were responsible for the symptoms, and we treated him with analgesics. Thirty-six hours later, the ache had not resolved and the parents noticed petechiae where they had massaged the back of their son to soothe the pain. We asked them to bring the patient to our clinic.At the time point of admission the patient was cooperative, but seemed altered as far as behavior was concerned. He displayed signs of dehydration. Other than the petechiae mentioned earlier, the skin was normal; in particular, there was no ef¯orescence of any kind throughout the following episode. The liver was enlarged, whereas the spleen was not palpable. The remainder of the physical examination was unremarkable.We had begun intravenous rehydration, when ®rst laboratory results became available. It was noteworthy that the hemoglobin level of 17.5 g/dl was markedly elevated, whereas the total protein level of 5.0 g/dl was low. This was a sign of liver failure and was more reliable than coagulation parameters, which were still affected by recent asparaginase treatment. The laboratory values of liver enzymes and lactate dehydrogenase were indicative of an overwhelming disintegration of hepatocytes (Table I). The situation became worse, when overnight the patient needed oxygen insuf¯ation because of respiratory insuf®ciency. Simultaneously, the liver grew enormously and clinical symptoms of liver failure such as confusion, dizziness, and sleepiness were aggravated. In the morning, a complete perfusion block in the portal vein was diagnosed by ultrasound. Only a few hours later, the patient developed profound gastrointestinal bleeding. Intensive efforts to compensate the severe hypovolemia became complicated by disseminated intravasal coagulopathy, and the patient died of complications of fulminate liver failure within 24 h after admission.The pathogenetic mechanism was completely unclear, and we hypothesized that either pharmacologic toxicity or an as yet unidenti®ed infection caused the fatal liver failure. First, we analyzed the serum of the last days. There was neither elevation of asparaginase levels, nor toxic concentrations of acetaminophen or metamizole. Acetylsalicylate had not been administered. Hence, the most feasible direct pharmacologic causes were excluded. Postmortem liver biopsy was impressive, and showed that more than 80% of all hepatocytes had decomposed. Approximately one half of all vital hepatocytes were marked by macrovesicular lipid droplets ...

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Strategies for the Rational Use of Antivirals

Waugh

Carman

2005

Antibiotic Policies

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Chickenpox in childhood

Cited by 16 publications

References 44 publications

Majocchi Granuloma Superinfected With Herpes Zoster

Majocchi Granuloma Superinfected With Herpes Zoster

Noncutaneous varicella‐zoster virus (VZV) infection with fatal liver failure in a child with acute lymphoblastic leukemia (ALL)

Strategies for the Rational Use of Antivirals

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