PubMed Health⌕ Search

PubMed · 15938226

[Transverse testicular ectopia].

Abstract

Transverse testicular ectopia is an extremely rare anomaly, characterized by migration of one testis towards the opposite inguinal canal, usually associated with inguinal hernia. Spermatic cord of the ectopic testis originates from the appropriate side. In most reported cases, the accurate diagnosis has not been made before surgery. This is a case report of transverse testicular ectopia in eleven-year-old boy who had undergone an operation for the left inguinal hernia in age of ten months. At the time of herniorrhaphy, the right testis was absent. Ten years later, during re-operation of the left inguinal hernia, both testis were found in left inguinal canal and easily brought down sequentially through the left groin into the scrotum. The right testis was fixed in the left hemiscrotum, due to shorter funicular elements, and the left was trans-septally moved to the right hemiscrotum (a modified Ombrédanne operation). Ultrasonography and voiding cystoureterography showed no associated genitourinary anomalies and no Mülerian duct remnants. The rupture of gubernaculum and dysfunction of the genitofemoral nerve could explain the etiology of crossed testis ectopia. Although ectopic testis could be localized preoperatively by ultrasonography, CT, MRI, arteriography and venography, correct diagnosis was made intraoperatively in the majority of cases. Treatment modalities include laparoscopic and surgical procedures. Atrophic testis should be removed. If testes are fused, they have to be brought into one hemiscrotum. In cases where testes are completely separated with individual funicular elements and vas deferens, an ipsilateral or contralateral orchiopexy should be performed depending on the length of funicular elements.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

Dragoljub Zivanović, Andjelka Slavković, Jelica Madić, Dejan Novaković. [Transverse testicular ectopia].. https://doi.org/10.2298/sarh0412438z

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

Prevalence and risk factors for persistent faecal carriage of extended spectrum beta-lactamase producing Escherichia coli in a paediatric community population.

OBJECTIVE: To investigate clinical and microbiological factors associated with persistent faecal carriage of extended spectrum beta-lactamase (ESBL) producing Escherichia coli in infants. METHODS: Between 2010 and 2022, children aged 3 months to 2 years old were sampled in a community setting in France, at two visits, V1 and V2, 3-24 months apart, to screen for prolonged faecal carriage of ESBL-producing E. coli. Patient clinical information and whole genome sequence of each isolate were used for association studies. RESULTS: A total of 4641 children were sampled. 375 (8%) carried an ESBL-producing Enterobacterales, among which 142 of ESBL-producing E. coli carriers were once again sampled at V2 and included in this study. 21.8% (n = 31/142) and 18.4% (n = 16/99) carried the same ESBL-producing E. coli clone for at least 3 and 6 months, respectively. B2 phylogroup, and among which ST131 clones were associated with an increased risk of persistent carriage. Multivariate analysis identified virulence associated genes involved in adhesion (papC/papGII allele and a tia-like gene) and encoding toxin (senB) as major risk factors for persistence. A genome wide association study highlighted the potential role of the frz metabolic operon, known to be involved in enterocytes adhesion/internalisation. CONCLUSION: Main extraintestinal pathogenic E. coli genomic features (phylogenetic background, adhesion properties) are associated with ESBL-producing E. coli gut colonisation persistence in infants, which could potentially lead to an increased risk of febrile urinary tract infection in these patients.

Child↗

Extensive and differential platinum chemotherapy mutagenesis in livers of children.

Childhood cancer survivors often experience late adverse effects that may be linked to chemotherapy mutagenesis. We studied chemotherapy mutagenesis in normal pediatric tissues using duplex sequencing (NanoSeq) to enable the detection of mutations from single DNA molecules. We found that platinum chemotherapeutics increased the mutation burdens of normal pediatric tissues to levels seen in adults. In the liver, platinum agents imparted a tissue-specific mutational signature that was absent from other tissues. Gene-focused duplex sequencing revealed that chemotherapy mutagenesis generates a great diversity of nonsynonymous variants, some of which may have functional potential, such as leukemogenic variants in blood. Our findings demonstrate extensive chemotherapy mutagenesis in normal tissues of children, which may provide a plausible link between chemotherapy exposure and adverse effects in later life.

Child↗

Clinical and immunological characterization of a child with a homozygous TBK1 kinase-domain truncation.

TBK1 is a serine-tyrosine kinase protein that transmits signals from pattern recognition receptors to the NF-κB pathway leading to production of Type 1 Interferons. Mutations in this protein have been associated with arthritis, vasculitis, herpes simplex encephalitis and amyotrophic lateral sclerosis. In the current study, we characterized the functional consequences of a TBK1-variant bearing a truncation in exon 4 and 5 in a patient with poly arthritis resembling juvenile idiopathic arthritis and necrotizing encephalitis. The truncation was associated with reduced TBK1 protein abundance and altered phosphorylation. The variant was associated with increased basal/and or Poly-I: C induced IL-6, TNFα, IL-1β and IL-18 and type 1 Interferon ex vivo. Our findings expand the phenotypic spectrum of TBK1 loss-of-function variants and may provide insight into the management of immune dysregulation in affected patients.

Child↗