PubMed Health⌕ Search

PubMed · 3284802

Congenital Leydig cell hyperplasia.

Abstract

The testes and epididymes collected at autopsy from 21 newborns showed apparent Leydig cell hyperplasia which was studied by light and electron microscopy. Twelve newborns were the sons of diabetic mothers, two had undergone rhesus isoimmunization, two were twins of a non-diabetic mother, three had Beckwitz-Widemann's syndrome, and two had leprechaunism. In the first two groups the placentas were also collected and studied. All the testes showed normal seminiferous tubules and diffuse Leydig cell hyperplasia in the testicular interstitium. In addition one son of a diabetic mother and another with Beckwitz-Widemann's syndrome presented multiple Leydig cell nodules in the mediastinum testis and epididymis. The number of Leydig cells per unit area of the testis was calculated on histological sections stained with the peroxidase-anti-peroxidase method for the detection of testosterone. These numbers varied from 1.4 to 3.2 times those found in age-matched controls, except for the two testes with nodular hyperplasia in which the increase in Leydig cells was even greater. The differential diagnosis between Leydig cell hyperplasia, ectopic adrenal cells and leydig cell tumour is discussed. It is proposed that the cause of congenital Leydig cell hyperplasia might be related to placental secretion of human chorionic gonadotrophin.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

M Nistal, P González-Peramato, R Paniagua. 1988. Congenital Leydig cell hyperplasia.. https://doi.org/10.1111/j.1365-2559.1988.tb01945.x

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

KEEP EXPLORING

Related citations

Langerhans cell histiocytosis infiltration into pancreas and kidney.

An 18-month-old male presented with a swelling of the neck for 2 months. A presumptive diagnosis of Langerhans cell histiocytosis (LCH) was made on fine needle aspiration cytology from the lymph node. The child received chemotherapy. He remained well for around 10 months, when he represented with loose stools, cough, and respiratory distress. His condition deteriorated over a few hours culminating in death. A partial autopsy revealed LCH infiltration in liver, pancreas, and kidneys along with bronchopneumonia. The pancreatic and renal infiltration by LCH is extremely rare.

Autopsy↗

Radiography after unexpected death in infants and children compared to autopsy.

BACKGROUND: Postmortem radiography may reveal skeletal and soft-tissue abnormalities of importance for the diagnosis of cause of death. OBJECTIVE: To review the radiographs of children under 3 years of age who had died suddenly and unexpectedly. To compare the radiological and autopsy findings evaluating possible differences in children dying of SIDS and of an explainable cause. MATERIALS AND METHODS: A total of 110 consecutive skeletal surveys performed between 1998 and 2002 were reviewed. All but one were performed before autopsy and comprised AP views of the appendicular and axial skeleton and thorax/abdomen, lateral views of the axial skeleton and thorax, and two oblique views of the ribs. Radiography and autopsy findings were compared. RESULTS: Causes of death were classified as SIDS/borderline SIDS (n = 52) and non-SIDS (n = 58), with one case of abuse. In 102 infants there were 150 pathological findings, 88 involving the chest, 24 skeletal, and 38 miscellaneous findings. The radiological-pathological agreement was poor concerning pulmonary findings. Skeletal findings were sometimes important for the final diagnosis. CONCLUSIONS: Radiography revealed many skeletal and soft-tissue findings. Pulmonary pathology was most frequently found, but showed poor agreement with autopsy findings. Recognizing skeletal findings related to abuse is important, as these may escape recognition at autopsy.

Autopsy↗

Autopsy-proven Huntington's disease with 29 trinucleotide repeats.

Huntington's disease (HD) is a neurodegenerative disorder associated with expansion of CAG trinucleotide repeats in the huntingtin gene. A minimum of 36 CAG repeats is usually reported in patients with clinical features of HD; 30 to 35 repeats represent an intermediate range. Here we report a 65-year-old male with autopsy-proven HD and 29 CAG repeats.

Autopsy↗