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Biomedical subjects

I Reintoft

Publications and source records attributed to I Reintoft.

29 records · Page 2Linked to original sources
PubMed1977

Lymphocytic thyroiditis. II. The course of the disease in relation to morphologic, immunologic and clinical findings at the time of biopsy.

Thirty-two patients with goitre and lymphocytic thyroiditis were followed for 1 1/2--19 years (average 7) after open surgical biopsy. Treatment with thyroid hormone was started when myxoedema was diagnosed. Five patients (group A) regained normal glandular size, remained euthyroid and had elevated antibody titres. Six patients (group B) continued to have goitre and elevated antibody titres and remained euthyroid. Thirteen patients (group C) developed myxoedema, while 8 (group D) demonstrated myxoedema at the time of biopsy. The patients in groups C and D had a higher average age and their biopsies showed more marked fibrosis compared with groups A and B. The goitre disappeared during treatment in 62% of the patients and the microsomal antibody titre also decreased in them, whereas the thyroglobulin antibody titre decreased in all treated patients. The results indicate that the degree of fibrosis in the thyroid gland is of overall importance for the prognosis with regard to glandular function. It seems evident that the treatment with thyroid hormone influences the autoimmune process so that the activity decreases.

Antibodies↗
PubMed1975

A cytogenetic study of gonadoblastoma tissue in two cases.

The hypothesis that gonadoblastoma (gonocytoma III) arises from gonadal tissue with a male chromosome complement has earlier been forwarded. In the literature there is no case with a well documented diagnosis of gonadoblastoma and absence of a Y chromosome. In the two presented cases, one a phenotypic female, the other a phenotypic male, gonadoblastoma was diagnosed. Cytogenetic studies of the removed gonadoblastomas revealed a Y chromosome in both cases. This is in accordance with the hypothesis.

Adolescent↗
PubMedDate not supplied

Dorsal root gangliopathia presenting with rapidly progressing sensory polyneuropathy.

A 52-year-old woman developed progressive sensory polyneuropathy leading to death in 1.5 years. Electromyography and peripheral nerve biopsy had revealed severe axonal degeneration. Neuropathological examination showed involvement of all dorsal root ganglia with loss of the bipolar nerve cells, degeneration of the remaining nerve cells, Nageotte's residual nodules, and scattered lymphocytes. The posterior columns of the spinal cord and the sensory spinal roots revealed secondary loss and degeneration of the nerve fibers. The etiology is unknown but an autoimmune-mediated reaction effecting the nervous system is strongly suggested.

Disease Progression↗
PubMedDate not supplied

A new craniofacial disorder involving hypertelorism and malformations of external nose, palate and pituitary gland.

The aim of the present study was to describe and pathologically evaluate an apparently unreported craniofacial malformation, based on comparison of the cranial midsagittal components with similar components under normal developmental conditions. A severely malformed fetus with a gestational age of about 17 weeks underwent whole body and special craniofacial radiography. Following autopsy dissection, the midsagittal segment of the cranial base, including the eyes, was radiographed in different projections. Midsagittal tissue blocks were serially sectioned for microscopy. Routine stains and immunohistochemical stains were applied. The face was characterized by hypertelorism, absence of external nose but with open shell-like cavities medio-cranially to the eyes, and by a palate fused in the midline and with extensive bony ridges laterally. There was absence of normal nasal cavities, presence of nasal septum and vomer, normal eyes, and nasal ducts covered with nasal mucosa ending blindly in the cartilage. No olfactory bulbs were found. The palatal ridges consisted of bony tissue. The pituitary gland was severely malformed and consisted solely of adenopituitary gland tissue, located in its full extent in the pharyngeal mucosa. There was no sella turcica. From a pathogenetic point of view, it is suggested that the neural crest cells in the frontonasal region of the crest were reduced in amount or late in migration to the midfacial region compared to the neural crest cells to the maxillary region. Therefore, we believe that the malformations observed in the nasal placodes and in the pituitary placode, combined with abnormal migration or abnormal timing of neural crest cells during the craniofacial development, are important factors behind this disorder.

Brain↗