Lymphocytic Adenohypophysitis and Lymphocytic Infundibuloneurohypophysitis.

Hashimoto, Kozo; Takao, Tosihiro; Makino, Shinya

doi:10.1507/endocrj.44.1

Cited by 144 publications

(136 citation statements)

References 69 publications

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“…The pituitary stalk usually survives after hypovolemia in Sheehan's syndrome that is because there is rich blood supply from the superior/inferior hypophyseal and the trabecular arteries [13]. Lymphocytic adenohypophysitis, an autoimmune disease of the anterior pituitary gland, is often observed after delivery and causes postpartum panhypopituitarism ending up in empty sella, the same as Sheehan's syndrome in chronic phase [14][15][16][17]. In acute phase, as we have described previously, lymphocytic adenohypophysitis shows a homogenous enhancement in the anterior lobe in typical MR image [14,15].…”

Section: Discussionmentioning

confidence: 99%

A novel hook-shaped enhancement on contrast-enhanced sagittal magnetic resonance image in acute Sheehan’s syndrome: a case report

et al. 2014

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Section: Discussionmentioning

confidence: 99%

A novel hook-shaped enhancement on contrast-enhanced sagittal magnetic resonance image in acute Sheehan’s syndrome: a case report

et al. 2014

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“…In a review article by Hashimoto et al [48] hyperprolactinemia was found to be reported in 32.4% of the cases. The hyperprolactinemia in our cases was attributed to stalk involvement and/or compression.…”

Section: Discussionmentioning

confidence: 93%

Lymphocytic Hypophysitis and Infundibuloneurohypophysitis. Clinical and Pathological Evaluations.

et al. 1999

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Abstract.This report describes the clinical and pathological characteristics of two patients with lymphocytic hypophysitis (LHy) and two with infundibuloneurohypophysitis (INHy). Two of the patients were women and two were men, and their ages were between 27 and 38 years old. This disease was not associated with either pregnancy or the postpartum period in the female patients.Two of the patients presented with diabetes insipidus, one with panhypopituitarism and right abducens paralysis and one with headache and galactorrhea. At presentation three of the patients had mild to moderate hyperprolactinemia and one had low prolactin levels. All four had abnormal magnetic resonance imaging (MRI): focal nodular enlarging of the infundibulum and normal hypophysis in one, expanding sellar masses in two, and diffusely thickened stalk with slightly enlarged pituitary gland in one. Three cases showed no sign of adenohypophysial deficiency with stimulation tests. One patient had associated chronic lymphocytic thyroiditis.Of the first three patients, one patient underwent transcranial and two underwent transnasal transsphenoidal (TNTS) surgery for mass excisions since they were thought to have pituitary tumors. Endoscopic endonasal transsphenoidal biopsy was performed in the last one with a suspicion of LHy. The pathological and immunohistochemical examinations revealed lymphocytic infiltration. Hyperprolactinemia resolved with surgery in two patients and one developed diabetes insipidus as a complication.We conclude that LHy and infundibuloneurohypophysitis should be considered in the differential diagnosis of the mass lesions of the sellar region and also should be kept in the mind for the etiopathogenesis of cases of hyperprolactinemia, galactorrhea and diabetes insipidus.In suspected cases endoscopic endonasal biopsy for the histopathological diagnosis can be a safe approach.

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“…Several reports have previously indicated that such combined pituitary hormone deficiency (CPHD) can be induced by lymphocytic hypophysitis [9] or through mutation of transcriptional factors such as Prop-1 or Pit-1 [10][11][12]. However, the patterns of ACTH and PRL deficiencies are very rare, and a report about such CPHD induced by lymphocytic hypophysitis or disorders of transcriptional factors is not unprecedented.…”

Section: Discussionmentioning

confidence: 99%

A Case of Prolactin Deficiency with Familial Puerperal Alactogenesis Accompanying Impaired ACTH Secretion

et al. 2007

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Abstract. We report here the case of a 34-year-old female with puerperal alactogenesis. Her menstrual cycle was regular and breast development normal. She had delivered a healthy boy but could not breast-feed after parturition. Endocrinological studies disclosed that the cause was a prolactin (PRL) deficiency. In addition, she showed accompanying impaired ACTH secretion that was believed to be triggered by encephalitis, although her plasma levels of GH, TSH, LH and FSH remained intact. Pituitary MRI showed no specific findings and anti-pituitary antibody tests were negative. Interestingly, both her mother and grandmother also reported puerperal alactogenesis. The sequences of all five exons of the PRL gene, including promoter region and transcription initiation point, were surveyed in order to examine for certain genetic disorders, but no mutations were identified. Although it cannot be definitively concluded that this PRL deficiency was not a genomic DNA disorder, in our case at least, her PRL gene was normal and, therefore, was not directly responsible for the patient's impaired PRL secretion. This evidence suggests that familial puerperal alactogenesis and PRL deficiency can be induced by other causes such as via disorders of unknown transcription factors or molecules that contribute to translation of PRL gene.

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Lymphocytic Adenohypophysitis and Lymphocytic Infundibuloneurohypophysitis.

Cited by 144 publications

References 69 publications

A novel hook-shaped enhancement on contrast-enhanced sagittal magnetic resonance image in acute Sheehan’s syndrome: a case report

A novel hook-shaped enhancement on contrast-enhanced sagittal magnetic resonance image in acute Sheehan’s syndrome: a case report

Lymphocytic Hypophysitis and Infundibuloneurohypophysitis. Clinical and Pathological Evaluations.

A Case of Prolactin Deficiency with Familial Puerperal Alactogenesis Accompanying Impaired ACTH Secretion

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