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Endocrine Reviews Nov 1988
Review
Topics: Adrenocorticotropic Hormone; Gonadotropins, Pituitary; Growth Hormone; Humans; Pituitary Gland, Anterior; Pituitary Hormones, Anterior; Pituitary Neoplasms; Prolactin; Somatostatin; Thyrotropin
PubMed: 2905987
DOI: 10.1210/edrv-9-4-417 -
World Journal of Gastroenterology Jul 2008To analyze pituitary hormone and melatonin circadian rhythms, and to correlate hormonal alterations with clinical performance, hepatic disease severity and diagnostic...
AIM
To analyze pituitary hormone and melatonin circadian rhythms, and to correlate hormonal alterations with clinical performance, hepatic disease severity and diagnostic tests used for the detection of hepatic encephalopathy in cirrhosis.
METHODS
Twenty-six patients with cirrhosis were enrolled in the study. Thirteen patients hospitalized for systemic diseases not affecting the liver were included as controls. Liver disease severity was assessed by the Child-Pugh score. All patients underwent detailed neurological assessment, electroencephalogram (EEG), brain magnetic resonance imaging (MRI), assays of pituitary hormone, cortisol and melatonin, and complete blood chemistry evaluation.
RESULTS
Pituitary hormone and melatonin circadian patterns were altered in cirrhosis patients without clinical encephalopathy. Circadian hormone alterations were different in cirrhosis patients compared with controls. Although cortisol secretion was not altered in any patient with cirrhosis, the basal cortisol levels were low and correlated with EEG and brain MRI abnormalities. Melatonin was the only hormone associated with the severity of liver insufficiency.
CONCLUSION
Abnormal pituitary hormone and melatonin circadian patterns are present in cirrhosis before the development of hepatic encephalopathy. These abnormalities may be early indicators of impending hepatic encephalopathy. Factors affecting the human biologic clock at the early stages of liver insufficiency require further study.
Topics: Aged; Circadian Rhythm; Electroencephalography; Female; Hepatic Encephalopathy; Humans; Hydrocortisone; Liver Cirrhosis; Male; Melatonin; Middle Aged; Pituitary Hormones; Prolactin; Thyrotropin
PubMed: 18636665
DOI: 10.3748/wjg.14.4190 -
Saishin Igaku. Modern Medicine Apr 1971
Review
Topics: Action Potentials; Animals; Calcium; Electric Stimulation; Male; Nerve Endings; Neurosecretory Systems; Oxytocin; Pituitary Gland, Posterior; Pituitary Hormones, Posterior; Rats; Vasopressins
PubMed: 4940014
DOI: No ID Found -
Annals of the New York Academy of... Dec 1995
Review
Topics: Animals; Corticotropin-Releasing Hormone; Cytokines; Gonadotropin-Releasing Hormone; Growth Hormone; Hypothalamo-Hypophyseal System; Interleukin-1; Pituitary Gland, Anterior; Pituitary Hormones; Prolactin; Rats
PubMed: 8597416
DOI: 10.1111/j.1749-6632.1995.tb44697.x -
BMC Pediatrics Nov 2019Pituitary tumors and/or their treatment are associated with multiple pituitary hormone deficiency (MPHD) in adults, but the distinct pituitary hormone profile of MPHD in...
BACKGROUND
Pituitary tumors and/or their treatment are associated with multiple pituitary hormone deficiency (MPHD) in adults, but the distinct pituitary hormone profile of MPHD in Chinese children and adolescents remains unclear.
METHODS
Patients with MPHD were divided into four groups according to their MRI results: 1) pituitary stalk interruption syndrome (PSIS); 2) hypoplasia; 3) normal; and 4) tumor survivor.
RESULTS
Among the 184 patients, 93 patients (50.5%) were with PSIS, 24 (13.0%) had hypoplastic pituitary gland, 10 (5.4%) patients were normal, and 57 (31.0%) were tumor survivors. There was an association between abnormal fetal position and PSIS (P ≤ 0.001). The CA/BA in PSIS, hypoplasia, normal, tumor survivor groups were 2.27 ± 1.05, 1.48 ± 0.39, 1.38 ± 0.57, 1.49 ± 0.33, and HtSDS were - 3.94 ± 1.39, - 2.89 ± 1.09, - 2.50 ± 1.05, - 1.38 ± 1.63. Patients in PSIS group had the largest CA/BA (P ≤ 0.001 vs. hypoplasia group, P = 0.009 vs. normal group, P ≤ 0.001 vs. tumor survivors) and lowest HtSDS (P ≤ 0.001 vs. hypoplasia group, P = 0.003 vs. normal group, P ≤ 0.001 vs. tumor survivors). The levels of TSH in the PSIS, hypoplasia, normal, and tumor survivor groups were 1.03 ± 1.08 (P = 0.149 vs. tumor survivors), 1.38 ± 1.47 (P = 0.045 vs. tumor survivors), 2.49 ± 1.53 (P < 0.001 vs. tumor survivors), and 0.76 ± 1.15 μIU/ml. The levels of GH peak in PSIS, hypoplasia, normal, tumor survivor groups were 1.37 ± 1.78, 1.27 ± 1.52, 3.36 ± 1.79, 0.53 ± 0.52 ng/ml and ACTH were 27.50 ± 20.72, 25.05 ± 14.64, 34.61 ± 59.35, 7.19 ± 8.63 ng/ml. Tumor survivors had the lowest levels of GH peak (P ≤ 0.001 vs. PSIS group, P = 0.002 vs. hypoplasia group, P ≤ 0.001 vs. normal group) and ACTH (all the P ≤ 0.001 vs. the other three groups).
CONCLUSION
The frequency of PSIS is high among children and adolescents with MPHD. The severity of hormone deficiencies in patients with MPHD was more important in the tumor survivor group compared with the other groups.
Topics: Adolescent; Asian People; Child; Child, Preschool; Female; Humans; Hypopituitarism; Infant; Male; Pituitary Hormones; Retrospective Studies
PubMed: 31722706
DOI: 10.1186/s12887-019-1819-6 -
The Journal of Clinical Investigation Nov 1987Approximately 25% of patients with pituitary adenomas have no clinical or biochemical evidence for excess hormone secretion and are classified as having null cell or...
Approximately 25% of patients with pituitary adenomas have no clinical or biochemical evidence for excess hormone secretion and are classified as having null cell or nonfunctioning adenomas. To characterize the cell type of these tumors, we analyzed pituitary hormone gene expression in clinically nonfunctioning pituitary adenomas using specific oligonucleotide probes for the messenger (m)RNAs encoding growth hormone, prolactin, ACTH, and the glycoprotein hormone subunits, alpha, luteinizing hormone (LH)beta, follicle-stimulating hormone (FSH)beta, and thyroid-stimulating hormone (TSH)beta. Expression of one or more of the anterior pituitary hormone genes was found in 12/14 (86%) of the patients with clinically classified nonfunctioning adenomas. Expression of one or more of the glycoprotein hormone genes (alpha, LH beta, FSH beta, TSH beta) was identified most commonly (79%) with expression of multiple beta-subunit genes in many cases. Expression of alpha-subunit mRNA was found in each of the adenomas from patients expressing one of the beta-subunit mRNAs and in three patients with no detectable beta-subunit mRNA. Although FSH beta and LH beta mRNAs were found with similar frequencies in nonfunctioning adenomas, expression of FSH beta mRNA was generally much more abundant. TSH beta mRNA was detected in only one adenoma. The levels of glycoprotein hormone subunit mRNAs were variable in different adenomas, but the lengths of the mRNAs and transcriptional start sites for the alpha- and beta-subunit genes were the same in the pituitary adenomas and in normal pituitary. Growth hormone and prolactin gene expression were not observed in the nonfunctioning adenomas, but ACTH mRNA was found in a single case. Immunohistochemistry of the adenomas confirmed production of one or more pituitary hormones in 13/14 (93%) nonfunctioning tumors, with a distribution of hormone production similar to that of the hormone mRNAs. These data indicate that pituitary adenomas originating from cells producing glycoprotein hormones are common, but are difficult to recognize clinically because of the absence of characteristic endocrine syndromes and defective hormone biosynthesis and secretion.
Topics: Adenoma; Adrenocorticotropic Hormone; Adult; Aged; Aged, 80 and over; Female; Follicle Stimulating Hormone; Follicle Stimulating Hormone, beta Subunit; Growth Hormone; Histocytochemistry; Humans; Immunoenzyme Techniques; Luteinizing Hormone; Male; Middle Aged; Nucleic Acid Hybridization; Pituitary Hormones; Pituitary Neoplasms; Prolactin; RNA, Messenger; Thyrotropin
PubMed: 2824561
DOI: 10.1172/JCI113228 -
Pediatric Endocrinology Reviews : PER Jan 2009Clinical manifestations of hypopituitarism are variable and depend on the severity of hormone deficiency, creating a diagnostic challenge for diagnosis of the... (Review)
Review
Clinical manifestations of hypopituitarism are variable and depend on the severity of hormone deficiency, creating a diagnostic challenge for diagnosis of the non-classical patient who may have a less severe growth hormone (GH) deficiency and only a suggestion of possible hypothyroidism. Laboratory tests contribute to the diagnostic process, but the tests for growth and thyroid dysfunction, two of the most common manifestations of multiple pituitary hormone deficiency, are some of the most problematic from a methodological perspective. Patients in the "grey zone" of diagnosis, for whom there is no distinct dividing line or gold standard diagnostic test, are the focus of this article. Issues relating to the use of laboratory tests involving GH, insulin-like growth factor-I, and free thyroxine in the diagnosis of GH and thyroid deficiency are reviewed. Assay harmonization initiatives are required before clinical research studies are performed to establish diagnostic thresholds for GH and thyroid hormone deficiencies.
Topics: Human Growth Hormone; Humans; Hypopituitarism; Hypothyroidism; Insulin-Like Growth Factor I; Pituitary Hormones; Thyroxine
PubMed: 19337184
DOI: No ID Found -
Andes Pediatrica : Revista Chilena de... Dec 2023The deficiency of two or more pituitary hormones is called multiple pituitary hormone deficiencies (MPHD). Its prevalence is estimated to be about 1/8,000 worldwide.
UNLABELLED
The deficiency of two or more pituitary hormones is called multiple pituitary hormone deficiencies (MPHD). Its prevalence is estimated to be about 1/8,000 worldwide.
OBJECTIVE
To present the diagnosis processes, clinical findings, and long-term follow-up of patients with MPHD.
PATIENTS AND METHOD
Between 1999 and 2015, patients diagnosed with MPHD were evaluated. Clinical presentation, anthropometry, imaging studies, and clinical evolution were analyzed. Hormone status was evaluated, including growth hormone (GH), thyroid-stimulating hormone (TSH), adrenocorticotropic hormone (ACTH), follicle-stimulating hormone/luteinizing hormone (FSH/LH), and prolactin (PRL). Data were assessed using the student's t-test and the Mann-Whitney U test. Spearman's correlation was used for correlations. A p-value < 0.05 was considered statistically significant.
RESULTS
Forty-five patients were included; 55.6% were male, the mean age at presentation was 5.6 ± 3.9 (0-14.4) years, and the median bone age was 3.5 ± 2.3 (0.5-11) years. At admission, GH deficiency was found in 88.9% of the cases, TSH deficiency in 77.8%, ACTH deficiency in 33.3%, FSH/LH deficiency in 22.2%, and PRL deficiency in 17.8%. During the follow-up, 62% of the cases added other hormone deficiencies. The mean follow-up period was 9.18 ± 3.6 (3.02-17.2) years.
CONCLUSION
Patients with MPHD have very different clinical presentations, with GH and TSH deficiency being the most common in this study. Additional hormonal deficiencies can occur even years after the initial diagnosis and our results demonstrate that genetic height potential is achieved with GH treatment.
Topics: Humans; Male; Infant; Child, Preschool; Female; Follow-Up Studies; Pituitary Hormones; Hypopituitarism; Human Growth Hormone; Growth Hormone; Adrenocorticotropic Hormone; Follicle Stimulating Hormone; Hypothyroidism
PubMed: 38329304
DOI: 10.32641/andespediatr.v94i6.4680 -
Circulatory Shock Sep 1994Recent studies have led to the re-discovery of the protein originally described as macrophage-migration inhibitory factor (MIF) to be both a pituitary hormone and a... (Review)
Review
Recent studies have led to the re-discovery of the protein originally described as macrophage-migration inhibitory factor (MIF) to be both a pituitary hormone and a pro-inflammatory, macrophage cytokine. MIF is a pivotal mediator in endotoxic shock and may serve as a pituitary "stress" hormone that regulates systemic inflammatory responses.
Topics: Animals; Humans; Inflammation; Macrophage Migration-Inhibitory Factors; Pituitary Hormones; Shock, Septic
PubMed: 7704936
DOI: No ID Found -
Bailliere's Clinical Endocrinology and... Jul 1995In this chapter, we have reviewed the fast-moving area of the molecular pathology of pituitary hormone deficiencies and resistance. Examples have been described... (Review)
Review
In this chapter, we have reviewed the fast-moving area of the molecular pathology of pituitary hormone deficiencies and resistance. Examples have been described affecting all levels of pituitary function, i.e. the releasing hormone, its receptor, the pituitary hormone and its receptor, and the development of the pituitary gland. Other examples in these genes, and in those in which no mutation has yet been found, will undoubtedly be discovered in the next few years, throwing light on the structural basis of the gene product's function and allowing a greater understanding of endocrine physiology and pathophysiology. The main reason for this rapid progress in knowledge is the recent technological advances in mutation detection, which bring this activity within the grasp of the majority of reasonably equipped laboratories. Technological advancement, however is not all that it takes to carry out this work. The conditions caused by genetic damage such as we have described are rare, and there is clearly a requirement for great awareness on the part of the clinical endocrinologist. Patients in whom it is suspected that mutations such as these may occur require careful clinical and biochemical work-up. Indeed, in many instances, careful thought has to go into deciding what the phenotype of a particular mutation might be. Thus, the requirement for close collaboration between clinical and molecular endocrinologists has to be the important message for the future in this area of research.
Topics: Adrenocorticotropic Hormone; Follicle Stimulating Hormone; Gonadotropin-Releasing Hormone; Growth Disorders; Growth Hormone; Humans; Luteinizing Hormone; Mutation; Pituitary Hormones; Receptors, Somatotropin; Thyroid Hormones
PubMed: 7575328
DOI: 10.1016/s0950-351x(95)80536-2