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At least 19 recordsLinked to original sources
PubMed1994

Hypopituitarism with invisible pituitary stalk: two case reports of males with micropenis suggesting fetal onset of hypopituitarism.

The presence of hypopituitarism and invisible pituitary stalk on a magnetic resonance image (MRI) is commonly attributed to birth trauma. Two patients with severe hypopituitarism and invisible pituitary stalk are presented. One was born by breech delivery, the other by Cesarean section. The presence of a micropenis since early infancy in these two patients suggested that their hypopituitarism might have begun during early fetal life thus effecting penile growth during the second and third triministers of gestation. These findings raise the possibility that the association of hypopituitarism and invisible pituitary stalk may have multiple etiologies including hormonal abnormalities during early fetal life.

Adolescent↗
PubMed1992

The association of hypopituitarism with small pituitary, invisible pituitary stalk, type 1 Arnold-Chiari malformation, and syringomyelia in seven patients born in breech position: a further proof of birth injury theory on the pathogenesis of "idiopathic hypopituitarism".

We report seven cases of hypopituitarism all having a history of breech delivery, asphyxia at birth, and syringomyelia. A small pituitary gland was found on MRI or CT in six cases, invisible pituitary stalk on MRI in five cases, and type 1 Arnold-Chiari malformation in six cases. A constellation of these abnormalities are best explained by traction of brain and spinal cord of the subjects exerted during breech delivery and further support the primary role of birth trauma in the genesis of "idiopathic hypopituitarism".

Adolescent↗
PubMed1975

Optic nerve hypoplasia with hypopituitarism. Septo-optic dysplasia with hypopituitarism.

Four children had optic nerve hypoplasia with hypopituitarism, and their clinical picture varied with age. The newborn had apnea, hypotonia, seizures, hyopglycemia, and prolong jaundice. The young infant had defective vision, behavioral delay, hypotonia, and seizures. Except for a mildly receding lower jaw and a high-arched palate, the appearance of the patients was not unusual. The fasting blood glucose level was mildly depressed. In two cases the liver was palpable and results of liver function tests were abnormal. The older child, who was blind and mentally retarded, had growth failure. The extent of the pituitary hormone deficiencies was variable, including diabetes insipidus. The septum pellucidum was not invariably absent. Clinical and pathological findings indicate that the brain lesion might be more diffuse than hitherto recognized. Early recognition of this syndrome and timely intervention might diminish serious sequels.

Abnormalities, Multiple↗
PubMed2001

Inflammatory cardiovascular risk markers in women with hypopituitarism.

Patients with hypopituitarism have increased cardiovascular mortality. A high prevalence of conventional cardiovascular risk factors, including obesity, central fat distribution, insulin resistance, and dyslipidemia, have been described in these patients. The inflammatory markers C-reactive protein (CRP) and IL-6 are predictors of cardiovascular events, and high levels of CRP have been reported in men with hypopituitarism and GH deficiency. However, little is known about inflammatory cardiovascular risk markers in women with hypopituitarism. We therefore investigated whether inflammatory and traditional cardiovascular risk markers are elevated in women with hypopituitarism. Fifty-three women with hypopituitarism and 111 healthy control women were included in this cross-sectional study. Morning blood samples were drawn after an overnight fast. Serum was assayed for CRP, IL-6, glucose, insulin, IGF-I, triglycerides, total cholesterol, low density lipoprotein cholesterol, high density lipoprotein (HDL) cholesterol, lipoprotein(a), E2, total testosterone (total T) and free testosterone (free T), and dehydroepiandrosterone sulfate. IL-6 and CRP levels were higher in women with hypopituitarism than in healthy controls (P < 0.0001 for comparison between groups). In a multivariate model, CRP levels depended on hypopituitarism, body mass index (BMI), and estrogen use. There was an interaction between the effect of BMI and hypopituitarism on CRP levels, such that the importance of hypopituitarism in determining CRP levels disappeared at high BMIs. In a similar multivariate model, IL-6 levels depended on hypopituitarism and BMI. Total cholesterol, the total to HDL cholesterol ratio, and triglycerides were higher in hypopituitary patients, but only triglycerides and the total to HDL cholesterol ratio depended on hypopituitarism when controlling for BMI. There was no significant difference in lipoprotein(a) levels between hypopituitary women and control subjects. However, when controlling for estrogen use, lipoprotein(a) levels showed a trend toward being lower in the hypopituitary group (P = 0.075). In patients with hypopituitarism, CRP correlated negatively with IGF-I (r = -0.35; P = 0.010), total T (r = -0.42; P = 0.0020), and free T (r = -0.30; P = 0.031). Similarly, IL-6 correlated negatively with total T (r = -0.39; P = 0.0040) and androstenedione (r = -0.27; P = 0.048) in hypopituitary patients. In conclusion, hypopituitary women have increased levels of IL-6 and CRP, both of which are inflammatory markers of atherosclerosis. GH deficiency and androgen deficiency may contribute to these findings. Chronic inflammation may contribute to the high cardiovascular risk seen in this population.

Biomarkers↗
PubMed2001

Prevalence and incidence of hypopituitarism in an adult Caucasian population in northwestern Spain.

OBJECTIVE: To determine the prevalence and incidence of hypopituitarism in the general population. POPULATION: The study population comprised an average population sample of 146,000 adult inhabitants in South Galicia (northwestern Spain). The Medical Register of the General Hospital of Vigo ensured virtually complete case ascertainment for diagnosed hypopituitarism in this sample population. Only patients residing in the study area were included. The diagnosis of hypopituitarism was based on baseline and hormonal dynamic tests. DESIGN: The study comprised two cross-sectional surveys, the first from January to December 1992 and the second from January to December 1999, together with a longitudinal survey performed between January 1993 and December 1999. MAIN RESULTS: In the first survey the prevalence of hypopituitarism was 29/100,000 (CI, 19.88-37.72), without sex differences. In the second survey, the prevalence observed was higher than in the first, 45.5/100,000 (CI, 34.92-56.08). In the second survey, which included almost all cases registered in the first study, the cause of hypopituitarism was a pituitary tumour in 61%, a non-pituitary tumour in 9% and a non-tumour cause in 30%. Around 50% of patients had 3-5 pituitary hormonal deficiencies, with LH/FSH being the most prevalent. Patients with tumour-induced hypopituitarism showed a tendency to suffer GH deficiency more frequently than those due to non-tumour causes. In the longitudinal study with a population of 1,020,764 people-years of observation, the average annual incidence rate of hypopituitarism was 4.21 cases/100,000 (CI, 2.95-5.47), with this incidence being similar for both sexes. The annual incidence of hypopituitarism remained stable during the study period. CONCLUSION: We present for the first time data on the prevalence and incidence of hypopituitarism in the general adult population. These patients showed a tendency to suffer LH/FSH deficiency as the most prevalent hormone deficit. Furthermore, patients with hypopituitarism due to a tumour or its treatment showed a greater tendency to suffer GH deficiency than those with a non-tumour cause. These data may be useful for producing a rational programme for patients suffering from this condition and also for comparison with future data in our country and elsewhere in the world.

Adolescent↗
PubMed2005

Hypopituitarism induced by traumatic brain injury in the transition phase.

Traumatic brain injury (TBI) has been associated with hypopituitarism in general and GH deficiency (GHD) in particular; the consequences of this on growth and development are likely to be critical in children and adolescents in the so-called "transition phase". In order to verify the consequences of TBI on pituitary function in the transition phase, we studied a population of adolescents and young adults 3 and 12 months after brain injury [no. = 23, 9 females, 14 males; age: 16-25 yr; body mass index (BMI): 21.9 +/- 0.6 kg/m2]. At 3 months, hypopituitarism was present in 34.6%. Total, multiple and isolated deficits were present in 8.6, 4.3 and 21.7%, respectively. Diabetes insipidus (DI) was present in 8.6% patients and mild hyperprolactinemia in 4.3%. At 12 months, hypopituitarism was present in 30.3%. Total, multiple and isolated deficits were present in 8.6, 4.3 and 17.4%, respectively. DI was present in 4.3% of patients and mild hyperprolactinemia in 4.3%. Total hypopituitarism was always confirmed at retesting. Multiple and isolated hypopituitarism were confirmed in 0/1 and 2/5, respectively. Two/23 patients showed isolated hypopituitarism at 12 months only; 1 patient with isolated at 3 months showed multiple hypopituitarism at retesting. GHD and secondary hypogonadism were the most common acquired pituitary deficits. These results show the high risk of TBI-induced hypopituitarism also in the transition age. Thus it is recommended that pediatric endocrinologists follow-up pituitary function of children and adolescents after brain injuries.

Adolescent↗
PubMed2006

Hypopituitarism: a sequela of severe hypoxic encephalopathy.

BACKGROUND/PURPOSE: Central diabetes insipidus (DI) is an established phenomenon after hypoxic encephalopathy or brain death, but hypopituitarism is seldom described. This study investigated the characteristics of 11 patients with DI and hypopituitarism which developed after severe hypoxic encephalopathy. METHODS: The medical records of patients with DI and hypopituitarism after severe hypoxic encephalopathy from 1997 to 2002 were retrospectively reviewed. Eleven patients with DI and hypopituitarism after severe hypoxic episodes were included. Demographic data, primary diagnosis, the time of onset of DI, the time of diagnosis of hypopituitarism, the presence of symptoms of hypopituitarism, and outcome of these patients were analyzed. RESULTS: Eleven patients comprising nine females and two males aged 47.4 +/- 19.3 years (range, 24-74 years) were included. The mean interval from the precipitating event to the onset of DI was 60 +/- 46 hours (range, 11-131 hours). The mean interval from the precipitating event to the diagnosis of hypopituitarism was 423 +/- 182 hours (range, 132-672 hours). The average duration of hospitalization was 63 +/- 35 days (range, 9-113 days). The overall mortality rate during hospitalization was 45%. Four patients died of sepsis and one died of heart failure due to acute myocardial infarction. CONCLUSION: The development of DI after severe hypoxic encephalopathy is a sign of severe brain damage. It usually ensues immediately or days after loss of brain stem reflexes. Hypopituitarism developed several weeks later than DI in these patients. Recognition and treatment of these deficiencies may prevent organ dysfunction.

Adrenocorticotropic Hormone↗
PubMed2002

Medical management of hypopituitarism in patients with pituitary adenomas.

Hypopituitarism is a disease complex with variable clinical manifestations. Recent studies have improved our understanding of its pathophysiology, particularly in patients with pituitary adenomas. In that setting, hypopituitarism was previously considered a permanent and irreversible process, requiring life-long hormone replacement therapy. While this could be true in some instances, recent data demonstrated recovery of pituitary function in a large number of patients with hypopituitarism following surgical decompression. Mechanical compression of portal vessels and the pituitary stalk, by the expanding adenoma was postulated to be the predominant mechanism causing hypopituitarism in this setting. Since portal vessels also provide blood supply to the anterior lobe, ischemic necrosis of portions of the pituitary can occur as a result of increased and prolonged compression by the expanding adenoma. Recent data demonstrated increases in intrasellar pressure (ISP) in patients with pituitary macroadenomas, particularly those with hypopituitarism. The data showed that ISP measurements correlated positively with the serum prolactin levels but not with tumor sizes. It is postulated that increased ISP has predominant role in the pathogenesis of hypopituitarism in patients with pituitary adenomas while. The increase in ISP results in decreased blood flow through the portal vessels and the pituitary stalk. The latter will result in diminished delivery of hypothalamic hormones to the anterior pituitary and may also cause ischemia and/or necrosis in some portions of the normal gland. Recovery of pituitary function can thus be anticipated after surgical decompression, in patients who have viable pituitary cells. Understanding the pathophysiology of hypopituitarism and recognizing the probability for recovery of function should be emphasized in the management of patients with this disease. An important aspect of the management is patients' education about their disease, including the use of medic alert identification. The managing physician should appreciate the variable clinical manifestations of the disease and the possible occurrence of other associated neuroendocrine, neurological and neuro-ophthalmologic signs and symptoms. Treatment of hypopituitarism should not be rigid but instead, always individualized. Management should take into consideration the patients' age, sex, education, original disease process and clinical history.

Adenoma↗
PubMed2005

Consensus guidelines on screening for hypopituitarism following traumatic brain injury.

PRIMARY OBJECTIVE: The goal of this consensus statement is to increase awareness among endocrinologists and physicians treating patients with traumatic brain injury (TBI) of the incidence and risks of hypopituitarism among patients with TBI. RATIONALE: TBI poses significant risk to the pituitary gland, leading to elevated risks of diabetes, hypopituitarism and other endocrinopathies. Signs and symptoms associated with hypopituitarism often mimic the sequellae of TBI, although the severity of symptoms is not necessarily related to the severity of the injury. Patients with TBI-induced hypopituitarism may benefit both physically and psychologically from appropriate hormone replacement therapy (HRT). Participants at this unique consensus meeting attempted to define and spearhead an approach to increase awareness of the risks of TBI-induced endocrinopathies, in particular growth hormone deficiency (GHD), and to outline necessary and practical objectives for managing this condition. RECOMMENDATIONS: Systematic screening of pituitary function is recommended for all patients with moderate-to-severe TBI at risk of developing pituitary deficits. Patients with hypopituitarism benefit from appropriate hormonal replacement and prospects for rehabilitation of patients with TBI-induced hypopituitarism may be enhanced by appropriate HRT. Further exploration of this possibility requires: (1) active collaboration between divisions of endocrinology and rehabilitation at the local level to perform a screening of pituitary function in patients after TBI, (2) creation of a consultancy service by endocrine societies for use by rehabilitation centres, (3) development of continuing medical education (CME) programmes that can be offered as crossover training to the physicians who manage the care of patients with TBIs, (4) targeting of patient organizations with educational information for dissemination to patients and their families, (5) continued efforts to more clearly define the population at greatest risk of TBI-induced hypopituitarism and (6) monitor results of efficacy studies as they become available to evaluate whether and how much replacement therapy can improve the symptoms of individuals with TBI-induced hypopituitarism.

Brain Injuries↗
PubMed2004

Traumatic brain injury and subarachnoid haemorrhage are conditions at high risk for hypopituitarism: screening study at 3 months after the brain injury.

OBJECTIVE: Acquired hypopituitarism in adults is obviously suspected in patients with primary hypothalamic-pituitary diseases, particularly after neurosurgery and/or radiotherapy. That brain injuries (BI) can cause hypopituitarism is commonly stated and has been recently emphasized but the management of BI patients does not routinely include neuroendocrine evaluations. AIM: To clarify the occurrence of hypopituitarism in patients after traumatic brain injury (TBI) or subarachnoid haemorrhage (SAH) 3 months after the BI. SUBJECTS AND METHODS: The occurrence of hypopituitarism in conscious patients after traumatic brain injury [TBI, n = 100, 31 women, 69 men; age 37.1 +/- 1.8 years; body mass index (BMI) 23.7 +/- 0.4 kg/m(2); Glasgow Coma Scale (GCS) 3-15] or subarachnoid haemorrhage [SAH, n = 40, 14 men, 26 wpmen, 51.0 +/- 2.0 years; 25.0 +/- 0.6 kg/m(2); Fisher's scale 1-4] was studied in a multicentre study 3 months after the BI. All patients underwent wide basal hormonal evaluation; the GH/IGF-I axis was evaluated by GHRH + arginine test and IGF-I measurement. RESULTS: In TBI patients, some degree of hypopituitarism was shown in 35%. Total, multiple and isolated deficits were present in 4, 6 and 25%, respectively. Diabetes insipidus was present in 4%. Secondary adrenal, thyroid and gonadal deficit was present in 8, 5 and 17%, respectively. Severe GH deficiency (GHD) was the most frequent pituitary defect (25%). In SAH patients, some degree of hypopituitarism was shown in 37.5%. Despite no total hypopituitarism, multiple and isolated deficits were present in 10 and 27.5%, respectively. Diabetes insipidus was present in 7.5%. Secondary adrenal, thyroid and gonadal deficit was present in 2.5, 7.5 and 12.5%, respectively. Severe GHD was the most frequent defect (25%). CONCLUSIONS: TBI and SAH are conditions associated with high risk of acquired hypopituitarism. The pituitary defect is often multiple and severe GHD is the most frequent defect. Thus neuroendocrine evaluations are always mandatory in patients after brain injuries.

Adult↗
PubMedDate not supplied

Hypopituitarism in childhood.

BACKGROUND: Childhood hypopituitarism may be present at birth or may be acquired. Early diagnosis and treatment promote the best possible outcomes. METHODS: The anatomy, etiologies, clinical presentation, diagnostic testing strategies, and current treatments relevant to childhood hypopituitarism are reviewed. RESULTS: Children with congenital hypopituitarism may present with life-threatening hypoglycemia, abnormal serum sodium concentrations, shock, microphallus in males, and, only later, growth failure. Causes of congenital hypopituitarism include septo-optic dysplasia, other midline syndromes, and mutations of transcription factors involved in pituitary gland development. Children with acquired hypopituitarism typically present with growth failure and may have other complaints depending on the etiology and the extent of missing pituitary hormones. Acquired hypopituitarism may result from tumors (most commonly craniopharyngioma), radiation, infection, hydrocephalus, vascular anomalies, and trauma. CONCLUSIONS: An MRI of the head is critical in determining the etiology. Testing for pituitary hormone deficiencies is undertaken along with appropriate hormonal replacement and, in some cases, direct treatment of the cause of the hypopituitarism. All children with hypopituitarism require coordination of medical care by a pediatric endocrinologist and, when older, transition to the care of an internist endocrinologist. Referrals to a reproductive endocrinologist may be required as fertility issues arise.

Age of Onset↗
PubMed2004

Direct causes of death in Japanese patients with hypopituitarism as analyzed from a nation-wide autopsy database.

OBJECTIVES: The direct causes of death in Japanese patients with hypopituitarism remain unclear. In this study, the direct causes of death were investigated and compared between Japanese patients with hypopituitarism from a nation-wide autopsy database and an age- and gender-matched control population from national reports. SUBJECTS: Three hundred and ninety-one subjects with hypopituitarism who had died were selected from a nation-wide autopsy database (1984-1993). The ratios of each cause of death among the age- and gender-matched control population were derived from national reports. RESULTS: In subjects with hypopituitarism, an increased relative frequency of death from cerebrovascular diseases (male; 2.02 (95% confidence interval (CI) 1.45-2.82), female; 1.73 (95% CI 1.18-2.52)) was found. In particular, the relative frequency of death from cerebral hemorrhage was 4.60 (95% CI 2.95-7.17) in male and 4.80 (95% CI 2.90-7.94) in female subjects with hypopituitarism. Unexpectedly, a decreased relative frequency of death from all heart diseases (male; 0.439 (95% CI 0.277-0.696), female; 0.267 (95% CI 0.149-0.478)) was found in subjects with hypopituitarism, although there was no difference between subjects with hypopituitarism and controls in the frequency of death from ischemic heart disease. CONCLUSIONS: These results provide useful information for the long-term care of Japanese patients with hypopituitarism.

Adolescent↗
PubMed1998

Effect of acute pharmacological reduction of plasma free fatty acids on growth hormone (GH) releasing hormone-induced GH secretion in obese adults with and without hypopituitarism.

In obesity, there is a markedly decreased GH secretion. The diagnosis of GH deficiency (GHD) in adults is based on peak GH responses to stimulation tests. In the severely obese, peak GH levels after pharmacological stimulation are often in the range that is observed in hypopituitary patients. To distinguish obese subjects from GHD patients, it will be necessary to demonstrate that reduced GH responsiveness to a given test is reversible in the former, but not in the latter, group. Recent studies have shown that reduction of plasma free fatty acids (FFA) with acipimox in obese patients restores their somatotrope responsiveness. There are no data evaluating GH responsiveness to acipimox plus GHRH in obese adults with hypopituitarism. The aim of the present study was to evaluate the effect of acute pharmacological reduction of plasma FFA on GHRH-mediated GH secretion in obese normal subjects and obese adults with hypopituitarism. Eight obese patients with a body mass index of 34.2+/-1.2; eight obese adults with hypopituitarism, with a body mass index of 35.5+/-1.9; and six control subjects were studied. All the patients showed an impaired response to an insulin-tolerance test (0.15 U/kg, i.v.), with a peak GH secretion of less than 3 microg/L. Two tests were carried out. On one day, they were given GHRH (100 microg, i.v., 0 min), preceded by placebo; and blood samples were taken every 15 min for 60 min. On the second day, they were given GHRH (100 microg, i.v., 0 min), preceded by acipimox (250 mg, orally, at -270 min and -60 min); and blood samples were taken every 15 min for 60 min. The administration of acipimox induced a FFA reduction during the entire test. Normal control subjects had a mean peak (microg/L) of 23.8+/-4.8 after GHRH-induced GH secretion; previous acipimox administration increased GHRH-induced GH secretion, with a mean peak of 54.7+/-14.5. In obese patients, GHRH-induced GH secretion was markedly reduced, with a mean peak (microg/L) of 3.9+/-1; previous administration of acipimox markedly increased GHRH-mediated GH secretion, with a mean peak of 16.0+/-3.2 (P < 0.05). In obese adults with hypopituitarism, GHRH-induced GH secretion was markedly reduced, with a mean peak (microg/L) of 2+/-0.7; previous acipimox administration did not significantly modify GHRH-mediated GH secretion, with a mean peak of 3.3+/-1.1 (P < 0.05). The GH response of obese patients and obese adults with hypopituitarism was similar after GHRH alone. In contrast, the GH response after GHRH plus acipimox, was markedly decreased in obese adults with hypopituitarism (mean peak, 3.3+/-1.1), compared with obese patients (mean peak, 16.0+/-3.2) (P < 0.05) and control subjects (mean peak, 54.7+/-14.5) (P < 0.01). In conclusion, GH secretion, after GHRH-plus-acipimox administration, is reduced in obese adults with hypopituitarism patients, when compared with obese normal patients. Testing with GHRH plus acipimox is safe and is free from side effects and could be used for the diagnosis of GHD in adults.

Adult↗
PubMed2003

Severe hyponatremia due to hypopituitarism with adrenal insufficiency: report on 28 cases.

OBJECTIVE: Severe hyponatremia due to hypopituitarism and adrenal insufficiency can be life-threatening, and treatment with glucocorticoids is very effective once the diagnosis of the underlying disorder has been made. In our experience, the diagnosis of hypopituitarism in hyponatremic patients is often overlooked. METHODS: In a retrospective study we screened the files of 185 patients with severe hyponatremia (<130 mmol/l) that had been seen in one endocrinological unit of a university hospital between 1981 and 2001 in order to describe the clinical spectrum of patients with hyponatremia and hypopituitarism including secondary adrenal insufficiency. RESULTS: In 139 cases it was possible to clearly ascribe the patients to the pathophysiological groups of (i) primary sodium deficiency, (ii) edematous disorders, and (iii) normovolemic disorders including the "syndrome of inappropriate secretion of antidiuretic hormone" (SIADH). Twenty-eight patients with severe "normovolemic hyponatremia" (serum sodium: 116+/-7 mmol/l, mean+/-s.d.) had hypopituitarism and secondary adrenal insufficiency as shown by basal cortisol measurements and dynamic tests of adrenal function. In 25 cases of this group hypopituitarism (mostly due to empty sella, Sheehan's syndrome and pituitary tumors) had not been recognized previously, and in 12 cases recurrent hyponatremia during previous hospital admissions (up to four times) could be documented. The mean age of these patients (21 women, seven men) was 68 Years. The most frequently occurring clinical signs were missing or scanty pubic and axillary hair, pale and doughy skin, and small testicles in the men. Frequent symptoms like nausea and vomiting, confusion, disorientation, somnolence or coma were similar to those in 91 patients with SIADH. Basal serum cortisol levels in the acutely ill state ranged from 20 to 439 nmol/l (mean+/-s.d.: 157+/-123), while in 30 other severely hyponatremic patients it ranged from 274 to 1732 nmol/l (732+/-351 nmol/l). In most patients with hyponatremic hypopituitarism, plasma antidiuretic hormone levels were inappropriately high, probably due to a failure of endogenous cortisol to suppress the hormone in a stressful situation. All patients recovered after low-dose hydrocortisone substitution. Most patients had other pituitary hormone deficiencies and were appropriately substituted subsequently. CONCLUSIONS: Hypopituitarism including secondary adrenal insufficiency seems to be a frequently overlooked cause of severe hyponatremia. A high level of suspicion is the best way to recognize the underlying disorder. Treatment with hydrocortisone is very effective.

Adrenal Glands↗
PubMed2000

Cost of illness in adult patients with hypopituitarism.

OBJECTIVE: To compare the healthcare costs of patients with hypopituitarism with those of individuals from the general population. DESIGN: A retrospective study of costs over 1 year. Estimates of direct and indirect health-related costs were calculated for patients from the general population using existing databases, and for patients with hypopituitarism using records of all patients eligible to participate on 31 December 1989 who could be traced, were willing to participate and had not been treated for acromegaly or Cushing's disease. SETTING: The catchment area of the Endocrine Unit, Sahlgrenska Hospital, Gothenburg. The study was conducted from the societal perspective. Reference data were collected from official regional and national registries. PATIENTS: 199 patients with adult-onset hypopituitarism in whom replacement therapy was given to maintain the adrenal, thyroid and gonadal (but not the somatotropic) axes. MAIN OUTCOME MEASURES AND RESULTS: Direct and indirect costs incurred by patients with hypopituitarism were higher than those incurred by individuals from the general population. The total direct costs per patient were Swedish Crowns (SEK)22,920 vs SEK12,080 (p < 0.003) in the general population, and the highest costs were related to inpatient care. Of the patients aged 16 to 64 years, 22% had drawn a disability pension versus the expected 11.3% (p < 0.003) in the general population, and the patients had a mean sick leave of 38.4 days vs 23.5 (p < 0.001). Total excess costs for all patients with hypopituitarism were SEK 35,768 per patient (p < 0.007). CONCLUSIONS: Patients with hypopituitarism incur more health-related costs than individuals from the general population. They also take more sick leave days and are more likely to claim a disability pension than members of the general population. Further cost analyses are needed to determine whether improvements in diagnostic and surgical procedures, and hormone replacement therapy, can reduce the healthcare costs of patients with hypopituitarism.

Adult↗
PubMedDate not supplied

[Primary hypothyroidism associated with empty sella turcica and hypopituitarism].

INTRODUCTION: Empty sella syndrome is a rather frequent neuroradiological finding in the general population and can be associated with hypopituitarism. Examinations reveal low pituitary hormone levels and lack of response to stimuli. Most patients suffer from central hypothyroidism as part of pituitary insufficiency. Primary hypothyroidism is a rare finding in these patients. CASE REPORT: We present 3 patients: one female and two male, suffering from complete hypopituitarism, as part of the empty sella syndrome diagnosed due to low concentrations of all pituitary hormones, elevated TSH and low thyroid hormones. TRH, LHRH, ACTH and ITT tests, as well as IGF1 have confirmed hypopituitarism and primary hypothyroidism. CT and NMR in all three patients showed empty sella without a tumor in it. The diagnosis of primary hypothyrodism in the first patient was made before hypopituitarism has taken place, or at the same time in the second patient, whereas in the third patient it was diagnosed twenty years later. In two patients anti-TPO and anti-Tg antibody levels were high, and in the third patient they were not elevated. It can be assumed that the etiology of primary hypothyrodism in all three patients was of autoimmune origin, which caused thyroid hypofunction. High level of TSH in all three patients and especially in the patient whose hypopituitarism was diagnosed twenty years later, showed presence of thyrotrophic cells in the pituitary. Evaluation of the hypothalamic-pituitary-thyroid axis was carried out during the complete substitution therapy of hypopituitarism. CONCLUSION: Diagnosing primary hypothyroidism associated with hypopituitarism helps improving the knowledge on empty sella syndrome and points to different clinical syndromes characterized by lack of mixoedema, although approach to therapy is the same for both primary and central hypothyroidism.

Adult↗