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Sheehan syndrome is a potentially serious complication in the postpartum period corresponding to ischemic necrosis of the anterior pituitary related to postpartum haemorrhage. We report three original observations showing an unusual mode of revelation of this syndrome. The first observation is that of a 46-year-old patient admitted initially to resuscitation for a recovered cardiorespiratory arrest, severe hypoglycemia and profound hyponatremia. The second is that of a 45-year-old patient, admitted for recurrent cardiac tamponade after pericardial and pleural puncture and pericardial drainage; clinical survey found signs of slight panhypopituitarism. The latest case is that of a patient of 44 years, admitted to pericardial effusion average abundance revealed by dyspnea and tachypnea with hypotension. The interrogation of all patients revealed the concept of an old hemorrhagic syndrome, absence of lactation and secondary amenorrhea thereafter. Laboratory tests showed insufficient thyroid-stimulating, low cortisol, a hypogonadism hypogonadism. The pituitary magnetic resonance imaging showed an empty sella in the three cases. Patients were placed under replacement therapy with L-thyroxine and hydrocortisone with good clinical, biological and echocardiographic evolution. The three cases illustrate a rare heart atypical presentation for Sheehan's syndrome and underline the importance of early diagnosis and suitable replacement therapy of this syndrome to avoid this complication that can be life threatening., (Copyright © 2016 Elsevier Masson SAS. All rights reserved.)

Hypotension is defined by a low blood pressure either permanently or only in upright posture (orthostatic hypotension). In contrast to hypertension, there is no threshold defining hypotension. The occurrence of symptoms for systolic and diastolic measurements respectively below 90 and 60 mm Hg establishes the diagnosis. Every acute hypotensive event should suggest shock, adrenal failure or an iatrogenic cause. Chronic hypotension from endocrine origin may be linked to adrenal failure from adrenal or central origin, isolated hypoaldosteronism, pseudohypoaldosteronism, pheochromocytoma, neuro-endocrine tumors (carcinoïd syndrome) or diabetic dysautonomia. Hypotension related to hypoaldosteronism associates low blood sodium and above all high blood potassium levels. They are generally classified according to their primary (hyperreninism) or secondary (hyporeninism) adrenal origin. Isolated primary hypoaldosteronisms are rare in adults (intensive care unit, selective injury of the glomerulosa area) and in children (aldosterone synthase deficiency). Isolated secondary hypoaldosteronism is related to mellitus diabetes complicated with dysautonomia, kidney failure, age, iatrogenic factors, and HIV infections. In both cases, they can be associated to glucocorticoid insufficiency from primary adrenal origin (adrenal failure of various origins with hyperreninism, among which congenital 21 hydroxylase deficiency with salt loss) or from central origin (hypopituitarism with hypo-reninism). Pseudohypoaldosteronisms are linked to congenital (type 1 pseudohypoaldosteronism) or acquired states of resistance to aldosterone. Acquired salt losses from enteric (total colectomy with ileostomy) or renal (interstitial nephropathy, Bartter and Gitelman syndromes…) origin might be responsible for hypotension and are associated with hyperreninism-hyperaldosteronism. Hypotension is a rare manifestation of pheochromocytomas, especially during surgical removal when the patient has not been prepared with calcium inhibitors. Every flush with hypotension should suggest a carcinoid crisis, which is very sensitive to subcutaneous somatostatin analog. An accurate etiological diagnosis should allow treat efficiently endocrine hypotension without inducing hypertension in supine posture., (Copyright © 2012. Published by Elsevier Masson SAS.)

Traumatic brain injury has been considered for long as a rare cause of hypopituitarism. Recent studies have already shown a prevalence of 30% of pituitary dysfunction following moderate or severe head injury that may persist into the chronic phase of recovery, hypogonadism and GH deficiency being the most common hormonal deficiencies. Hypopituitarism may impede recovery and contribute to chronic disability in these patients. However, there are limited data available regarding the impact of hypopituitarism, and the indications of hormonal replacement (especially GH replacement and hypogonadism treatment) still remain to be defined. The screening strategy for TBI - induced hypopituitarism has recently been revised., (Copyright © 2012 Société française d’anesthésie et de réanimation (Sfar). Published by Elsevier SAS. All rights reserved.)

We describe the case of a young woman admitted for severe hyponatremia due to hypopituitarism caused by a Sheehan's syndrome. Sheehan's syndrome is a rare disorder. It develops after obstetrical hemorrhage that causes ischemic necrosis of the pituitary gland. In most cases, illness appears progressively and diagnosis is made after variable delay. Acute syndrome may develop immediately after delivery in some rare cases. Hyponatremia is a frequent manifestation and may be severe. It is principally caused by secondary adrenal failure.

Antiphospholipid syndrome (APS) is an acquired thrombotic disorder. It mainly occurs with systemic disease or as a primary disorder. All organs may be involved by thrombosis, but to date the most common endocrine manifestation is chronic adrenal insufficiency. Very few cases of hypopituitarism with primary APS have been reported. We report the case of a 27-year-old woman, victim of a stroke leading to double vision and intracranial hypertension. Magnetic resonance imaging showed a macro-adenoma with hemorrhage of a suprasellar lesion. Hormone assessment showed hyper prolactinemia with positive anticardiolipin antibody. Our case is the second reported associating APS with apoplexy. We discuss the clinical, biological and radiological features observed in our case. We conclude that APS should be searched for whenever a history of adenoma with apoplexy is found associated with recurrent thrombosis.

Fatigue is frequent and disabling in patients with traumatic brain injury (TBI). Its mechanisms are complex and multifactorial. We performed a literature review of reports of the condition using the following key words: brain injury, depression, neuroendocrine dysfunction, and treatment. Five scales have been used to evaluate fatigue in TBI patients: the Fatigue Severity Scale, the visual analog scale (VAS) for fatigue, the Fatigue Impact Scale, the Barrow Neurological Institute (BNI) Fatigue Scale and the Cause of Fatigue (COF) Questionnaire. The BNI Fatigue Scale and the COF Questionnaire have been designed specifically for brain-injured patients. Fatigue is present in 43-73% of patients and is one of the first symptoms for 7% of them. Fatigue does not seem to be significantly related to injury severity not to time since injury. It can be related to mental effort necessary to overcome attention deficit and slowed processing ("coping hypothesis"). It can also be related to sleeping disorders and depression, although the relation between fatigue and depression are debated. Finally, fatigue can also be related to infraclinical pituitary insufficiency (growth hormone insufficiency, hypocorticism). To date, no published study of treatment of fatigue after TBI exists.

Introduction: Treatment of pituitary macroadenoma frequently leads to nontraumatic cerebrospinal fistula and rhinorrhea. We report an unusual case of rhinorrhea in a woman with Sheehan's syndrome., Case: A 39-year-old woman receiving hormone replacement therapy for hypothyroidism diagnosed 13 years earlier (Sheehan's syndrome) developed metabolic syndrome, which combining obesity, type 2 diabetes, hypertension and mixed hyperlipidemia. Cerebrospinal fluid rhinorrhea was confirmed by measurement of the glucose concentration in her nasal discharge and by cerebral MRI, which revealed a fistula of the ethmoid bone and an empty sella. Etiological screening was negative, and normal bone densitometry as well as the absence of trauma ruled out any bone defects. Conversely, the metabolic syndrome, notably obesity, suggested a nontraumatic mechanism for the empty sella., Discussion: Onset of empty sella syndrome during treatment for Sheehan's syndrome may be the cause of the CSF rhinorrhea. The role of obesity requires further investigation.

Neurological manifestations of anterior pituitary deficiency are well known but their association remains rare. We report a woman who developed, insidiously over ten Years, a complex neurological disorder associating cognitive impairment, psychiatric disorder, cerebellar ataxia, demyelinating neuropathy, and myopathy with pseudomyotonia. After 18 Months of hormone substitution treatment, the patient fully recovered.

A 30-year-old women developed post-partum thyroiditis associated with post- partum pituitary infarction. Pituitary stimulation tests demonstrated global pituitary deficiency but there was no thyrotropin response to TRH stimulation and free T4 was normal. Associated goiter and high circulating levels of microsomal antibodies led to the diagnosis of post-partum thyroiditis associated with pituitary deficiency. Two cases of this unusual association have been reported. The underlying pathogenesis might involve post-partum immunological rebound and/or hypocorticism-induced immunological disorders.

To evaluate the frequency of clinical manifestations and to study the etiological aspects of hypothyroidism in hypothyroid patients in Cotonou, we carried out a retrospective analysis of the medical reports on hypothyroid patients followed in our clinical practice. A total of 33 patients was thus studied, comprising 8 men (24%) and 25 women (76%) with mean age of 45,8 years for men and 40,4 years for women. The more frequent clinical manifestations observed were: face edema (45%), weight gain (45%), paresthesia (42%), fatigue (39%), lethargy (30%) and bradycardia (24%). Constipation (12%), sensation of cold (9%), depilation (6%) and dry skin (6%) were less frequently observed. Myalgia, hoarseness and menstrual irregularities were present in 15% of the cases respectively. Regarding the etiology, 82% of the cases were primary hypothyroidism and only 18% were of central origin. Thyroidectomy was the leading cause in our hypothyroid patients, representing 70% of all cases and 85% of primary hypothyroidism. Radioiodine treatment and autoimmune thyroiditis were equally found in 6% of the cases. Central hypothyroidism was related to a pituitary adenoma in four cases (12%) and to Sheehan syndrome in two cases (6%). As it can be expected, hypercholesterolemia was present in 82% of the patients but creatine phosphokinase elevation was more frequent (94% of the patients). Compared to the data reported in the literature, the frequency of the symptoms and signs of hypothyroidism seems to be underevaluated in our study and the frequency of autoimmune thyroiditis as a cause of hypothyroidism is low.

6 years after surgery for epidermoid lung cancer, a 58-year-old man presented with atopic dermatitis and a high level of IgE, primary hypothyroidism of autoimmune origin, slight hyperprolactinemia and adrenal insufficiency of pituitary origin. ACTH levels were low and unresponsive to CRH. There was no deficiency of the other pituitary hormones and the MRI of the pituitary was normal. The other instances of autoimmune thyroiditis associated with ACTH deficiency are reviewed. The etiology of the deficiency is discussed in the context of a possible hypophysitis.

A 14 year old patient had both Moebius anomalad with arthrogryposis and growth hormone deficiency due to a midline defect. This combination suggests an abnormality in the organization of the neural crest and homologous neural tube segment.

We report two new cases of isolated corticotropin deficiency, associated with TSH deficiency in one of the two patient. The diagnostic was made difficult because the symptoms were mainly psychiatric. Low plasmatic cortisol and ACTH level were found, with low T3, T4 and TSH in the second patient. The TSH did not respond to the stimulation by TRH. The cerebral tomodensitometry and magnetic resonance imaging focused on the sella turcica were normal, eliminated a tumor and showed an empty sella turcica. The patients have to be followed-up because an isolated deficiency may further complete to panhypopituitarism.

There have only been thirty cases of total post-partum hypopituitarism published in the literature and these have nearly all been secondary to Sheehan's syndrome. The authors report a case of partial anterior hypopituitarism associated with diabetes insipidus which arose after an uneventful Caesarean operation and the origin of which seems to lie in auto-immune hypophysitis. The authors first describe the morphological and endocrine changes that the hypophysis undergoes during pregnancy and then point out that auto-immune hypophysitis seems to have been only recently recognised. This can be used to explain some cases of post-partum hypophyseal insufficiency occurring almost silently without any history of third haemorrhage. Research has been made systematically for anti-hypophyseal antibodies and for specific antibodies of the organ, but has not always been positive. So the diagnosis of auto-immune hypophysitis is often made only after eliminating other reasons for it. A brief review of the physiopathological mechanisms of diabetes insipidus makes it possible to suggest that vasopressinase coming from the placenta together with prostaglandins could play a role.

A case of a 39 year old male patient with slipped capital femoral epiphysis and idiopathic panhypopituitarism is reported. A review of the literature shows that a slipped epiphysis with hypothalamo-hypophyseal dysfunction, may be observed either in a proportional pituitary dwarfism or in a skeletal disproportion of the eunuchoidal or even of the acromegalic type. This association leads to examine the causal role of the hormonal status.

Hypopituitarism and diabetes insipidus are often idiopathic conditions. A retrospective study of 6 cases of diabetes insipidus and 8 cases of partial or global idiopathic anterior hypopituitarism has shown that MRI is of considerable value to detect abnormalities of the pituitary stalk or hypothalamo-pituitary "relay". On the basis of MRI findings, some cases of idiopathic hypopituitarism can now be grouped together in a new entity which may be called hypopituitarism due to neonatal transection of the pituitary stalk.

Three cases of septo-optic dysplasia are related in infants. A neurogenic diabetes insipidus and an central adrenocortical insufficiency is proved. An growth hormone deficiency is founded in one case. The other anterior pituitary functions are normal. The pneumo-encephalography with congenital absence of septum lucidum and the ophtalmologic anomalies are typical. The treatment is envisaged. In one case an autopsy sustains the radiologic aspect.

Another case of flexion contracture in a 60 year-old patient with hypopituitarism, chronic alcoholism and starvation is reported. The contracture, as in the other cases, involved the lower limbs, but in this particular patient it extended to the abdominal and extensor neck muscles and neurological signs were associated: cerebellar atrophy and peripheral neuropathy of the lower limbs probably due to alcoholism. As in the other reported cases, severe hyponatremia was observed (105 mmol/l) the physiopathology of which is discussed: starvation and glucocorticoid deficiency alone or associated with aldosterone deficiency. The special feature of the anterior pituitary deficiency is that it is partly functional, at least with regards to the gonadotrophic secretion, perhaps related to the denutrition. The authors emphasize the necessity of searching for adrenal insufficiency in cases of abdomino-crural contracture because of the beneficial effects that result from hydrocortisone replacement therapy.

From February 1983 to December 1985, the authors investigated 19 african women with Sheehan's syndrome in Niamey (Republic of Niger). A 15 points diagnostic score was systematically used. Two signs were indispensable for the diagnosis: post-partum agalactia (or severe hypogalactia) and amenorrhea. At least 9 points score was found for every case. Eighteen patients lived along a major road in Niamey and in Dosso departments. The prevalence of this disease is probably important but many cases were not diagnosed since there was no medical examination. Sheehan's syndrome was predominantly diagnosed among Fulani women. Young women (mean age: 26 years) in intensive sexual life, primiparous (8/9) or multiparous (11/19) were concerned. Emergence circumstances of signs were: childbirth at home (18/19), severe vaginal bleeding at placental birth (14/19), rare transfusions (2/19). The infant of a mother with Sheehan's syndrome had a poor prognosis: 9 deaths among 11 deliveries for multiparous, 7/8 for monoparous. The infants were stillborn or more often dead during the first months. Deaths were in relation to absence of maternal lactation. For the primiparous, then infertile women because of hypopituitarism, the repudiation becomes often the only social way of life. Lasting hormonotherapy was not available because 18/19 patients were very poor. Prevention is not possible before long, especially in primiparous, because of: the mentality: the first delivery at home with the mother is the traditional habit; the importance of the required measures.

The diagnosis of anterior pituitary insufficiency is difficult in the elderly and frequently made when the patient become comatose. At this age hypoglycemia is rarely the exclusive factor of this coma. The authors report a case revealed by hypoglycemic coma and supported by the lack of stimulation by the releasing factors. None etiology was found. With hormone treatment the patient recovered a normal life.

The 20 women investigated were 22 to 59 years old (average 35.9 +/- 2.3 years) when the diagnosis of Sheehan's syndrome was confirmed. Fourteen had had previous pregnancies, 6 were primiparas; average parity was 4. The patients were delivered in hospital, in France, in 14 cases, and abroad (Algeria, Portugal) at home in 6 cases. A history of severe haemorrhage during delivery was recorded in all but 2 cases. This was serious enough to warrant hysterectomy in 2 cases. Agalactia and amenorrhea were observed in all but 1 case in the immediate post-partum period. Transient polyuria and polydipsia occurred in 3 patients. In the months following birth, most women lead restricted lives; they were apathetic, asthenic and indifferent. The diagnosis was established under three different circumstances: in the majority (15/20) on clinical grounds, in 3 cases after acute adrenal failure, in 2 cases, fortuitously. Clinical examination showed signs of global anterior hypophyseal insufficiency involving thyroid, adrenal and gonad stimulating hormones in 14 cases; in 6 cases, the pituitary failure was dissociated. Corticotrophin, somatotropin and prolactin deficiencies were observed in all patients; gonadotrophin (17/20) and thyrotrophin (16/20) deficiencies were common. The diagnosis was confirmed less than 1 month (2 cases) to over 12 years (7 cases) after obstetric haemorrhage (average 6.9 +/- 1.9 years). No correlation was observed between the severity of the syndrome and this time interval. The short term outcome was favourable with return of menstruation and even pregnancy in one patient.(ABSTRACT TRUNCATED AT 250 WORDS)

There are many methods that can be used to induce ovulation when there is a fault in ovulation in patients who have normal prolactin levels. These are: Bringing the weight to a normal level. Giving Clomiphene. Giving Tamoxifen. Giving cyclofenil and bromocriptine, which really have no more effect than giving a placebo. Giving gonadotrophins in a classical way. This is very useful where there is hypogonadic amenorrhoea but much less useful when the failure of ovulation occurs with normal gonadic function. It is accompanied by a risk of multiple pregnancies and of hyperstimulation, which should be monitored by ultrasound very strictly so that it cannot become too serious. The use of purified FSH which theoretically should be more adequate, at least in cases where the gonadic function is normal in spite of failure of ovulation. Pulsatile administration of LHRH, which in cases of hypothalamic amenorrhoea carries less total risk than giving gonadotrophins. Finally, wedge resection of the ovaries which is reversed for polycystic ovaries that are larger than normal in size, and allied methods. The first choice for hypogonadic hypothalamic amenorrhoea would seem to be the LHRH pump; and for failure of ovulation with normal gonadic function Clomiphene or Tamoxifen. When anti-oestrogens fail to correct these latter cases one can choose according to the case between gonadotrophins, choosing if possible pure FSH, and/or wedge resection. In the last resort in these cases the LHRH pump can be used. The frequent failure of these methods show that perhaps it is possible to create a hypogonadotrophic hypogonadism by giving agonists for a long time or antagonists to LHRH in such a way that a second attempt can be made to induce ovulation using gonadotrophins in better conditions of efficacy and safety.

Thirty five patients with hypopituitarism have been studied. Nine had a mild hyponatremia (126-137 mEq/l) and five a profound hyponatremia (105-124 mEq/l). None of them had hemodilution (plasma protein, potassium were normal). Hyponatremia was present even in the absence of deficit in GH and/or TSH, and/or FSH-LH. All the pateints had a complete ACTH deficiency. There was a negative correlation between age and natremia (r = -0,39; p0.02). 2/5 patients with severe hyponatremia had mental confusion. These two patients had a complete TSH deficiency. Natremia increased with cortisone therapy in all cases but reached the normal range only in one case. Mental confusion disappeared and natremia became normal in all patients with therapy with cortisone and thyroid hormones.