Clinical Overview > Condition/ Syndrome > Hyponatraemia
You are looking at 1 - 10 of 23 items
Search for other papers by Tzy Harn Chua in
Google Scholar
PubMed
Search for other papers by Wann Jia Loh in
Google Scholar
PubMed
Summary
Severe hyponatremia and osmotic demyelination syndrome (ODS) are opposite ends of a spectrum of emergency disorders related to sodium concentrations. Management of severe hyponatremia is challenging because of the difficulty in balancing the risk of overcorrection leading to ODS as well as under-correction causing cerebral oedema, particularly in a patient with chronic hypocortisolism and hypothyroidism. We report a case of a patient with Noonan syndrome and untreated anterior hypopituitarism who presented with symptomatic hyponatremia and developed transient ODS.
Learning points:
-
Patients with severe anterior hypopituitarism with severe hyponatremia are susceptible to the rapid rise of sodium level with a small amount of fluid and hydrocortisone.
-
These patients with chronic anterior hypopituitarism are at high risk of developing ODS and therefore, care should be taken to avoid a rise of more than 4–6 mmol/L per day.
-
Early recognition and rescue desmopressin and i.v. dextrose 5% fluids to reduce serum sodium concentration may be helpful in treating acute ODS.
Search for other papers by Raku Son in
Google Scholar
PubMed
Search for other papers by Masahiko Nagahama in
Google Scholar
PubMed
Search for other papers by Fumiaki Tanemoto in
Google Scholar
PubMed
Search for other papers by Yugo Ito in
Google Scholar
PubMed
Search for other papers by Fumika Taki in
Google Scholar
PubMed
Search for other papers by Ryosuke Tsugitomi in
Google Scholar
PubMed
Search for other papers by Masaaki Nakayama in
Google Scholar
PubMed
Summary
The etiology of hyponatremia is assessed based on urine osmolality and sodium. We herein describe a 35-year-old Asian man with pulmonary tuberculosis and perforated duodenal ulcer who presented with hyponatremia with hourly fluctuating urine osmolality ranging from 100 to 600 mosmol/kg, which resembled urine osmolality observed in typical polydipsia and SIADH simultaneously. Further review revealed correlation of body temperature and urine osmolality. Since fever is a known non-osmotic stimulus of ADH secretion, we theorized that hyponatremia in this patient was due to transient ADH secretion due to fever. In our case, empiric exogenous glucocorticoid suppressed transient non-osmotic ADH secretion and urine osmolality showed highly variable concentrations. Transient ADH secretion-related hyponatremia may be underrecognized due to occasional empiric glucocorticoid administration in patients with critical illnesses. Repeatedly monitoring of urine chemistries and interpretation of urine chemistries with careful review of non-osmotic stimuli of ADH including fever is crucial in recognition of this etiology.
Learning points:
-
Hourly fluctuations in urine osmolality can be observed in patients with fever, which is a non-osmotic stimulant of ADH secretion.
-
Repeated monitoring of urine chemistries aids in the diagnosis of the etiology underlying hyponatremia, including fever, in patients with transient ADH secretion.
-
Glucocorticoid administration suppresses ADH secretion and improves hyponatremia even in the absence of adrenal insufficiency; the etiology of hyponatremia should be determined carefully in these patients.
Search for other papers by Anna Popławska-Kita in
Google Scholar
PubMed
Search for other papers by Marta Wielogórska in
Google Scholar
PubMed
Search for other papers by Łukasz Poplawski in
Google Scholar
PubMed
Search for other papers by Katarzyna Siewko in
Google Scholar
PubMed
Search for other papers by Agnieszka Adamska in
Google Scholar
PubMed
Search for other papers by Piotr Szumowski in
Google Scholar
PubMed
Search for other papers by Piotr Myśliwiec in
Google Scholar
PubMed
Search for other papers by Janusz Myśliwiec in
Google Scholar
PubMed
Search for other papers by Joanna Reszeć in
Google Scholar
PubMed
Search for other papers by Grzegorz Kamiński in
Google Scholar
PubMed
Search for other papers by Janusz Dzięcioł in
Google Scholar
PubMed
Search for other papers by Dorota Tobiaszewska in
Google Scholar
PubMed
Search for other papers by Małgorzata Szelachowska in
Google Scholar
PubMed
Search for other papers by Adam Jacek Krętowski in
Google Scholar
PubMed
Summary
Papillary thyroid gland carcinoma is the most common type of malignancy of the endocrine system. Metastases to the pituitary gland have been described as a complication of papillary thyroid cancer in few reported cases since 1965. We report the case of a 68-year-old female patient with a well-differentiated form of thyroid gland cancer. Despite it being the most common malignant cancer of the endocrine system, with its papillary form being one of the two most frequently diagnosed thyroid cancers, the case we present is extremely rare. Sudden cardiac arrest during ventricular fibrillation occurred during hospitalization. Autopsy of the patient revealed papillary carcinoma of the thyroid, follicular variant, with metastasis to the sella turcica, and concomitant sarcoidosis of heart, lung, and mediastinal and hilar lymph nodes. Not only does atypical metastasis make our patient’s case most remarkable, but also the postmortem diagnosis of sarcoidosis makes her case particularly unusual.
Learning points:
-
The goal of presenting this case is to raise awareness of the clinical heterogeneity of papillary cancer and promote early diagnosis of unexpected metastasis and coexisting diseases to improve clinical outcomes.
-
Clinicians must be skeptical. They should not fall into the trap of diagnostic momentum or accept diagnostic labels at face value. Regardless of the potential mechanisms, clinicians should be aware of the possibility of the coexistence of thyroid cancer and sarcoidosis as a differential diagnosis of lymphadenopathy.
-
This case highlights the importance of the diagnostic and therapeutic planning process and raises awareness of the fact that one uncommon disease could be masked by another extremely rare disorder.
Search for other papers by Isabella Lupi in
Google Scholar
PubMed
Search for other papers by Alessandro Brancatella in
Google Scholar
PubMed
Search for other papers by Mirco Cosottini in
Google Scholar
PubMed
Search for other papers by Nicola Viola in
Google Scholar
PubMed
Search for other papers by Giulia Lanzolla in
Google Scholar
PubMed
Search for other papers by Daniele Sgrò in
Google Scholar
PubMed
Search for other papers by Giulia Di Dalmazi in
Google Scholar
PubMed
Search for other papers by Francesco Latrofa in
Google Scholar
PubMed
Search for other papers by Patrizio Caturegli in
Google Scholar
PubMed
Search for other papers by Claudio Marcocci in
Google Scholar
PubMed
Summary
Programmed cell death protein 1/programmed cell death protein ligand 1 (PD-1/PD-L1) and cytotoxic T-lymphocyte antigen 4/B7 (CTLA-4/B7) pathways are key regulators in T-cell activation and tolerance. Nivolumab, pembrolizumab (PD-1 inhibitors), atezolizumab (PD-L1 inhibitor) and ipilimumab (CTLA-4 inhibitor) are monoclonal antibodies approved for treatment of several advanced cancers. Immune checkpoint inhibitors (ICIs)-related hypophysitis is described more frequently in patients treated with anti-CTLA-4; however, recent studies reported an increasing prevalence of anti-PD-1/PD-L1-induced hypophysitis which also exhibits slightly different clinical features. We report our experience on hypophysitis induced by anti-PD-1/anti-PD-L1 treatment. We present four cases, diagnosed in the past 12 months, of hypophysitis occurring in two patients receiving anti-PD-1, in one patient receiving anti-PD-1 and anti-CTLA-4 combined therapy and in one patient receiving anti-PD-L1. In this case series, timing, clinical presentation and association with other immune-related adverse events appeared to be extremely variable; central hypoadrenalism and hyponatremia were constantly detected although sellar magnetic resonance imaging did not reveal specific signs of pituitary inflammation. These differences highlight the complexity of ICI-related hypophysitis and the existence of different mechanisms of action leading to heterogeneity of clinical presentation in patients receiving immunotherapy.
Learning points:
-
PD-1/PD-L1 blockade can induce hypophysitis with a different clinical presentation when compared to CTLA-4 blockade.
-
Diagnosis of PD-1/PD-L1 induced hypophysitis is mainly made on clinical grounds and sellar MRI does not show radiological abnormalities.
-
Hyponatremia due to acute secondary adrenal insufficiency is often the principal sign of PD-1/PD-L1-induced hypophysitis and can be masked by other symptoms due to oncologic disease.
-
PD-1/PD-L1-induced hypophysitis can present as an isolated manifestation of irAEs or be in association with other autoimmune diseases
Search for other papers by E Sanz-Sapera in
Google Scholar
PubMed
Search for other papers by S Sarria-Estrada in
Google Scholar
PubMed
Search for other papers by F Arikan in
Google Scholar
PubMed
Search for other papers by B Biagetti in
Google Scholar
PubMed
Summary
Pituitary apoplexy is a rare but potentially life-threatening clinical syndrome characterised by ischaemic infarction or haemorrhage into a pituitary tumour that can lead to spontaneous remission of hormonal hypersecretion. We report the case of a 50-year-old man who attended the emergency department for sudden onset of headache. A computed tomography (CT) scan at admission revealed pituitary haemorrhage and the blood test confirmed the clinical suspicion of acromegaly and an associated hypopituitarism. The T1-weighted magnetic resonance imaging (MRI) showed the classic pituitary ring sign on the right side of the pituitary. Following admission, he developed acute-onset hyponatraemia that required hypertonic saline administration, improving progressively. Surprisingly, during the follow-up, IGF1 levels became normal and he progressively recovered pituitary function.
Learning points:
-
Patients with pituitary apoplexy may have spontaneous remission of hormonal hypersecretion. If it is not an emergency, we should delay a decision to undertake surgery following apoplexy and re-evaluate hormone secretion.
-
Hyponatraemia is an acute sign of hypocortisolism in pituitary apoplexy. However, SIADH although uncommon, could appear later as a consequence of direct hypothalamic insult and requires active and individualised treatment. For this reason, closely monitoring sodium at the beginning of the episode and throughout the first week is advisable to guard against SIADH.
-
Despite being less frequent, if pituitary apoplexy is limited to the tumour, the patient can recover pituitary function previously damaged by the undiagnosed macroadenoma.
Search for other papers by Jose León Mengíbar in
Google Scholar
PubMed
Search for other papers by Ismael Capel in
Google Scholar
PubMed
Search for other papers by Teresa Bonfill in
Google Scholar
PubMed
Search for other papers by Isabel Mazarico in
Google Scholar
PubMed
Search for other papers by Laia Casamitjana Espuña in
Google Scholar
PubMed
Search for other papers by Assumpta Caixàs in
Google Scholar
PubMed
Search for other papers by Mercedes Rigla in
Google Scholar
PubMed
Summary
Durvalumab, a human immunoglobulin G1 kappa monoclonal antibody that blocks the interaction of programmed cell death ligand 1 (PD-L1) with the PD-1 and CD80 (B7.1) molecules, is increasingly used in advanced neoplasias. Durvalumab use is associated with increased immune-related adverse events. We report a case of a 55-year-old man who presented to our emergency room with hyperglycaemia after receiving durvalumab for urothelial high-grade non-muscle-invasive bladder cancer. On presentation, he had polyuria, polyphagia, nausea and vomiting, and laboratory test revealed diabetic ketoacidosis (DKA). Other than durvalumab, no precipitating factors were identified. Pre-durvalumab blood glucose was normal. The patient responded to treatment with intravenous fluids, insulin and electrolyte replacement. Simultaneously, he presented a thyroid hormone pattern that evolved in 10 weeks from subclinical hyperthyroidism (initially attributed to iodinated contrast used in a previous computerised tomography) to overt hyperthyroidism and then to severe primary hypothyroidism (TSH: 34.40 µU/mL, free thyroxine (FT4): <0.23 ng/dL and free tri-iodothyronine (FT3): 0.57 pg/mL). Replacement therapy with levothyroxine was initiated. Finally, he was tested positive for anti-glutamic acid decarboxylase (GAD65), anti-thyroglobulin (Tg) and antithyroid peroxidase (TPO) antibodies (Abs) and diagnosed with type 1 diabetes mellitus (DM) and silent thyroiditis caused by durvalumab. When durvalumab was stopped, he maintained the treatment of multiple daily insulin doses and levothyroxine. Clinicians need to be alerted about the development of endocrinopathies, such as DM, DKA and primary hypothyroidism in the patients receiving durvalumab.
Learning points:
-
Patients treated with anti-PD-L1 should be screened for the most common immune-related adverse events (irAEs).
-
Glucose levels and thyroid function should be monitored before and during the treatment.
-
Durvalumab is mainly associated with thyroid and endocrine pancreas dysfunction.
-
In the patients with significant autoimmune background, risk–benefit balance of antineoplastic immunotherapy should be accurately assessed.
Search for other papers by Ilan Rahmani Tzvi-Ran in
Google Scholar
PubMed
Search for other papers by Judith Olchowski in
Google Scholar
PubMed
Search for other papers by Merav Fraenkel in
Google Scholar
PubMed
Search for other papers by Asher Bashiri in
Google Scholar
PubMed
Search for other papers by Leonid Barski in
Google Scholar
PubMed
Summary
A previously healthy 24-year-old female underwent an emergent caesarean section without a major bleeding described. During the first post-operative days (POD) she complained of fatigue, headache and a failure to lactate with no specific and conclusive findings on head CT. On the following days, fever rose with a suspicion of an obstetric surgery-related infection, again with no evidence to support the diagnosis. On POD5 a new-onset hyponatremia was documented. The urine analysis suggested SIADH, and following a treatment failure, further investigation was performed and demonstrated both central hypothyroidism and adrenal insufficiency. The patient was immediately treated with hydrocortisone followed by levothyroxine with a rapid resolution of symptoms and hyponatremia. Further laboratory investigation demonstrated anterior hypopituitarism. The main differential diagnosis was Sheehan’s syndrome vs lymphocytic hypophysitis. Brain MRI was performed as soon as it was available and findings consistent with Sheehan’s syndrome confirmed the diagnosis. Lifelong hormonal replacement therapy was initiated. Further complaints on polyuria and polydipsia have led to a water deprivation testing and the diagnosis of partial central insipidus and appropriate treatment with DDAVP.
Learning points:
-
Sheehan’s syndrome can occur, though rarely, without an obvious major post-partum hemorrhage.
-
The syndrome may resemble lymphocytic hypophysitis clinically and imaging studies may be crucial in order to differentiate both conditions.
-
Hypopituitarism presentation may be variable and depends on the specific hormone deficit.
-
Euvolemic hyponatremia workup must include thyroid function test and 08:00 AM cortisol levels.
Search for other papers by Danielle R Bullock in
Google Scholar
PubMed
Search for other papers by Bradley S Miller in
Google Scholar
PubMed
Search for other papers by H Brent Clark in
Google Scholar
PubMed
Search for other papers by Patricia M Hobday in
Google Scholar
PubMed
Summary
IgG4-related hypophysitis is an important diagnostic consideration in patients with a pituitary mass or pituitary dysfunction and can initially present with headaches, visual field deficits and/or endocrine dysfunction. Isolated IgG4-related pituitary disease is rare, with most cases of IgG4-related disease involving additional organ systems. We report the case of a teenage female patient with isolated IgG4-related hypophysitis, diagnosed after initially presenting with headaches. Our patient had no presenting endocrinologic abnormalities. She was treated with surgical resection, prednisolone and rituximab with no further progression of disease and sustained normal endocrine function. This case, the youngest described patient with isolated IgG4-related hypophysitis and uniquely lacking endocrinologic abnormalities, adds to the limited reports of isolated pituitary disease. The use of rituximab for isolated pituitary disease has never been described. While IgG4-related hypophysitis has been increasingly recognized, substantial evidence concerning the appropriate treatment and follow-up of these patients is largely lacking.
Learning points:
-
IgG4-related hypophysitis most often occurs in the setting of additional organ involvement but can be an isolated finding. This diagnosis should therefore be considered in a patient presenting with pituitary abnormalities.
-
Most patients with IgG4-related hypophysitis will have abnormal pituitary function, but normal functioning does not exclude this diagnosis.
-
Corticosteroids have been the mainstay of therapy for IgG4-related disease, with other immunosuppressive regimens being reserved for refractory cases. Further research is needed to understand the effectiveness of corticosteroid-sparing regimens and whether there is utility in using these agents as first-line therapies.
Search for other papers by Benedetta Zampetti in
Google Scholar
PubMed
Search for other papers by Roberto Attanasio in
Google Scholar
PubMed
Search for other papers by Renato Cozzi in
Google Scholar
PubMed
Summary
A 69-year-old male was admitted for severe hyponatremia disclosed after an accidental fall. He was anticoagulated from 2 months after the implantation of a biologic aortic valve prosthesis. The work-up disclosed adrenal failure and MRI showed bilateral adrenal hemorrhage. Clinical picture and lab parameters normalized quickly after the appropriate replacement treatment. Anticoagulation excess should be added to the list of drugs potentially causing hyponatremia.
Learning points:
-
Hyponatremia requires a complete and timely workup in order to start an appropriate treatment for the improvement of clinical conditions.
-
History is crucial: a detailed list of drugs potentially causing hyponatremia should be collected. Anticoagulants should be added to the list, mostly in the event of excessive anticoagulation.
-
Intra-adrenal hemorrhage is a rare cause of hyponatremia and adrenal failure.
-
The ACTH test is still the gold standard for the diagnosis of hypoadrenalism.
Search for other papers by Shunsuke Funazaki in
Google Scholar
PubMed
Search for other papers by Hodaka Yamada in
Google Scholar
PubMed
Search for other papers by Kazuo Hara in
Google Scholar
PubMed
Division of Endocrinology and Metabolism Division of Endocrinology and Metabolism, International University of Health and Welfare Hospital, Tochigi, Japan
Search for other papers by San-e Ishikawa in
Google Scholar
PubMed
Summary
Lymphocytic hypophysitis (LyH) has been known to be associated with pregnancy. We herein report the case of a 33-year-old woman who underwent vaginal delivery without massive bleeding at 40 weeks of gestation. Because of the presence of headache and terrible fatigue after childbirth, she visited our hospital. Severe hyponatremia (Na, 118 mEq/L) and visual field abnormality was noted upon examination. MRI revealed pituitary enlargement with a swollen pituitary stalk, albeit at low signal intensity. Basal pituitary hormone levels were all reduced and remained low after exogenous administration of hypothalamic-releasing hormones. She was diagnosed with LyH and was started on prednisolone 60 mg/day. A month later, her pituitary function had gradually improved together with a decrease in pituitary enlargement and recovery of her visual field. The dose of prednisolone was gradually reduced and finally withdrawn 27 months later. After prednisolone withdrawal, her pituitary function remained normal despite the absence of any hormonal replacement. A year later, she became pregnant without medication and delivered a second baby without LyH recurrence. Thereafter, her pituitary function has been normal for more than 5 years. Two valuable observations can be highlighted from the case. First, the patient completely recovered from LyH through prompt prednisolone therapy during its initial phase and had almost normal pituitary function. Second, after recovery from LyH, she was able to undergo spontaneous pregnancy and deliver a baby. We believe that reporting incidences of spontaneous pregnancy after complete normalization of pituitary function in patients with LyH is of great significance.
Learning points:
-
Females are more affected by LyH than males given its strong association with pregnancy.
-
LyH possesses characteristic findings on pituitary MRI.
-
Glucocorticoid therapy for LyH has been recommended as an effective treatment.
-
A history of previous pregnancies does not increase the risk of developing AH in subsequent pregnancies.
-
Early induction of high-dose prednisolone was therapeutically effective in treating LyH.
