Diagnosis and Treatment > Signs and Symptoms > Constipation

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Marlene Tarvainen School of Medicine, University of Tampere, Tampere, Finland

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Satu Mäkelä School of Medicine, University of Tampere, Tampere, Finland
Department of Internal Medicine, Tampere University Hospital, Tampere, Finland

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Jukka Mustonen School of Medicine, University of Tampere, Tampere, Finland
Department of Internal Medicine, Tampere University Hospital, Tampere, Finland

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Pia Jaatinen School of Medicine, University of Tampere, Tampere, Finland
Department of Internal Medicine, Tampere University Hospital, Tampere, Finland
Division of Internal Medicine, Seinäjoki Central Hospital, Seinäjoki, Finland

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Summary

Puumala hantavirus (PUUV) infection causes nephropathia epidemica (NE), a relatively mild form of haemorrhagic fever with renal syndrome (HFRS). Hypophyseal haemorrhage and hypopituitarism have been described in case reports on patients with acute NE. Chronic hypopituitarism diagnosed months or years after the acute illness has also been reported, without any signs of a haemorrhagic aetiology. The mechanisms leading to the late-onset hormonal defects remain unknown. Here, we present a case of NE-associated autoimmune polyendocrinopathy and hypopituitarism presumably due to autoimmune hypophysitis. Thyroid peroxidase antibody seroconversion occurred between 6 and 12 months, and ovarian as well as glutamate decarboxylase antibodies were found 18 months after acute NE. Brain MRI revealed an atrophic adenohypophysis with a heterogeneous, low signal intensity compatible with a sequela of hypophysitis. The patient developed central (or mixed central and peripheral) hypothyroidism, hypogonadism and diabetes insipidus, all requiring hormonal replacement therapy. This case report suggests that late-onset hormonal defects after PUUV infection may develop by an autoimmune mechanism. This hypothesis needs to be confirmed by prospective studies with sufficient numbers of patients.

Learning points:

  • Pituitary haemorrhage resulting in hypopituitarism has been reported during acute HFRS caused by PUUV and other hantaviruses.

  • Central and peripheral hormone deficiencies developing months or years after HFRS have also been found, with an incidence higher than that in the general population. The pathogenesis of these late-onset hormonal defects remains unknown.

  • This case report suggests that the late-onset hypopituitarism and peripheral endocrine defects after HFRS could evolve via autoimmune mechanisms.

  • The sensitivity of current anti-pituitary antibody (APA) tests is low. A characteristic clinical course, together with typical brain MRI and endocrine findings may be sufficient for a non-invasive diagnosis of autoimmune hypophysitis, despite negative APAs.

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Benjamin G Challis Wellcome Trust–MRC Institute of Metabolic Science, University of Cambridge, Cambridge, CB2 0QQ, UK
Wolfson Diabetes and Endocrinology Clinic, Institute of Metabolic Science, Cambridge University Hospitals NHS Foundation Trust, Addenbrookes Hospital, Box 281, Cambridge, CB2 0QQ, UK

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Nicolai J Wewer Albrechtsen Department of Biomedical Sciences, Faculty of Health and Medical Sciences, University of Copenhagen, Blegdamsvej 3B, Copenhagen, DK-2200, Denmark
Faculty of Health and Medical Sciences, Novo Nordisk Foundation Center for Basic Metabolic Research, University of Copenhagen, Blegdamsvej 3B, Copenhagen, DK-2200, Denmark

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Vishakha Bansiya Wolfson Diabetes and Endocrinology Clinic, Institute of Metabolic Science, Cambridge University Hospitals NHS Foundation Trust, Addenbrookes Hospital, Box 281, Cambridge, CB2 0QQ, UK

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Keith Burling Wellcome Trust–MRC Institute of Metabolic Science, University of Cambridge, Cambridge, CB2 0QQ, UK

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Peter Barker Wellcome Trust–MRC Institute of Metabolic Science, University of Cambridge, Cambridge, CB2 0QQ, UK

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Bolette Hartmann Department of Biomedical Sciences, Faculty of Health and Medical Sciences, University of Copenhagen, Blegdamsvej 3B, Copenhagen, DK-2200, Denmark
Faculty of Health and Medical Sciences, Novo Nordisk Foundation Center for Basic Metabolic Research, University of Copenhagen, Blegdamsvej 3B, Copenhagen, DK-2200, Denmark

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Fiona Gribble Wellcome Trust–MRC Institute of Metabolic Science, University of Cambridge, Cambridge, CB2 0QQ, UK

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Stephen O'Rahilly Wellcome Trust–MRC Institute of Metabolic Science, University of Cambridge, Cambridge, CB2 0QQ, UK
Wolfson Diabetes and Endocrinology Clinic, Institute of Metabolic Science, Cambridge University Hospitals NHS Foundation Trust, Addenbrookes Hospital, Box 281, Cambridge, CB2 0QQ, UK

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Jens J Holst Department of Biomedical Sciences, Faculty of Health and Medical Sciences, University of Copenhagen, Blegdamsvej 3B, Copenhagen, DK-2200, Denmark
Faculty of Health and Medical Sciences, Novo Nordisk Foundation Center for Basic Metabolic Research, University of Copenhagen, Blegdamsvej 3B, Copenhagen, DK-2200, Denmark

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Helen L Simpson Wolfson Diabetes and Endocrinology Clinic, Institute of Metabolic Science, Cambridge University Hospitals NHS Foundation Trust, Addenbrookes Hospital, Box 281, Cambridge, CB2 0QQ, UK

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Summary

Pancreatic neuroendocrine tumours (pNETs) secreting proglucagon are associated with phenotypic heterogeneity. Here, we describe two patients with pNETs and varied clinical phenotypes due to differential processing and secretion of proglucagon-derived peptides (PGDPs). Case 1, a 57-year-old woman presented with necrolytic migratory erythema, anorexia, constipation and hyperinsulinaemic hypoglycaemia. She was found to have a grade 1 pNET, small bowel mucosal thickening and hyperglucagonaemia. Somatostatin analogue (SSA) therapy improved appetite, abolished hypoglycaemia and improved the rash. Case 2, a 48-year-old male presented with diabetes mellitus, diarrhoea, weight loss, nausea, vomiting and perineal rash due to a grade 1 metastatic pNET and hyperglucagonaemia. In both cases, plasma levels of all measured PGDPs were elevated and attenuated following SSA therapy. In case 1, there was increased production of intact glucagon-like peptide 1 (GLP-1) and GLP-2, similar to that of the enteroendocrine L cell. In case 2, pancreatic glucagon was elevated due to a pancreatic α-cell-like proglucagon processing profile. In summary, we describe two patients with pNETs and heterogeneous clinical phenotypes due to differential processing and secretion of PGDPs. This is the first description of a patient with symptomatic hyperinsulinaemic hypoglycaemia and marked gastrointestinal dysfunction due to, in part, a proglucagon-expressing pNET.

Learning points

  • PGDPs exhibit a diverse range of biological activities including critical roles in glucose and amino acid metabolism, energy homeostasis and gastrointestinal physiology.

  • The clinical manifestations of proglucagon-expressing tumours may exhibit marked phenotypic variation due to the biochemical heterogeneity of their secreted peptide repertoire.

  • Specific and precise biochemical assessment of individuals with proglucagon-expressing tumours may provide opportunities for improved diagnosis and clinical management.

Open access
Reiner Jumpertz von Schwartzenberg Department of Endocrinology and Metabolic Diseases, Charité – Universitätsmedizin, Charitéplatz 1, Berlin, 10117, Germany

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Ulf Elbelt Department of Endocrinology and Metabolic Diseases, Charité – Universitätsmedizin, Charitéplatz 1, Berlin, 10117, Germany

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Manfred Ventz Department of Endocrinology and Metabolic Diseases, Charité – Universitätsmedizin, Charitéplatz 1, Berlin, 10117, Germany

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Knut Mai Department of Endocrinology and Metabolic Diseases, Charité – Universitätsmedizin, Charitéplatz 1, Berlin, 10117, Germany

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Tina Kienitz Department of Endocrinology and Metabolic Diseases, Charité – Universitätsmedizin, Charitéplatz 1, Berlin, 10117, Germany

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Lukas Maurer Department of Endocrinology and Metabolic Diseases, Charité – Universitätsmedizin, Charitéplatz 1, Berlin, 10117, Germany

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Thomas Rose Division of Rheumatology and Clinical Immunology, Medical Department, Charité – Universitätsmedizin, Charitéplatz 1, Berlin, 10117, Germany

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Jens C Rückert Department of General Visceral Vascular and Thoracic Surgery, Charité – Universitätsmedizin, Charitéplatz 1, Berlin, 10117, Germany

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Christian J Strasburger Department of Endocrinology and Metabolic Diseases, Charité – Universitätsmedizin, Charitéplatz 1, Berlin, 10117, Germany

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Joachim Spranger Department of Endocrinology and Metabolic Diseases, Charité – Universitätsmedizin, Charitéplatz 1, Berlin, 10117, Germany

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Parathyroid carcinoma is a rare disease leading to severe hypercalcemia due to hyperparathyroidism. Surgery is the primary treatment option. A more progressive form of the disease is characterized by parathyrotoxicosis, and subsequent hypercalcemia is the most common cause of death. We report a case presenting with severe hypercalcemia due to parathyrotoxicosis from parathyroid carcinoma treated for the first time using the monoclonal antibody denosumab as a rescue therapy and present long-term follow-up data. The 71-year-old patient presented with severe hypercalcemia due to metastatic parathyroid carcinoma. Despite undergoing treatment with bisphosphonates, cinacalcet hydrochloride, and forced diuresis, the patient`s condition deteriorated rapidly due to resistant hypercalcemia. Surgery performed because of spinal metastasis and forced diuresis lowered calcium levels, albeit they remained in the hypercalcemic range and significantly increased when forced diuresis was stopped. Considering a palliative situation to overcome hypercalcemia, we decided to administer denosumab, a monoclonal antibody that binds to the receptor activator of nuclear factor-kappa B ligand. After a single subcutaneous administration of 60 mg denosumab, calcium levels normalized within one day. Subsequent denosumab injections led to permanent control of serum calcium for more than 2 years despite rising parathyroid hormone levels and repeated surgeries. Together with recent cases in the literature supporting our observation, we believe that denosumab is relevant for future trials and represents an effective tool to control hypercalcemia in patients with advanced stages of parathyroid cancer.

Learning points

  • Severe hypercalcemia is the most common cause of death in patients with parathyroid carcinoma.

  • The monoclonal antibody denosumab rapidly lowered severely elevated serum calcium levels due to parathyrotoxicosis.

  • Denosumab was effective in the long-term treatment of hypercalcemia despite progression of parathyroid carcinoma.

Open access
Mohammed Al-Sofiani
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Dhimitri Nikolla Lake Erie College of Osteopathic Medicine, Erie, Pennsylvania, USA

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V V S Ramesh Metta
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Summary

We report the case of a 42-year-old female with a history of hypothyroidism and asthma presenting with progressive dyspnea and orthopnea after 2 days of an upper respiratory tract infection (URTI). Based on the clinical and radiological findings, the patient was admitted as a case of cardiogenic pulmonary edema secondary to possible viral myocarditis. However, a normal brain natriuretic peptide (BNP) level with a normal ejection fraction (EF) on echocardiogram changed our working diagnosis from cardiogenic to non-cardiogenic pulmonary edema. Further questioning revealed a history of nocturnal snoring, frequent awakening, and daytime fatigue, suggesting a possible sleep apnea syndrome (SAS). In conclusion, we believe that SAS was the missing link between our patient's hypothyroidism and non-cardiogenic pulmonary edema.

Learning points

  • Always keep an open mind and look for a pathology that would explain the whole clinical scenario.

  • The involvement of the respiratory system in hypothyroidism can range from SAS, pulmonary hypertension, hypoventilation, and severe respiratory failure.

  • Hypothyroidism and SAS should be considered in the differential diagnosis of non-cardiogenic pulmonary edema.

  • Patients should be instructed to take levothyroxine on an empty stomach 30–60 min before food to avoid erratic absorption of the hormone.

Open access
Beverly T Rodrigues Department of Diabetes and Endocrinology, The Townsville Hospital, Townsville, Queensland, Australia
School of Medicine and Dentistry, James Cook University, Douglas, Queensland, Australia

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Zulfiquer Otty Department of Oncology, The Townsville Hospital, Townsville, Queensland, Australia

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Kunwarjit Sangla Department of Diabetes and Endocrinology, The Townsville Hospital, Townsville, Queensland, Australia

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Vasant V Shenoy Department of Diabetes and Endocrinology, The Townsville Hospital, Townsville, Queensland, Australia
School of Medicine and Dentistry, James Cook University, Douglas, Queensland, Australia

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Summary

Autoimmune hypophysitis (AH) has been previously described in a typical demographic population, primarily women in the reproductive age group and perinatal period. The era of immune modulation using anti-cytotoxic T-lymphocyte-associated antigen 4 biological therapy (ipilimumab) against advanced cancers like metastatic melanomas has now resulted in a new form of hypophysitis being increasingly recognised under a spectrum of immune-related adverse events. Drug-related AH often presents with subtle symptoms and a pituitary mass, with the potential for fatality necessitating wide awareness and a high index of clinical suspicion given that it is usually treatable. We describe below two cases of AH within the last three months at our centre, which were treated with different regimens and produced good endocrine outcomes.

Learning points

  • AH is a new and defined clinical entity occurring as a side effect of ipilimumab, which enhances immune-mediated destruction of metastatic melanoma.

  • It can present insidiously and have life-threatening complications related to hypocortisolism, hence a high index of clinical suspicion must be exerted by treating physicians, and seems to result in resolution of pituitary masses and variable improvements of pituitary function.

  • Clinical improvement, radiological resolution of pituitary masses and variable normalisation of pituitary function are possible with early treatment with high-dose oral or i.v. steroids and hormone replacement therapy, although duration and dosing protocols are unclear at this stage.

  • Ipilimumab should continue to be prescribed as treatment for metastatic melanoma; however, close clinical observation of patient's progress must be maintained while they are on this drug.

  • Predictive factors for onset of AH remain unclear and it is imperative that AH is distinguished from pituitary metastases.

  • Further studies are required to determine the safety of continuing therapy with ipilimumab in patients who have developed AH while on treatment.

Open access
K Nadarasa Department of Endocrinology, St Bartholomew's Hospital, London, UK

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M Bailey Department of Endocrinology, St Bartholomew's Hospital, London, UK

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H Chahal Imperial Centre for Endocrinology, Imperial College Healthcare NHS Trust, London, UK

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O Raja Department of Endocrinology, St Bartholomew's Hospital, London, UK

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R Bhat Department of Neonatology, King's College Hospital, London, UK

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C Gayle Department of Diabetes, King's College Hospital, London, UK

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A B Grossman Department of Endocrinology, St Bartholomew's Hospital, London, UK

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M R Druce Department of Endocrinology, St Bartholomew's Hospital, London, UK

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Summary

We present the case of a patient with metastatic parathyroid carcinoma whose hypercalcaemia was medically managed through two pregnancies. The diagnosis was made when the patient presented with chronic knee pain and radiological findings consistent with a brown tumour, at the age of 30. Her corrected calcium and parathyroid hormone (PTH) levels were significantly elevated. Following localisation studies, a right parathyroidectomy was performed with histology revealing parathyroid carcinoma, adherent to thyroid tissue. Aged 33, following biochemical recurrence of disease, the patient underwent a second operation. A subsequent CT and FDG–PET revealed bibasal pulmonary metastases. Aged 35, the patient was referred to our unit for treatment of persistent hypercalcaemia. The focus of treatment at this time was debulking metastatic disease using radiofrequency ablation. Despite advice to the contrary, the patient conceived twice while taking cinacalcet. Even though there are limited available data regarding the use of cinacalcet in pregnancy, both pregnancies continued to term with the delivery of healthy infants, using intensive medical management for persistent hypercalcaemia.

Learning points

  • Parathyroid carcinoma is a rare cause of primary hyperparathyroidism.

  • Hypercalcaemia during pregnancy can result in significant complications for both the mother and the foetus.

  • The use of high-dose cinacalcet in pregnancy has been shown, in this case, to aid in the management of resistant hypercalcaemia without teratogenicity.

Open access