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      Pulmonary Artery Calcification in a 57-Year-Old Man

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          Case Presentation

          A 57-year-old man was admitted to our hospital via the ED presenting in reduced general condition because of an infection of unknown origin, generalized edema, and dyspnea at rest (peripheral capillary oxygen saturation, 89%) that required 2 L/min intranasal oxygen. Anamnesis was complicated by an infection-triggered delirium, but his wife reported an increasing physical decay that had led to bed confinement. The BP was reduced at 88/55 mm Hg with a normal heart rate of 86 beats/min. Lung auscultation showed mild bipulmonal rales. Previous comorbidities were a BMI of 42 kg/m 2, an insulin-dependent type 2 diabetes mellitus with a severe diabetes-related chronic kidney disease stage G4A3, and systemic arterial hypertension.

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          Most cited references12

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          2015 ESC/ERS Guidelines for the diagnosis and treatment of pulmonary hypertension: The Joint Task Force for the Diagnosis and Treatment of Pulmonary Hypertension of the European Society of Cardiology (ESC) and the European Respiratory Society (ERS): Endorsed by: Association for European Paediatric and Congenital Cardiology (AEPC), International Society for Heart and Lung Transplantation (ISHLT).

          Guidelines summarize and evaluate all available evidence on a particular issue at the time of the writing process, with the aim of assisting health professionals in selecting the best management strategies for an individual patient with a given condition, taking into account the impact on outcome, as well as the risk-benefit ratio of particular diagnostic or therapeutic means. Guidelines and recommendations should help health professionals to make decisions in their daily practice. However, the final decisions concerning an individual patient must be made by the responsible health professional(s) in consultation with the patient and caregiver as appropriate.
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            Primary hyperparathyroidism.

            Primary hyperparathyroidism (PHPT) is a common disorder in which parathyroid hormone (PTH) is excessively secreted from one or more of the four parathyroid glands. A single benign parathyroid adenoma is the cause in most people. However, multiglandular disease is not rare and is typically seen in familial PHPT syndromes. The genetics of PHPT is usually monoclonal when a single gland is involved and polyclonal when multiglandular disease is present. The genes that have been implicated in PHPT include proto-oncogenes and tumour-suppressor genes. Hypercalcaemia is the biochemical hallmark of PHPT. Usually, the concentration of PTH is frankly increased but can remain within the normal range, which is abnormal in the setting of hypercalcaemia. Normocalcaemic PHPT, a variant in which the serum calcium level is persistently normal but PTH levels are increased in the absence of an obvious inciting stimulus, is now recognized. The clinical presentation of PHPT varies from asymptomatic disease (seen in countries where biochemical screening is routine) to classic symptomatic disease in which renal and/or skeletal complications are observed. Management guidelines have recently been revised to help the clinician to decide on the merits of a parathyroidectomy or a non-surgical course. This Primer covers these areas with particular attention to the epidemiology, clinical presentations, genetics, evaluation and guidelines for the management of PHPT.
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              Nephrolithiasis and renal calcifications in primary hyperparathyroidism.

              Renal complications in terms of hypercalciuria, nephrolithiasis, and nephrocalcinosis are well-known risks in primary hyperparathyroidism (PHPT) and may lead to impaired renal function. We reviewed published evidence on the occurrence, pathophysiology, and consequences of renal complications in PHPT and highlighted areas of uncertainty that should be investigated further. In asymptomatic PHPT, renal stones are present in approximately 7% of the patients, which is a significantly higher prevalence than among patients without PHPT (1.6%). Also, before diagnosis of PHPT, risk of hospital admissions due to renal stones is increased compared with the background population, and the risk remains increased for at least 10 yr after surgical cure from PHPT. However, shortly after parathyroidectomy, risk of recurrent stone episodes is reduced to the recurrence rate among patients with idiopathic renal stone disease. In general, patients with PHPT who develop nephrolithiasis are of younger age and more often are males, compared with those who do not form renal calcifications. Although 24-h urinary calcium is decreased after parathyroidectomy, studies have shown a higher renal calcium excretion and lower serum phosphate levels in former PHPT patients compared with healthy controls, suggesting that these patients have some additional mineral disorder. All patients with a diagnosis of PHPT should initially be evaluated for renal calcifications by unenhanced helical computed tomography. If calcifications are present, parathyroidectomy is recommended. If symptoms develop after parathyroidectomy, patients should be evaluated and treated similar to other patients with renal stones.
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                Author and article information

                Contributors
                Journal
                Chest
                Chest
                Chest
                American College of Chest Physicians
                0012-3692
                1931-3543
                07 June 2024
                June 2024
                07 June 2024
                : 165
                : 6
                : e191-e198
                Affiliations
                [a ]Department of Internal Medicine III, Nephrology, University Hospital Jena, Jena, Germany
                [b ]Forensic Medicine, Section of Pathology, University Hospital Jena, Jena, Germany
                [c ]Forensic Medicine, University Hospital Jena, Jena, Germany
                [d ]Institute for Diagnostic and Interventional Radiology, University Hospital Jena, Jena, Germany
                Author notes
                [] CORRESPONDENCE TO: Martin Busch, MD martin.busch@ 123456med.uni-jena.de
                Article
                S0012-3692(24)00257-5
                10.1016/j.chest.2024.02.022
                11177096
                38852977
                67d904aa-76b8-485b-81e4-0038ee7f84c7
                © 2024 The Author(s)

                This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/4.0/).

                History
                Categories
                Chest Imaging and Pathology for Clinicians

                Respiratory medicine
                Respiratory medicine

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