Der Internist
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In many cases primary hyperparathyroidism (PHPT) remains asymptomatic for years and is only detected by abnormalities in routine diagnostics. While symptomatic disease almost always requires surgical treatment, in symptom-free patients the question of whether and in what form treatment should be carried out is particularly important. ⋯ The diagnostics of asymptomatic PHPT is the same as for symptomatic disease. The diagnosis is made in the presence of elevated parathyroid hormone and balanced vitamin D levels when a combination of hypercalcemia, hypophosphatemia and hypercalciuria is present. Borderline laboratory findings occur especially in asymptomatic PHPT and the differential diagnosis of familial hypocalciuric hypercalcemia must be considered. Once the diagnosis is made sonography, radiography or computed tomography (CT) is used to search for nephrolithiasis or nephrocalcinosis. Regarding bone mineral density (BMD) measurements, in addition to routine measurements at the lumbar spine and femur, measurement at the distal radius is important as it is the most sensitive site for detecting osteoporosis in PHPT. An indication for parathyroidectomy is confirmed in the case of hypercalcemia > 1.0 mg/dl (>0.25 mmol/l) above the upper limit of normal, hypercalciuria > 400 mg/day (>10 mmol/day), renal insufficiency, proven osteoporosis or age < 50 years. If none of these criteria are fulfilled and surgery is not desired by the patient, annual laboratory check-ups and assessment of BMD every 1-2 years are recommended.
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Case Reports
[A several-week history of inflammatory changes in the right foot and right hand of a 57-year-old male patient].
Metastatic fat necrosis due to inflammatory or neoplastic pancreatic diseases is rare. This phenomenon is attributed to systemic effects of pancreatic enzymes. ⋯ Many case reports describe the phenomenon of skin, joint and bone manifestations of fat necrosis under the acronym PPP (pancreatic, panniculits, polyarthritis) syndrome. The management of "autodigestion" primarily consists of treating the underlying pancreatic disease.
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A 61-year-old female patient presented to the emergency room with nausea. Laboratory findings revealed metabolic acidosis, which had to be associated with a sodium-glucose co-transporter‑2 (SGLT2) inhibitor. ⋯ Calculating the anion gap can provide orientation in the case of acidosis of unknown origin. Presumably, a relevant proportion of such cases of ketoacidosis is currently being overlooked or its diagnosis delayed.
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Gout is the most common inflammatory arthritis in men with a rising incidence worldwide. It is a metabolic disease caused by hyperuricemia. Common causes of hyperuricemia, in addition to hereditary reduced renal excretion of urate, include purine over-nutrition, aging, comorbidities and associated medications, some of which increase serum urate levels. ⋯ Gout patients often exhibit other metabolic, renal and cardiovascular co-morbidities and have higher (cardiovascular) mortality. Therefore, guidelines call for consequent urate lowering strategies to bring serum urate levels to a target at least below 360 µmol/l. The following article summarizes the recent state of knowledge regarding the diagnosis and therapy of gout.