ArticleCureus2026
Chronic Musculoskeletal Pain as an Initial Presentation of Gitelman Syndrome in Adulthood: A Case Report.
Article in Cureus, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Gitelman syndrome is an autosomal recessive salt-wasting tubulopathy characterized by hypokalemia, metabolic alkalosis, hypomagnesaemia and hypocalciuria. It may present in adulthood with nonspecific symptoms including cramps, fatigue and musculoskeletal complaints. We report the case of a 34-year-old male electrical engineer with a three-year history of low back pain, neck and shoulder pain, and radiculopathy. His spinal history is briefly noted as contextual. He was found to have persistent hypokalemia (serum K⁺ ~2.9-3.4 mmol/L), hypomagnesaemia (serum Mg²⁺ ~0.97-1.16 mmol/L), metabolic alkalosis (serum HCO₃⁻ ~28-31 mmol/L, arterial blood gas pH ~7.49) and low urinary fractional excretion of calcium (FECa ~0.002). Work-up excluded other causes of potassium and magnesium wasting; normal blood pressure was noted. A clinical diagnosis of Gitelman syndrome was made. Management included counselling regarding a high-sodium diet together with potassium-rich and magnesium-rich foods, supplementation of potassium and magnesium, and planned initiation of eplerenone and sodium chloride supplementation. We discuss the pathophysiology of Gitelman syndrome, its typical biochemical profile, differential diagnosis (including Bartter syndrome), the relevance of the patient's musculoskeletal pain in the setting of electrolyte imbalance, and therapeutic considerations. This case underscores the importance of considering Gitelman syndrome in adults presenting with persistent hypokalemia, hypomagnesaemia and metabolic alkalosis, even when musculoskeletal symptoms dominate the presentation. Early recognition allows targeted therapy, potentially improving quality of life.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.