Skip to main content
NCBI home page
Clinical Case Reports logoLink to Clinical Case Reports
. 2026 Feb 25;14(3):e72086. doi: 10.1002/ccr3.72086

Unraveling the Complexities of Kartagener's Syndrome: A Case of Bronchiectasis, Isolated Dextrocardia, and Primary Ciliary Dyskinesia in an Adult With Chronic Respiratory Symptoms

Ibrahim Khalil 1,✉, Sakib Abrar 2, Shah Tanvir Ahmed 1, Md Imran Hossain 3
PMCID: PMC12935558  PMID: 41767071

ABSTRACT

Kartagener's Syndrome (KS), a rare autosomal recessive disorder and a subset of Primary Ciliary Dyskinesia (PCD), is characterized by chronic sinusitis, bronchiectasis, and, in approximately 50% of cases, situs inversus. This condition arises from genetic mutations that impair motile cilia function, leading to defective mucociliary clearance, recurrent respiratory infections, and progressive lung damage. While KS is typically diagnosed in childhood, its recognition in adults is often delayed due to symptom overlap with common respiratory conditions such as asthma, chronic obstructive pulmonary disease (COPD), or cystic fibrosis. This case report describes a 40‐year‐old male who presented with a 10–12‐day history of productive cough, intermittent left‐sided chest pain, and a longstanding history of recurrent respiratory infections and chronic sinusitis. Diagnostic imaging, including chest X‐rays and computed tomography (CT) scans, revealed bilateral bronchiectasis, right lung atelectasis, and isolated dextrocardia, with all other organs maintaining normal anatomical positions (situs solitus), an atypical presentation of KS. Laboratory findings indicated mild neutrophilic leukocytosis, and sputum cultures confirmed Pseudomonas aeruginosa infection, a common pathogen in bronchiectasis. The patient was managed with inhaled bronchodilators, corticosteroids, targeted antibiotic therapy, and chest physiotherapy to enhance mucociliary clearance. A multidisciplinary team, including pulmonologists and cardiologists, was engaged to address the complex, multisystem nature of KS and provide long‐term care. This case underscores the diagnostic challenges of identifying KS in adults, particularly with atypical features like isolated dextrocardia, and emphasizes the critical need for comprehensive clinical evaluation, advanced imaging, and consideration of rare genetic disorders in patients with chronic respiratory symptoms.

Keywords: adult respiratory disease, bronchiectasis, chronic sinusitis, isolated dextrocardia, Kartagener's syndrome, primary ciliary dyskinesia

Key Clinical Message

Kartagener's Syndrome in adults with chronic respiratory symptoms and isolated dextrocardia requires comprehensive evaluation, including advanced imaging, to distinguish it from common respiratory conditions. Multidisciplinary management with targeted therapies improves outcomes in this rare genetic disorder.

graphic file with name CCR3-14-e72086-g003.jpg

1. Introduction

Kartagener's Syndrome (KS), a rare genetic disorder classified as a subset of Primary Ciliary Dyskinesia (PCD), results from mutations in genes encoding proteins essential for the structure and function of motile cilia. These mutations disrupt ciliary motility, impairing mucociliary clearance in the respiratory tract and leading to chronic infections, bronchiectasis, and sinusitis. Additionally, defective ciliary function during embryogenesis may alter the establishment of left–right organ asymmetry, resulting in situs inversus totalis or, less commonly, isolated laterality defects such as dextrocardia [1, 2]. The estimated incidence of PCD varies widely, ranging from 1:12,500 to 1:50,000 live births, with KS representing a subset characterized by the clinical triad of chronic sinusitis, bronchiectasis, and situs inversus in approximately 50% of cases [3, 4]. The genetic underpinnings of KS involve mutations in over 40 genes, including DNAH5 (dynein axonemal heavy chain 5), DNAI1 (dynein axonemal intermediate chain 1), and CCDC39 (coiled‐coil domain containing 39), which encode components of the ciliary axoneme responsible for coordinated ciliary beating [5, 6].

Patients with KS typically experience recurrent respiratory tract infections, including sinusitis, bronchitis, and otitis media, due to mucus stasis and subsequent bacterial colonization. Chronic inflammation from these infections leads to irreversible airway damage, manifesting as bronchiectasis, a hallmark feature of the condition [7, 8]. During embryonic development, nodal cilia generate leftward fluid flow to establish left–right asymmetry; dysfunction of these cilia may cause complete organ reversal (situs inversus totalis) or partial defects, such as isolated dextrocardia, as observed in this case [9, 10]. Infertility is another common manifestation, resulting from impaired ciliary function in sperm flagella or fallopian tubes, affecting both male and female reproductive capacity [11]. The phenotypic variability of KS, particularly in organ laterality, poses significant diagnostic challenges, especially in adults, where symptoms may be mistaken for more prevalent respiratory conditions like asthma or COPD [12].

The diagnosis of KS requires a comprehensive, multifaceted approach that integrates detailed clinical history, advanced imaging, ciliary function assessments, and genetic analysis. Chest X‐rays and CT scans are instrumental in identifying bronchiectasis and laterality defects, while low nasal nitric oxide (nNO) levels and abnormal ciliary beat patterns observed via high‐speed video microscopy are highly suggestive of PCD [13, 14]. Genetic testing to identify pathogenic mutations in ciliary protein genes provides definitive confirmation, although the genetic heterogeneity of PCD means that some cases remain undiagnosed even with advanced sequencing techniques [15]. Management of KS is inherently multidisciplinary, focusing on alleviating symptoms, preventing complications, and addressing the hereditary implications of the condition. Regular airway clearance techniques, such as chest physiotherapy and mucolytics, are essential to reduce mucus accumulation, while antibiotics target recurrent infections, and corticosteroids manage airway inflammation [16, 17]. Genetic counseling is a critical component of care, given the autosomal recessive inheritance pattern and the high prevalence of infertility among affected individuals [18].

KS exemplifies the intricate relationship between genetic mutations and multisystem clinical manifestations, affecting the respiratory, cardiovascular, and reproductive systems. Early recognition and intervention are paramount to preventing progressive lung damage and improving long‐term prognosis, yet adult diagnoses are frequently delayed due to the nonspecific nature of symptoms and the rarity of the condition [19]. Ongoing research into ciliary biology, genetic diagnostics, and novel therapeutic strategies continues to enhance our understanding of KS and PCD, offering potential avenues for improved diagnosis and treatment [19, 20]. This case report aims to contribute to the medical literature by detailing the diagnostic and management challenges of KS in an adult patient presenting with chronic respiratory symptoms and isolated dextrocardia, an atypical manifestation of the syndrome.

2. Case History

A 40‐year‐old male presented to a tertiary care hospital with a 10–12‐day history of intermittent left anterior chest pain and a persistent productive cough. The chest pain was described as sharp, localized to the left anterior thorax, and exacerbated by deep inspiration and coughing, significantly limiting the patient's ability to perform routine activities. The cough produced clear sputum, with no associated hemoptysis, fever, night sweats, weight loss, or other systemic symptoms. The patient reported intermittent episodes of hemoptysis, a recognized complication of bronchiectasis, though no massive hemoptysis requiring embolization was noted. The patient's medical history was notable for recurrent respiratory infections since childhood, often requiring antibiotic therapy, and chronic sinusitis managed with nasal decongestants and intermittent antibiotics. He also had a history of hypertension, controlled with amlodipine 5 mg daily, and bronchial asthma, managed with as‐needed albuterol inhalations. There was no prior history of cardiac disease, diabetes mellitus, chronic kidney disease, or significant surgical interventions. The patient was a non‐smoker, did not consume alcohol or illicit drugs, and worked as an office administrator with no known occupational exposures to respiratory irritants. There was no family history of chronic respiratory infections, sinusitis, bronchiectasis, situs inversus, dextrocardia, or infertility suggestive of Kartagener's Syndrome.

Physical examination revealed stable vital signs: blood pressure 120/80 mmHg, pulse rate 72 beats per minute, respiratory rate 16 breaths per minute, temperature 36.7°C, and oxygen saturation 98% on room air. There was no evidence of respiratory distress, cyanosis, digital clubbing, or pallor. Respiratory examination disclosed crepitations in the left lower lung field, raising suspicion of consolidation or an infectious process. Cardiovascular examination confirmed heart sounds on the right side of the thorax, consistent with dextrocardia, with no murmurs, gallops, or signs of elevated jugular venous pressure, effectively ruling out acute heart failure. Abdominal examination was unremarkable, with no hepatosplenomegaly, tenderness, or masses. Neurological, musculoskeletal, and dermatological examinations showed no abnormalities.

3. Differential Diagnosis, Investigations and Treatment

Laboratory investigations revealed a mild elevation in white blood cell count (6.06 × 103/μL, with 70% neutrophils), suggestive of an inflammatory or infectious process. Hemoglobin was 13 g/dL, and platelet count was normal at 210 × 103/μL. Biochemical markers, including serum creatinine (0.96 mg/dL), sodium (147 mmol/L), potassium (3.5 mmol/L), and liver function tests (alanine aminotransferase 25 U/L, aspartate aminotransferase 22 U/L), were within normal limits. C‐reactive protein was mildly elevated at 12 mg/L, further supporting an inflammatory state. Urinalysis was unremarkable, showing clear, straw‐colored urine with no red blood cells, pus cells, or casts. Sputum culture identified Pseudomonas aeruginosa , a frequent pathogen in bronchiectasis, with sensitivity to ceftazidime, tobramycin, and piperacillin‐tazobactam.

Imaging studies played a pivotal role in elucidating the underlying pathology. A chest X‐ray demonstrated an inhomogeneous opacity in the right lung, accompanied by fibrosis, cavity formation, and a blunted right costophrenic angle, suggestive of collapse or consolidation (Figure 1). The mediastinum was shifted to the right, and the cardiac silhouette was prominently located on the right side, confirming dextrocardia. A subsequent chest CT scan provided detailed insights, revealing bilateral lung abnormalities: the left lung exhibited hyperinflation, pronounced bronchial dilatation, and fibrosis, consistent with bronchiectasis, particularly affecting the lower lobe, while the right lung showed significant atelectasis without evidence of pleural effusion (Figures 2 and 3). These findings indicated severe, chronic lung damage likely resulting from recurrent infections and persistent inflammation. Echocardiography further confirmed isolated dextrocardia, with the heart positioned on the right side of the thorax, but no structural or functional cardiac abnormalities were identified, left ventricular ejection fraction 65%, normal valvular function, no septal defects, and the standard left‐sided (conventional) 12‐lead ECG shown in Figure 4. Abdominal CT verified situs solitus, with the liver located on the right, spleen on the left, and stomach and intestines in their normal anatomical positions, ruling out situs inversus totalis or partial visceral reversal. A sinus CT, prompted by the history of chronic sinusitis, revealed mucosal thickening and opacification of the maxillary sinuses, consistent with chronic rhinosinusitis.

FIGURE 1.

FIGURE 1

Open in a new tab

The chest X‐rays reveal agenesis of the right lung and dextrocardia. In the images, the absence of the right lung is apparent, with no visible lung tissue on the right side of the chest in both the posterior–anterior and lateral views. Additionally, the heart is positioned on the right side of the chest, confirming the presence of dextrocardia, a condition commonly associated with situs inversus. These findings align with the patient's clinical history of Kartagener's syndrome, which often includes these congenital anomalies.

FIGURE 2.

FIGURE 2

Open in a new tab

Axial HRCT scan of the chest showing significant bilateral lung abnormalities. The left lung exhibits a large area of expansion and possible hyperinflation, with pronounced bronchial dilatation and fibrosis, consistent with bronchiectasis. The right lung demonstrates significant atelectasis and compression, with no signs of pleural effusion. These findings indicate severe structural lung damage, predominantly affecting the left lung, likely due to chronic inflammatory processes. The right lung is notably compromised. The heart is positioned on the right side, as indicated by the yellow arrow.

FIGURE 3.

FIGURE 3

Open in a new tab

Axial CT scan of the chest showing significant bilateral lung abnormalities. The right lung demonstrates significant atelectasis and compression. The right lung is notably compromised. The heart is positioned on the right side, as indicated by the yellow arrow.

FIGURE 4.

FIGURE 4

Open in a new tab

(A) The ECG reveals several abnormalities that are consistent with the patient's clinical presentation. First, sinus rhythm is noted, with a normal heart rate and consistent P waves preceding each QRS complex, indicating normal electrical activity originating from the sinoatrial (SA) node. However, T wave abnormalities are present, with mild inversion or flattening in some leads. This is likely due to the chronic respiratory condition and recurrent infections, which can influence the cardiac repolarization process. Another potential abnormality is right ventricular hypertrophy (RVH). Given the structural changes in the lungs, including atelectasis and hyperinflation, there may be increased pressure and workload on the right ventricle, and signs of RVH were noted on the ECG, such as prominent R waves in lead V1 or deep S waves in lead V6 with poor R wave progression. (B) The echocardiogram report reveals several abnormalities. Dextrocardia is noted, a condition commonly associated with Kartagener's syndrome, where the heart is located on the right side of the chest rather than the left. Additionally, aortic sclerosis is observed, which refers to the thickening and hardening of the aortic valve, though no significant stenosis is detected. A trace amount of aortic regurgitation (AR) is present, suggesting mild backflow of blood into the left ventricle during diastole; however, this is not considered clinically significant at this time. The report also notes that there is no regional wall motion abnormality at rest, indicating the absence of acute ischemia or dysfunction in the heart's walls. While the left and right ventricular functions are both within normal limits, the right ventricular function appears normal despite the patient's respiratory issues.

4. Results (Outcome and Follow‐Up)

The patient's clinical history of recurrent respiratory infections, chronic sinusitis, and bronchiectasis, combined with the finding of isolated dextrocardia, strongly suggested Kartagener's Syndrome (KS), a subset of Primary Ciliary Dyskinesia (PCD). The absence of motile cilia was inferred from the clinical presentation, as nasal ciliary motion studies using high‐speed video microscopy were not available due to lack of specialized facilities. Genetic testing for mutations in PCD‐associated genes, such as DNAH5 or DNAI1, was recommended but could not be performed due to resource constraints, reflecting a common challenge in diagnosing rare disorders in certain healthcare settings.

Management was initiated promptly to address both the acute infection and the chronic respiratory symptoms. Intravenous antibiotics, including ceftazidime (2 g every 8 h) and tobramycin (5 mg/kg daily), were administered for 14 days to target the Pseudomonas aeruginosa infection, guided by culture sensitivity results. Inhaled bronchodilators (albuterol 2.5 mg nebulized as needed) and corticosteroids (budesonide 0.5 mg twice daily) were continued to manage airway obstruction and inflammation, building on the patient's existing asthma regimen. Daily chest physiotherapy, incorporating postural drainage, percussion, and positive expiratory pressure devices, was instituted to enhance mucociliary clearance and prevent further progression of bronchiectasis. Nasal saline irrigations (twice daily) were prescribed to alleviate sinus congestion and reduce the frequency of sinus infections. The patient was educated on the importance of adherence to these therapies and the need for regular follow‐up to monitor disease progression.

Given the complexity and multisystem nature of KS, the patient was referred to a multidisciplinary team comprising a pulmonologist, cardiologist, otolaryngologist, and genetic counselor. The pulmonologist coordinated respiratory management, including pulmonary function testing and annual imaging to assess lung damage. The cardiologist confirmed the benign nature of the isolated dextrocardia but recommended periodic echocardiograms to monitor for any latent cardiac complications. The otolaryngologist evaluated the chronic sinusitis, considering endoscopic sinus surgery if medical management failed. Genetic counseling was emphasized as a critical component of care, given the autosomal recessive inheritance pattern of KS and the potential for infertility, which could impact the patient or his family's future reproductive decisions. Although the patient reported no current fertility concerns, he was informed of the possibility of subclinical sperm motility issues and the importance of genetic testing for definitive diagnosis and family planning.

Over the course of two weeks, the patient's symptoms improved significantly, with a marked reduction in cough frequency, chest pain, and sputum production. Follow‐up chest X‐ray showed partial resolution of the right lung opacity, though CT findings of bronchiectasis and fibrosis remained unchanged, indicating irreversible structural damage. Pulmonary function tests revealed mild obstructive lung disease (forced expiratory volume in 1 s [FEV1] 75% predicted), consistent with bronchiectasis and asthma. Long‐term management plans included regular pulmonary function monitoring, annual chest imaging, and vaccinations against influenza and pneumococcus to reduce the risk of respiratory infections. The patient was also enrolled in a pulmonary rehabilitation program to improve exercise tolerance and quality of life.

5. Discussion

Kartagener's Syndrome (KS), a rare subset of Primary Ciliary Dyskinesia (PCD), arises from defective motile cilia due to mutations in genes such as DNAH5 and DNAI1, which encode dynein arm components essential for ciliary motility. This impairs mucociliary clearance, causing chronic respiratory infections, sinusitis, and bronchiectasis, while embryonic nodal cilia dysfunction disrupts left–right asymmetry, leading to situs inversus in ~50% of cases or rarer partial defects like isolated dextrocardia [1, 2, 3, 4, 5, 6, 9, 10]. This case highlights an atypical presentation with isolated dextrocardia and situs solitus, distinguishing it from the classic triad and illustrating phenotypic variability [21, 22, 23, 24].

The patient's longstanding recurrent infections, chronic sinusitis, productive cough, intermittent hemoptysis, and CT‐confirmed bilateral bronchiectasis (prominent left lower lobe dilatation, hyperinflation, right atelectasis) align with KS respiratory manifestations. Pseudomonas aeruginosa colonization, a common bronchiectasis pathogen, exacerbated damage. Isolated dextrocardia on echocardiography, with normal cardiac function, was a pivotal clue, as laterality defects remain a hallmark even without complete situs inversus [23, 24]. The asthma history was confounding but insufficient to explain bronchiectasis severity or dextrocardia.

Complications stem from chronic ciliary dysfunction: progressive bronchiectasis risks respiratory failure; chronic rhinosinusitis requires ongoing management; opportunistic infections drive hemoptysis and decline; and infertility affects up to 50% due to impaired sperm flagella or fallopian tube cilia [24, 25, 26]. These underscore the multisystem, progressive nature of KS and the need for proactive care.

The differential included cystic fibrosis (excluded by absent extrapulmonary features and presence of dextrocardia), allergic bronchopulmonary aspergillosis (no eosinophilia or elevated IgE), alpha‐1 antitrypsin deficiency (no emphysema/liver disease), COPD/asthma (inadequate to explain full picture), and other ciliopathies like Bardet‐Biedl syndrome (absent systemic features) [25, 26, 27, 28, 29]. Thorough history, imaging, and specialized testing are essential to differentiate KS.

Adult diagnosis remains challenging due to symptom overlap with common disorders and resource limitations. Nasal nitric oxide and high‐speed video microscopy are key but often unavailable; genetic testing is gold standard yet constrained here, leading to presumptive diagnosis via clinical/imaging findings [13, 14, 30, 31]. Chest/abdominal CT and echocardiography were crucial for identifying bronchiectasis, sinusitis, and isolated dextrocardia.

Management was multidisciplinary: targeted antibiotics (ceftazidime/tobramycin) cleared infection; inhaled bronchodilators/corticosteroids addressed obstruction/inflammation; chest physiotherapy and nasal irrigations enhanced clearance; and referrals to pulmonology, cardiology, otolaryngology, and genetics ensured comprehensive care, including monitoring, vaccinations, rehabilitation, and counseling on inheritance/infertility [16, 17, 31, 32, 33, 34].

Prognosis improves with early, consistent intervention to stabilize lung function and prevent decline, though untreated progression risks respiratory failure [34, 35]. Limitations include absent genetic/ciliary studies due to resources, symptom overlap risking misdiagnosis, and reliance on CF‐adapted therapies amid limited KS‐specific trials. Future efforts should enhance diagnostic access (portable nNO, affordable sequencing) and explore targeted therapies like gene editing.

Author Contributions

Ibrahim Khalil: conceptualization, data curation, formal analysis, methodology, project administration, validation, writing – original draft, writing – review and editing. Sakib Abrar: conceptualization, formal analysis, investigation, project administration, resources, supervision, validation, visualization, writing – original draft. Shah Tanvir Ahmed: conceptualization, data curation, writing – original draft. Md. Imran Hossain: writing – review and editing.

Funding

The authors have nothing to report.

Consent

Written informed consent was obtained from the patient to publish this report in accordance with the journal's patient consent policy.

Conflicts of Interest

The authors declare no conflicts of interest.

Acknowledgments

The authors have nothing to report.

Data Availability Statement

The data that support the findings of this study are available from the corresponding author upon reasonable request.

References

  • 1. Shapiro A. J., Davis S. D., Polineni D., et al., “Diagnosis of Primary Ciliary Dyskinesia. An Official American Thoracic Society Clinical Practice Guideline,” American Journal of Respiratory and Critical Care Medicine 197, no. 12 (2018): e24–e39, 10.1164/rccm.201805-0819ST. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 2. Knowles M. R., Daniels L. A., Davis S. D., Zariwala M. A., and Leigh M. W., “Primary Ciliary Dyskinesia. Recent Advances in Diagnostics, Genetics, and Characterization of Clinical Disease,” American Journal of Respiratory and Critical Care Medicine 188, no. 8 (2013): 913–922, 10.1164/rccm.201301-0059CI. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 3. Raidt J., Loges N. T., Olbrich H., Wallmeier J., Pennekamp P., and Omran H., “Primary Ciliary Dyskinesia,” La Presse Médicale 52, no. 3 (2023): 104171, 10.1016/j.lpm.2023.104171. [DOI] [PubMed] [Google Scholar]
  • 4. Hannah W. B., Seifert B. A., Truty R., et al., “The Global Prevalence and Ethnic Heterogeneity of Primary Ciliary Dyskinesia Gene Variants: A Genetic Database Analysis,” Lancet. Respiratory Medicine 10, no. 5 (2022): 459–468, 10.1016/S2213-2600(21)00453-7. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 5. Ferkol T., “Understanding Primary Ciliary Dyskinesia,” Pediatric Pulmonology 60, no. Suppl 1 (2025): S86–S87, 10.1002/ppul.27360. [DOI] [PubMed] [Google Scholar]
  • 6. Horani A., Ferkol T. W., Dutcher S. K., and Brody S. L., “Genetics and Biology of Primary Ciliary Dyskinesia,” Paediatric Respiratory Reviews 18 (2016): 18–24, 10.1016/j.prrv.2015.09.001. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 7. Leigh M. W., Pittman J. E., Carson J. L., et al., “Clinical and Genetic Aspects of Primary Ciliary Dyskinesia/Kartagener Syndrome,” Genetics in Medicine: Official Journal of the American College of Medical Genetics 11, no. 7 (2009): 473–487, 10.1097/GIM.0b013e3181a53562. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 8. Lucas J. S., Alanin M. C., Collins S., et al., “Clinical Care of Children With Primary Ciliary Dyskinesia,” Expert Review of Respiratory Medicine 11, no. 10 (2017): 779–790, 10.1080/17476348.2017.1360770. [DOI] [PubMed] [Google Scholar]
  • 9. Nonaka S., Tanaka Y., Okada Y., et al., “Randomization of Left‐Right Asymmetry due to Loss of Nodal Cilia Generating Leftward Flow of Extraembryonic Fluid in Mice Lacking KIF3B Motor Protein,” Cell 95, no. 6 (1998): 829–837, 10.1016/s0092-8674(00)81705-5. [DOI] [PubMed] [Google Scholar]
  • 10. Wallmeier J., Nielsen K. G., Kuehni C. E., et al., “Motile Ciliopathies,” Nature Reviews. Disease Primers 6, no. 1 (2020): 77, 10.1038/s41572-020-0209-6. [DOI] [PubMed] [Google Scholar]
  • 11. Raidt J., Wallmeier J., Hjeij R., et al., “Ciliary Beat Pattern and Frequency in Genetic Variants of Primary Ciliary Dyskinesia,” European Respiratory Journal 44, no. 6 (2014): 1579–1588, 10.1183/09031936.00052014. [DOI] [PubMed] [Google Scholar]
  • 12. Popatia R., Haver K., and Casey A., “Primary Ciliary Dyskinesia: An Update on New Diagnostic Modalities and Review of the Literature,” Pediatric Allergy, Immunology and Pulmonology 27, no. 2 (2014): 51–59, 10.1089/ped.2013.0314. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 13. Lucas J. S., Barbato A., Collins S. A., et al., “European Respiratory Society Guidelines for the Diagnosis of Primary Ciliary Dyskinesia,” European Respiratory Journal 49, no. 1 (2017): 1601090, 10.1183/13993003.01090-2016. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 14. O'Connor M. G., Griffiths A., Iyer N. P., Shapiro A. J., Wilson K. C., and Thomson C. C., “Summary for Clinicians: Diagnosis of Primary Ciliary Dyskinesia,” Ann Am Thorac Soc 16, no. 2 (2019): 171–174, 10.1513/AnnalsATS.201810-693CME. PMID: 30433820; PMCID: PMC7336768. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 15. Ibrahim R. and Daood H., “Kartagener Syndrome: A Case Report,” Canadian Journal of Respiratory Therapy: CJRT = Revue Canadienne de la Therapie Respiratoire: RCTR 57 (2021): 44–48, 10.29390/cjrt-2020-064. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 16. Schofield L. M., Duff A., and Brennan C., “Airway Clearance Techniques for Primary Ciliary Dyskinesia; Is the Cystic Fibrosis Literature Portable?,” Paediatric Respiratory Reviews 25 (2018): 73–77, 10.1016/j.prrv.2017.03.011. [DOI] [PubMed] [Google Scholar]
  • 17. Goyal V. and Chang A. B., “Combination Inhaled Corticosteroids and Long‐Acting beta2‐Agonists for Children and Adults With Bronchiectasis,” Cochrane Database of Systematic Reviews 2014, no. 6 (2014): CD010327, 10.1002/14651858.CD010327.pub2. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 18. Afzelius B. A. and Stenram U., “Prevalence and Genetics of Immotile‐Cilia Syndrome and Left‐Handedness,” International Journal of Developmental Biology 50, no. 6 (2006): 571–573, 10.1387/ijdb.052132ba. [DOI] [PubMed] [Google Scholar]
  • 19. Bush A. and Hogg C., “Primary Ciliary Dyskinesia: Recent Advances in Epidemiology, Diagnosis, Management and Relationship With the Expanding Spectrum of Ciliopathy,” Expert Review of Respiratory Medicine 6, no. 6 (2012): 663–682, 10.1586/ers.12.60. [DOI] [PubMed] [Google Scholar]
  • 20. Sahu S., Ranganatha R., Batura U., et al., “A Case of Unusual Presentation of Kartagener's Syndrome in a 22‐Year‐Old Female Patient,” Cureus 14, no. 8 (2022): e28119, 10.7759/cureus.28119. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 21. Novák J., Horáková L., Puchmajerová A., Vik V., Krátká Z., and Thon V., “Primary Ciliary Dyskinesia as a Rare Cause of Male Infertility: Case Report and Literature Overview,” Basic Clin. Androl 34 (2024): 27, 10.1186/s12610-024-00244-z. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 22. Chalmers J. D., Elborn S., and Greene C. M., “Basic, Translational and Clinical Aspects of Bronchiectasis in Adults,” European Respiratory Review: An Official Journal of the European Respiratory Society 32, no. 168 (2023): 230015, 10.1183/16000617.0015-2023. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 23. Kobbernagel H. E., Buchvald F. F., Haarman E. G., et al., “Study Protocol, Rationale and Recruitment in a European Multi‐Centre Randomized Controlled Trial to Determine the Efficacy and Safety of Azithromycin Maintenance Therapy for 6 Months in Primary Ciliary Dyskinesia,” BMC Pulmonary Medicine 16, no. 1 (2016): 104, 10.1186/s12890-016-0261-x. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 24. Alanin M. C., Aanaes K., Høiby N., et al., “Sinus Surgery Can Improve Quality of Life, Lung Infections, and Lung Function in Patients With Primary Ciliary Dyskinesia,” International Forum of Allergy & Rhinology 7, no. 3 (2017): 240–247, 10.1002/alr.21873. [DOI] [PubMed] [Google Scholar]
  • 25. Ratjen F., Bell S. C., Rowe S. M., Goss C. H., Quittner A. L., and Bush A., “Cystic Fibrosis,” Nature Reviews. Disease Primers 1 (2015): 15010, 10.1038/nrdp.2015.10. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 26. Agarwal R., Chakrabarti A., Shah A., et al., “Allergic Bronchopulmonary Aspergillosis: Review of Literature and Proposal of New Diagnostic and Classification Criteria,” Clinical & Experimental Allergy 43, no. 8 (2013): 850–873, 10.1111/cea.12141. [DOI] [PubMed] [Google Scholar]
  • 27. Greene C. M., Marciniak S. J., Teckman J., et al., “α1‐Antitrypsin Deficiency,” Nature Reviews. Disease Primers 2 (2016): 16051, 10.1038/nrdp.2016.51. [DOI] [PubMed] [Google Scholar]
  • 28. Celli B. R., Decramer M., Wedzicha J. A., et al., “An Official American Thoracic Society/European Respiratory Society Statement: Research Questions in COPD,” European Respiratory Journal 45, no. 4 (2015): 879–905, 10.1183/09031936.00009015. [DOI] [PubMed] [Google Scholar]
  • 29. Forsythe E., Kenny J., Bacchelli C., and Beales P. L., “Managing Bardet‐Biedl Syndrome‐Now and in the Future,” Frontiers in Pediatrics 6 (2018): 23, 10.3389/fped.2018.00023. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 30. Perloff J. K., “The Cardiac Malpositions,” American Journal of Cardiology 108, no. 9 (2011): 1352–1361, 10.1016/j.amjcard.2011.06.055. [DOI] [PubMed] [Google Scholar]
  • 31. Surdut S. P., van der Merwe E., Goussard P., and Urban M. F., “Which Side Are They on? Diagnosing Primary Ciliary Dyskinesias in Low‐ Or Middle‐Income Countries: A Review and Case Series,” African Journal of Thoracic and Critical Care Medicine 29, no. 3 (2023): 131–138, 10.7196/AJTCCM.2023.v29i3.425. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 32. Hosie P. H., Fitzgerald D. A., Jaffe A., Birman C. S., Rutland J., and Morgan L. C., “Presentation of Primary Ciliary Dyskinesia in Children: 30 Years' Experience,” Journal of Paediatrics and Child Health 51, no. 7 (2015): 722–726, 10.1111/jpc.12791. [DOI] [PubMed] [Google Scholar]
  • 33. Behan L., Dimitrov B. D., Kuehni C. E., et al., “PICADAR: A Diagnostic Predictive Tool for Primary Ciliary Dyskinesia,” European Respiratory Journal 47, no. 4 (2016): 1103–1112, 10.1183/13993003.01551-2015. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 34. Rubbo B. and Lucas J. S., “Clinical Care for Primary Ciliary Dyskinesia: Current Challenges and Future Directions,” European Respiratory Review 26, no. 145 (2017): 170023, 10.1183/16000617.0023-2017. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 35. Gebray H. M., Chekol A. L., Mihiretie S. A., Boye A. T., Wendimagegn Z. S., and Getachew Z. D., “Kartagener Syndrome in a Young Ethiopian Boy: A Case Report,” Journal of Medical Case Reports 19, no. 1 (2025): 230, 10.1186/s13256-025-05245-8. [DOI] [PMC free article] [PubMed] [Google Scholar]

Associated Data

This section collects any data citations, data availability statements, or supplementary materials included in this article.

Data Availability Statement

The data that support the findings of this study are available from the corresponding author upon reasonable request.

Articles from Clinical Case Reports are provided here courtesy of Wiley

RESOURCES