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Case Report

Special form of osteoporosis in a 53-year-old man, simon lampart.

1 Department of Internal Medicine, Luzerner Kantonsspital, Luzern, Switzerland

Silvia Azzarello-Burri

2 Institute of Medical Genetics, University of Zurich, Schlieren-Zurich, Switzerland

Christoph Henzen

3 Division of Endocrinology and Diabetes, Luzerner Kantonsspital, Luzern, Switzerland

Stefan Fischli

Male osteoporosis often remains unrecognised. Osteoporotic fractures occur approximately 10 years later in men than in women due to higher peak bone mass. However, 30% of all hip fractures occur in men. Risk factors of osteoporotic fractures can be grouped into primary and secondary causes. We present the case of a 53-year-old man, who suffered a compression fracture of a lumbar vertebra after a generalised seizure and an atraumatic rib fracture 5 months later. We could exclude secondary causes of bone mineral loss such as primary hyperparathyroidism, glucocorticoid use and hypogonadism. However, a heterozygous missense mutation of the COL1A1 gene in exon 48 in further search of a secondary cause was found. Therapy was changed from bisphosphonate treatment to teriparatide. Considering the lack of other osteogenesis imperfecta (OI) symptoms and signs, the patient’s illness can be classified as mild. OI should be considered as differential diagnosis in unexplained cases with osteoporosis.

In contrast to female patients, osteoporosis in men often remains an unrecognised and untreated condition. Due to the higher peak bone mass in men, osteoporotic fractures (ie, hip or vertebrae) normally occur 10 years later than in women. 1 However, male osteoporosis is a relevant and common clinical problem with high morbidity and mortality. 2 Thirty per cent of all hip fractures are arising in men 3 and sustaining a hip fracture is associated with twofold to threefold increased mortality risk relative to women. 4

As in women, risk factors for bone loss and osteoporotic fractures in men can be grouped into primary (age-related, idiopathic) and secondary causes. Among secondary causes, multiple risk factors for osteoporotic fractures in men have been identified, 5 that is, hypogonadism, low body mass index (BMI), smoking, excessive alcohol drinking and the use of glucocorticoid medications. Of these, a single or a combination of multiple risk factors can lead to a reduction of bone mineral density (BMD) or even superimpose the age-related bone loss.

Therefore, a thorough identification of potential risk factors is crucial to identify persons at risk 6 and to guide further diagnostic (ie, BMD assessment by Dual Energy X-Ray Absorptiometry (DEXA)) and therapeutic (ie, bisphosphonate treatment) measures.

In this case report, we describe a patient with a rare secondary form of osteoporosis.

Case presentation

A 53-year-old man presented at our hospital with a generalised seizure for the first time, which had caused a compression fracture of the first lumbar vertebra. The medical history of the patient was uneventful, he took no medications and he denied smoking, excessive alcohol consumption and the use of glucocorticoids in the past. Although older fractures were seen on the CT scan, there was no history of previous back pain. Symptoms of hypogonadism (ie, loss of libido or decreased spontaneous/morning erections) were absent as was a reduction of his height.

Clinical examination found a patient in good clinical conditions (weight 70 kg, height 170 cm, BMI 25.1 kg/m 2 , blood pressure 152/92 mm Hg, heart rate 78/min). Further examination revealed a normal configured spine with tenderness over the lumbar spine and absence of sensorimotoric deficits in the lower extremities. There were no signs suggestive of hypercortisolism or hearing loss; sclerae were normal.

Investigations

Laboratory analysis demonstrated normal values for creatinine, transaminases, serum calcium, phosphorus, parathyroid hormone, alkaline phosphatase, total testosterone, vitamin D and thyroid stimulating hormone. Protein electrophoresis with immune fixation was normal and coeliac disease was excluded by determination of antitransglutaminase antibodies. Adult systemic mastocytosis was ruled out by a normal serum tryptase and normal examination of bone marrow aspirate (including unremarkable immunophenotyping and moleculargenetic analysis of the aspirate).

Conventional X-ray imaging and a CT scan of the whole spine found older vertebral fractures at the thoracic (Th 6, 7, 8, 9 and 11) and lumbar (L3 and 4) level with the appearance of codfish vertebrae ( figures 1 and 2 ). BMD assessed by DEXA scan demonstrated a T-score of −3.3 at the lumbar spine and a T-score of −1.5 at the femoral neck.

X-ray, lateral view showing a new fracture of L1 and older fractures of Th11, L3 and L4.

CT scan, lateral view showing multiple older fractures Th 6, 7, 8, 9 and 11, L3 and L4, and a new fracture L1.

Due to the instability of the L1 fracture, kyphoplasty with internal fixation was performed. The patient was started on a combination therapy with calcium and vitamin D and he received bisphosphonate treatment with ibandronic acid.

Outcome and follow-up

Five months later, the patient returned and was diagnosed with rib fractures, which had occurred without trauma. In a further attempt to secure a secondary cause, a molecular genetic analysis for osteogenesis imperfecta (OI) was performed. This revealed a heterozygous missense variant of the COL1A1 gene ( {"type":"entrez-nucleotide","attrs":{"text":"NM_000088","term_id":"1777425449","term_text":"NM_000088"}} NM_000088 ; c.3688G>A, p.(Glu1230Lys)). This variant has a very low minor allele frequency of 0.001% and six different in silico prediction tools indicate a deleterious effect. The affected amino acid is located in the C-terminal propeptide, and with reference to the structure, the exchange would not be expected to cause a major structural disturbance. However, the reversal of charging could lead to reduced stability of the helix. Such a mild functional effect would be in line with the mild phenotype. We therefore assume that this variant is causative, although according to the current guidelines of the American College of Medical Genetics (ACMG), it would have to be classified as variant of unknown significance.

The treatment with bisphosphonates was re-evaluated in this patient after new fractures had occurred. It was decided to change the therapy to an osteoanabolic regimen with teriparatide. This led to a clear improvement of bone density in follow-up DEXA measurements and the absence of new fractures.

Initially, the patient was only aware of postmenopausal osteoporosis in his mother. However, after the diagnosis in the patient, it became apparent that further family members showed mild signs of OI. The brother of the patient suffered an osteoporotic vertebral fracture at the age of 52. Moreover, the patients’ son was said to have had three fractures after mild traumata (hand, finger, skull) and an abnormal audiogram, and he also suffered from tinnitus. Genetic testing in the patient’s brother and son confirmed that they are also carriers of the same COL1A1 variant.

OI (‘brittle bone disease’) is a group of disorders affecting connective tissue and bone structure. OI is rare with an estimated incidence of 1 in 20 000 7 or up to 1 in 10 000 births (Orphanet report series number 2 [2018]). Most of the cases are caused by autosomal-dominant inherited mutations in genes encoding alpha-1 and alpha-2 chains of type I collagen (COL1A1 and COL1A2). 8 Rarer forms include mutations of genes that encode proteins promoting post-translational modifications of type I collagen or bone formation and osteoblast maturation ( table 1 ).

Examples of mutations outside COL1A1/COL1A2 genes in mild OI forms overlapping with early-onset osteoporosis (adapted from 19 20 )

As type I collagen is an important protein for organic bone structure, typical osseous manifestation of OI include multiple/atypical fractures often caused by minimal trauma (‘brittle bones’), bowing and deformity of long bones, short stature, scoliosis and deformity of the skull. Extra skeletal manifestations include hearing loss, blue sclerae, dentinogenesis imperfecta and hyperlaxity of ligaments. The clinical spectrum of OI is very broad, depends on the type of mutation and ranges from mild manifestations (ie, accelerated postmenopausal osteoporosis) to severe forms in children (including perinatal lethal forms). 9 10

It is well known that peak bone mass 11 and the risk for osteoporosis are strongly determined by genetic 12 and epigenetic factors 13 following a complex mechanism. In rare cases, rare genetic variants with strong functional effects, that is, a COL1A1 mutation as in this patient, can play a critical role in the development of postmenopausal 14 or male osteoporosis.

Our patient presented with advanced osteoporosis and multiple low-trauma fractures. The L1 fracture was unstable and internal fixation/kyphoplasty was mandatory. At that time, the diagnosis of OI was not made. However, it should be emphasised that caution should be kept with kyphoplasty in patients with OI due to the increased risk of fractures in the adjacent vertebral bodies after such procedures.

The patient was initially treated with ibandronate. Later, therapy was changed to teriparatide after the patient had suffered new fractures. Bisphosphonates remain the mainstay of treatment in patients with moderate and severe forms of OI. 15 However, there is a growing body of evidence that teriparatide may be helpful in patient with milder forms of OI. 16 17

A thorough search for secondary causes of osteoporosis (ie, hypogonadism, systemic mastocytosis) remained uneventful. However, due to his multiple health complaints next to the osteoporosis, including seizures, migraine and a possible histamine intolerance, the patient was referred to genetic counselling to evaluate the possibility of a genetic condition. Because of the osteoporosis and low-trauma fractures in a male patient, genetic testing for the COL1A1 and COL1A2 genes were initiated and supported the clinical suspicion of OI. Based on the clinical findings and the lack of other OI typical features (ie, deformity of long bones, absence of hearing loss and blue sclerae), the OI in this case can be classified as mild. The heterozygous missense variant in the COL1A1 gene that was found in our patient has not been described in the literature to date. However, one case with mild OI was described in the literature to harbour a variant in a similar location. 18 Based on this report and the variant characteristics detailed above, we considered it likely causal for the advanced osteoporosis in our patient. It is unknown if it is a de novo mutation or if it was inherited in an autosomal-dominant manner. However, since the brother also carries the same variant, we assume that the mother with postmenopausal osteoporosis is also a carrier. Each carrier transmits the variant with a likelihood of 50% to her or his offspring. Therefore, the opportunity of molecular genetic testing and its possible implications (ie, early risk assessment by DEXA and medical treatment) must be discussed with the relatives at risk even in mild forms of OI.

Learning points

• Male osteoporosis is often unrecognised and remains untreated. It is associated with substantial morbidity and mortality.
• As in women, the aetiology of osteoporosis in men can be grouped into primary (age-related, idiopathic) and secondary causes (ie, hypogonadism, smoking, use of glucocorticoid medications).
• Osteogenesis imperfecta (OI) remains a rare secondary cause of osteoporosis. However, it can be hypothesised that the true prevalence of this condition remains underestimated due to lack of routine genetic screening and the multiple manifestations of the disease (ie, mild clinical phenotype with lack of ‘classical’ OI features).
• OI should be considered as differential diagnosis in unexplained cases with osteoporosis after exclusion of other secondary aetiologies. The possibility of molecular testing and its implications should be discussed with the patient and his/her relatives.

Contributors: SL wrote the first draft of the article. SF reviewed the article, making substantial alterations in order to completely present the case and to fully show the scientific intent of the presentation. SA-B reviewed the section on genetical information and provided further details in this respect. CH suggested that we present the case. The patient reviewed the article several times after providing his consent.

Funding: This research received no specific grant from any funding agency in the public, commercial or not-for-profit sectors.

Competing interests: None declared.

Patient consent: Obtained.

Provenance and peer review: Not commissioned; externally peer reviewed.

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Patient Case Presentation

Ms. C.S. is a 46-year-old white female, who presents to her primary care physician for further work up after being seen and treated by an orthopedic surgeon for a right distal radius fracture. Patient sustained a low impact fall from standing which led to her injury. She states generally she doesn’t have pain but rates pain in wrist seven out of ten on pain scale.

Pertinent Past Medical and Surgical History

Jones, R. (2013). Distal radius [Picture]. Retrieved from https://emrems.com/2013/10/02/distal-radius/

• Bipolar disorder, diagnosed age 23, medically treated with lithium and cognitive behavior therapy
• Hysterectomy, age 44
• Diabetes type 1, diagnosed age 2
• Depression, diagnosed age 17

Pertinent Social History

• One pack per day smoker since age 17
• Newly divorced after 25 years of marriage
• Height 5’2 weight 85 pounds

Pertinent Family History

• Father alive at age 76 with history of bipolar disorder
• Mother died of cardiac arrest after a myocardial infarction 60 days post hip replacement at age 66
• Brother alive at age 50 with history of hyperthyroidism
• Sister alive at age 52 with no pertinent medical history

The association between myasthenia gravis and risk of fracture: a systematic review and meta-analysis

• Published: 15 May 2024

Cite this article

• Chien-Ju Lin 1 ,
• Yu-Shan Lee 1 ,
• Jiann-Horng Yeh 2 , 3 ,
• Shu-Jung Liu 4 &
• Kuan-Yu Lin   ORCID: orcid.org/0000-0003-0559-3514 2  

Patients with myasthenia gravis (MG), because of their muscle weakness and exposure to corticosteroids treatment, are generally considered to be at increased risk for osteoporosis or fracture. However, clinical evidence of this issue is lacking. In this review, we systematically searched databases, including Cochrane Library, PubMed, Embase, and Airiti library from inception to the end of November 2023 for cohort studies that compared participants with MG and participants without MG for incidence of osteoporosis or fracture. We used the Newcastle–Ottawa Scale for quality assessment. In total, we included 3 studies with 34,865 participants. The pooled meta-analysis using the random effect model demonstrated no significant difference in risk of fracture in the MG group (odds ratio = 1.52; 95% confidence interval = 0.74 to 3.12; I 2  = 93%; between-study variance [τ 2 ] = 0.32) compared with that for the non-MG group. Due to limited studies, we could not perform a quantitative analysis for risk of osteoporosis. In conclusion, we found no robust evidence to support the proposition that patients with MG are at higher risk for fracture than general comparators. The explanations and underlying mechanisms of this finding remain unclear, we therefore conclude that additional studies are warranted.

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Lin, CJ., Lee, YS., Yeh, JH. et al. The association between myasthenia gravis and risk of fracture: a systematic review and meta-analysis. Osteoporos Int (2024). https://doi.org/10.1007/s00198-024-07097-2

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DOI : https://doi.org/10.1007/s00198-024-07097-2

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