Özlem Erol

An underdiagnosed hip pathology: apropos of two cases with gluteus medius tendon tears

Until recently, gluteus medius tendon tears have been the sort of hip pathology that is relatively unknown in the realm of rheumatology. Their diagnosis can pose a serious challenge to physicians, despite diligence. In this report we summarize two relevant cases and put forward some hints for their evaluation. Magnetic resonance imaging is quite beneficial in demonstrating the pathology and ruling out other likely pathologies after a prompt physical examination. Physicians should exercise care and vigilance in order not to overlook these cases, in which prompt physical examination and radiological interventions remain a prerequisite in the diagnostic algorithm.

Intravascular papillary endothelial hyperplasia in the finger: not a premier diagnosis

To the Editor, A 58-year-old lady was seen for a tender swelling in her left hand. Two days before, she had noticed a small purplish swelling on the dorsal side of her left fourth finger. Despite her medical history being otherwise non-contributory, on detailed questioning, she recalled having dealt with different types of vegetables (including squash, okra) just one day before she noticed the lesion. She also declared that the bruised area eventually became a lentil-sized nodule. On physical examination, a slightly tender moveable nodule was palpated adjacent to the proximal interphalangeal joint of the fourth finger in the left hand. There were no signs of local inflammation nor any problem pertaining to the tendons, and the digital nerves could be uncovered. An immediate sonography was performed and it revealed a 1.5 3 2.1 mm mass with mixed echogenicity without any relation to the extensor tendon. Then she was consulted to the hand surgeons and, as the patient also accepted, the mass was excised. The pathological diagnosis was established as intravascular papillary endothelial hyperplasia (IPEH). IPEH was first described by the French pathologist Masson as a neoplastic lesion vegetant intravascular hemangioendothelioma’. In 1976, Clerkin and Enzinger proposed the term IPEH, which is currently known as a non-neoplastic reactive endothelial proliferation. It is most commonly located in the skin or the subcutaneous tissue, usually in various vessels following thrombosis. Although there is a predilection for the deep dermis and subcutis of the head, neck, fingers and trunk; IPEH may occur in any location in the body. In subcutaneous localizations the lesion may appear clinically as a small, firm, superficial nodule imparting a red to blue discoloration of the overlying skin. The exact pathogenesis is unknown, but an unusual form of thrombus organization following a trauma is considered to play role. The release of b-fibroblast growth factor (b-FGF) from macrophages attracted to the site is proposed to trigger the proliferation of endothelial cells, which in turn release more b-FGF, leading to a vicious cycle. On the other hand, a history of trauma is rarely noted by the patients – in only 4%. Endothelial proliferation and obstruction of the luminal space of the vascular structures may lead to the enlargement of the mass lesion, necessitating differentiation from a neoplasm. In this regard, intravascular confinement of IPEH, absence of pleomorphism and mitotic atypia are helpful for histological distinction. Overall, excision of the lesion seems to be quite reasonable both for the diagnosis and the treatment.

A 17-Year-Old Girl With a Small Left Hand: Thoracic Outlet Syndrome Is on the Agenda:

the upper extremities were completely normal. Results of Adson, hyperabduction, and Roos tests were positive on the left side, with decreased radial pulse and aggravated aforementioned complaints. The clinical diagnosis was TOS, and further evaluations were performed to clarify the type of TOS and the underlying etiology. Cervical and hand radiographs were inconclusive, except for a length difference of 3 to 4 mm measured from the second metacarpal. Magnetic resonance (MR) angiography confirmed the left subclavian artery compromise during hyperabduction (Figure 2), and MR imaging clearly demonstrated the underlying cause to be hypertrophy of the left scalenus medius and posterior muscles. Results of electrodiagnostic studies of the upper extremities, including dynamic F-wave and medial antebrachial cutaneous nerve evaluations, were unremarkable. The patient was diagnosed as having vascular and disputed neurogenic TOS due to the hypertrophic scalene muscles. A home-based exercise regimen was prescribed for stretching and strengthening the shoulder elevators, along with reassurance and some daily life modifications. Her complaints were found to have improved on the follow-up visit after a month of exercise treatment, and accordingly, she was followed up conservatively.

Accessory nerve injury during amateur wrestling: silent but not overlooked

A 17 year old youth presented complaining of vague chest and back pain. His medical history was unremarkable except for a sports injury three to four months previously. The injury occurred during wrestling when his opponent had fallen on his chest and neck region. On physical examination, we noted an asymmetric neckline on the right, the result of atrophy in the superior portion of the right trapezius muscle. Neck and bilateral shoulder movement, both passive and active, were not limited and were painless. There were no functional deformities such as winging scapula or drooping shoulder. No loss of motor function was detected in the right sternocleidomastoid muscle or during right shoulder elevation. Radiographic examination …

BILATERAL FOOT DROP AFTER INTESTINAL SURGERY: PERONEAL NEUROPATHY UNABATED IN ELDERLY PATIENTS

between apolipoprotein E polymorphism and cardiovascular risk factors in an elderly population with longevity. Arq Bras Cardiol 2002;78:571–579. 5. Wilson PWF, Myers RH, Larson MG et al. Apolipoprotein E alleles, dyslipidemia, and coronary heart disease: The Framingham Offspring Study. JAMA 1995;272:1666–1671. 6. Formiga F, Alia P, Navarro MA et al. Apolipoprotein E genotypes in nonagenarians. J Am Geriatr Soc 2006;54:1471–1473. 7. Niu W, Guo X, Su Y et al. Apolipoprotein E and low-density lipoprotein receptor gene polymorphisms in dyslipidemias-associated essential hypertension. J Hum Hypertens 2007;21:337–339. 8. Imazu M, Yamamoto H, Toyofuku M et al. Association of apolipoprotein E phenotype with hypertension in Japanese-Americans: Data from the HawaiiLos Angeles-Hiroshima Study. Hypertens Res 2001;24:523–529. 9. Scuteri AS, Najjar SS, Muller D et al. ApoE4 allele and the natural history of cardiovascular risk factors. Am J Physiol Endocrinol Metab 2005;289: E322–E327. 10. Lima-Costa MF, Uchôa E, Guerra HL et al. The Bambuı́ Health and Ageing Study (BHAS). Methodological approach and preliminary results of a population-based cohort study of the elderly in Brazil. Rev Saude Pub 2000;34:126–135.

Unilateral Diaphragm Paralysis Possibly Due to Cervical Spine Involvement in Multiple Myeloma

Objective: To describe a patient with unilateral diaphragmatic paralysis due to multiple myeloma (MM) involving the cervical spine and related structures. Case Presentation and Intervention: A 52-year-old female presented with dyspnea, low back and widespread bone pain. She was diagnosed as having MM with vertebral involvement and unilateral paralysis of the diaphragm. She received two cycles of a chemotherapeutic regimen consisting of vincristine-Adriamycin-dexamethasone. The bisphosphonate zoledronic acid was also initiated at the same time. During follow-up, the back pain disappeared and the complaint of dyspnea decreased, although the paralysis persisted. Conclusion: As part of the differential diagnosis of bone and back pain, we draw attention to MMand the rare complication of diaphragmatic paralysis due to phrenic nerve involvement.

Effects of Exercise on Low Density Lipoprotein Receptor Related Protein 5 Gene Expression in Patients With Postmenopausal Osteoporosis

Objectives This study aims to investigate the effects of aerobic exercise on low density lipoprotein receptor related protein 5 (LRP5) gene messenger ribonucleic acid expression and evaluate the relationship between the clinical parameters and gene expression in patients with postmenopausal osteoporosis (OP). Patients and methods Seven patients with postmenopausal OP (mean age 60.0±5.3 years; range 51 to 66 years) were included in the study. An exercise protocol/program consisting of treadmill exercising for 30 minutes three days a week for six weeks was performed at a moderate intensity. LRP5 gene expression levels were evaluated before the onset of the exercise program and then four hours after the end of the first session and 12th (fourth week) and 18th (sixth week) sessions of exercise. Results Our results demonstrated variable changes in the LRP5 gene expression after the aerobic exercise sessions. Excluding one patient, the LRP5 gene expression levels showed a slight tendency to increase. In spite of this tendency, gene expression differences during the exercise sessions were not significant. Conclusion Our results suggest that interindividual variations of LRP5 gene expression exist after moderate intensity aerobic exercises in patients with postmenopausal OP. Despite of this variability, LRP5 gene expression levels increased slightly, except in peripheral blood in one patient. Future studies with larger sample sizes and different sampling time/tissues are required to shed more light on the impact of exercise at molecular level in OP.

Pteridine Pathway in Patients with Degenerative Diseases During Short Time Treatment with Low Dose of Meloxicam, as a Non-steroidal Anti-inflammatory Drug

Abstract The profiles of unconjugated pteridines such as neopterin and biopterin and of tryptophan metabolism change in many pathologic conditions such as rheumatoid arthritis, malignancies and autoimmune diseases and are related to the release of pro-inflammatory cytokines. However, studies on potential effects of drugs are very limited. This study investigates whether meloxicam, a non-steroidal anti-inflammatory drug, may cause any alteration of the pteridine pathway and tryptophan metabolism in 22 patients who admitted to the Physical and Rehabilitation Medicine outpatient clinic in the Hacettepe University Hospital and suffering from various musculoskeletal pain conditions without systemic inflammation. Urine concentrations of neopterin, biopterin and xanthopterin, and serum concentrations of neopterin, tryptophan, and kynurenine, and the activity of dihydropteridine reductase were measured at the beginning of the therapy and after a 15 days treatment with meloxicam. Average urine concentrations (± S.E.M.) of pterins before therapy (neopterin: 263 ± 15.6 μmol/mol creatinine, biopterin: 72.4 ± 13.4 μmol/mol creatinine, and xanthopterin: 675 ± 93.0 μmol/mol creatinine) were not changed during meloxicam therapy (neopterin: 230 ± 30.7 μmol/mol creatinine = 88% of baseline, biopterin 115 ± 26.5 μmol /mol creatinine = 159% of baseline, and xanthopterin 684 ± 88.0 μmol/mol creatinine = 101% of baseline; all differences not significant). The activity of dihydropteridine reductase was 6.02 ± 0.21 nmol/cytochrome C reduced/min/5 mm disc before and 6.28 ± 0.18 nmol/cytochrome C reduced/min/5 mm after treatment (= 104% of baseline; p = 0.088). Serum concentrations of neopterin 6.04 ± 0.33 nmol/L before treatment increased to 6.89 ± 0.48 nmol/L after treatment (= 114% of baseline; p <0.05, paired rank test). Likewise serum kynurenine concentrations increased from 1.52 ± 0.13 μmol/L to 1.87 ± 0.14 μmol/L after treatment (= 123% of baseline; p <0.01). There was a significant correlation between neopterin and kynurenine concentrations which corresponds with their common background of production, namely immune activation. However, also the mean tryptophan concentration in pretreatment samples 51.4 ± 3.34 increased to 59.3 ± 3.34 μmol/L post-treatment (= 115% of baseline; p <0.05). The change of kyn/trp was minor (at baseline: 30.4 ± 2.01, post-treatment: 32.2 ± 2.47 μmol/mmol; = 106% of baseline, not significant). Our findings show an influence of meloxicam treatment on neopterin and tryptophan metabolism in patients. However, significant differences were only found in serum but not in urine of patients. In serum, all marker concentrations increased including tryptophan and kynurenine.

Increased Factor VIII Level Lends Diversity to Ischemic Stroke Etiology

level; prothrombin time; and activated partial thromboplastin time were within normal limits. Further prothrombotic testing results were as follows: fibrinogen 536 mg/dL (144-430), protein C activity 97% (70-130), antithrombin 3 activity 84% (80-120); prothrombin 20210 A mutation, factor V Leiden mutant, and homozygosity for the thermolabile variant of the methylene tetrahydrofolate reductase gene were inconclusive. Anticardiolipin IgG and IgM, and antiphospholipid IgG and IgM were negative. Lipoprotein (a) level was 64.9 mg/dL (0-30), and factor VIII level was 230% (53-70). C reactive protein and erythrocyte sedimentation rate were elevated: 7.55 mg/dL (0-0.80) and 77 mm (0-20), respectively. Consequently, anticoagulation therapy was commenced with enoxaparin and continued with warfarin sodium, and the patient was prescribed antibiotics for his urinary tract infection. He was also started a rehabilitation program composed of active and passive range-of-motion exercises, strengthening exercises for the extremities, posture and balance exercises, gait training, and occupational therapy. The prevalence of increased factor VIII has been found to be 11% in the general population especially in the non-O blood groups. It is one of the most common leading causes of cerebral venous sinus (sinovenous) thrombosis in children, and it is reported to represent a 5-fold increased risk for venous thrombosis compared to individuals with normal levels. It has been reported that compared to controls, children with high factor VIII levels have a 5-fold increased risk for stroke. In 1982, Mettinger and Egberg suggested that high levels of factor VIII might predispose for thrombosis/atherosclerosis also in adults younger than 55 years of age. In addition, it has been found to be responsible for acute coronary syndromes especially in men. More recent literature confirms To the Editor: A 47-year-old man was admitted for left hemiparesia, imbalance in walking, and incontinence. His medical history revealed 2 similar previous attacks that had resolved. The first episode had occurred 6 years ago with right hemiparesia and dysarthria, after which he had been given aspirin and pentoxyphylline. When the symptoms recurred 7 months ago, a thorough evaluation was performed, including cerebral perfusion magnetic resonance imaging (MRI) and cerebral perfusion scintigraphy, the results of which were relevant with ischemia of the left frontoparietal cortex. The lumbar puncture and Doppler ultrasonography (DUS) of the vertebral and carotid arteries were then normal. His medical history regarding stroke risk factors, including age, smoking, hypertension, diabetes, hyperlipidemia, and cardiac disease except gender, was unremarkable. Current physical examination yielded weakness on the left side; normal light touch, pinprick, position, and vibratory sensations; and normal deep tendon reflexes. An MRI was consistent with acute ischemic findings in the right cerebral hemisphere, posterior frontal cortical area, and the right thalamus. Positron emission tomography and cerebral angiography, DUS of the lower extremities, and transthoracic and transesophageal echocardiography were normal. Serial DUS depicted occlusion of the right internal carotid artery initially, then it resolved during the follow-up. Laboratory evaluations consisting of complete blood count; renal, liver, and thyroid function tests; lipid profile; homocysteine