Exercise-Induced Mondor's Disease of the Chest Wall in a Nigerian Man: A Case Report.

BACKGROUND: Mondor's disease (MD) is a rare cause of chest pain, characterized by thrombophlebitis of the subcutaneous veins of the anterolateral thoracoabdominal wall. It is a benign, self-limiting condition that is often underdiagnosed due to lack of knowledge of the condition. Although the exact aetiology is unclear, several predisposing factors, including excessive physical activity have been postulated. To the best of our knowledge, there is no previous published report of MD of the chest wall in an adult Nigerian man. OBJECTIVE: To describe the association between muscular strain and the development of MD. CASE PRESENTATION: A 40-year-old Nigerian man presented with a one-month history of dull, aching right-sided chest pain. He gave a history of engaging in intense thoracoabdominal exercises for 6 weeks prior to onset of symptoms. Physical examination revealed a tender, subcutaneous cord-like swelling extending from below the right anterior axillary fold to the right hypochondrium and accentuated by overhead abduction of the right arm. Ultrasonography revealed a hypoechoic, noncompressible right thoracoepigastric vein with no flow on Doppler interrogation, in keeping with superficial venous thrombosis. He was treated with nonsteroidal anti-inflammatory agents and paracetamol. The pain and lesion resolved completely within two weeks after presentation and there was no recurrence over the subsequent four months of follow-up. CONCLUSION: MD is an uncommon cause of chest pain that is often underdiagnosed and underreported due to lack of awareness. It can suddenly appear in persons performing extreme thoracoabdominal exercises. Treatment is essentially symptomatic. Prompt diagnosis of this self-limiting condition is essential in distinguishing it from malignant diseases.

CONTEXTE: La maladie de Mondor (MD) est une cause rare de douleur thoracique, caractérisée par une thrombophlébite des veines sous-cutanées de la paroi thoraco-abdominale antérolatérale. Il s'agit d'une maladie bénigne et spontanément résolutive qui est souvent sous-diagnostiquée en raison d'un manque de connaissance de la maladie. Bien que l'étiologie exacte ne soit pas claire, plusieurs facteurs prédisposants, y compris une activité physique excessive, ont été postulés. Au meilleur de notre connaissance, il n'y a aucun rapport publié précédemment de MD de la paroi thoracique chez un homme Nigérian adulte. OBJECTIF: Décrire l'association entre la tension musculaire et le développement de la MD. PRÉSENTATION DE CAS: Un homme Nigérian de 40 ans s'est présenté avec une histoire d'un mois de douleur thoracique sourde et douloureuse du côté droit. Il a indiqué qu'il s'était engagé dans des exercices thoraco-abdominaux intenses pendant 6 semaines avant l'apparition des symptômes. L'examen physique a révélé une tuméfaction sous-cutanée semblable à un cordon s'étendant du dessous du pli axillaire antérieur droit à l'hypochondre droit et accentuée par une abduction au-dessus du bras droit. L'échographie a révélé une veine thoraco-épigastrique droite hypoéchogène, non compressible et sans débit à l'examen Doppler, en rapport avec une thrombose veineuse superficielle. Il a été traité avec des anti-inflammatoires non stéroïdiens et du paracétamol. La douleur et la lésion ont complètement disparu dans les deux semaines suivant la présentation et il n'y a eu aucune récidive au cours des quatre mois suivants de suivi. CONCLUSION: La MD est une cause rare de douleur thoracique qui est souvent sous-diagnostiquée et sous-déclarée en raison d'un manque de sensibilisation. Il peut apparaître soudainement chez les personnes effectuant des exercices thoraco-abdominaux extrêmes. Le traitement est essentiellement symptomatique. Un diagnostic rapide de cette maladie spontanément résolutive est essentiel pour la distinguer des maladies malignes. Mots clés: maladie de Mondor, exercice, douleur thoracique, thrombophlébite.

Identification of blood biomarkers for psychosis using convergent functional genomics.

There are to date no objective clinical laboratory blood tests for psychotic disease states. We provide proof of principle for a convergent functional genomics (CFG) approach to help identify and prioritize blood biomarkers for two key psychotic symptoms, one sensory (hallucinations) and one cognitive (delusions). We used gene expression profiling in whole blood samples from patients with schizophrenia and related disorders, with phenotypic information collected at the time of blood draw, then cross-matched the data with other human and animal model lines of evidence. Topping our list of candidate blood biomarkers for hallucinations, we have four genes decreased in expression in high hallucinations states (Fn1, Rhobtb3, Aldh1l1, Mpp3), and three genes increased in high hallucinations states (Arhgef9, Phlda1, S100a6). All of these genes have prior evidence of differential expression in schizophrenia patients. At the top of our list of candidate blood biomarkers for delusions, we have 15 genes decreased in expression in high delusions states (such as Drd2, Apoe, Scamp1, Fn1, Idh1, Aldh1l1), and 16 genes increased in high delusions states (such as Nrg1, Egr1, Pvalb, Dctn1, Nmt1, Tob2). Twenty-five of these genes have prior evidence of differential expression in schizophrenia patients. Predictive scores, based on panels of top candidate biomarkers, show good sensitivity and negative predictive value for detecting high psychosis states in the original cohort as well as in three additional cohorts. These results have implications for the development of objective laboratory tests to measure illness severity and response to treatment in devastating disorders such as schizophrenia.

Identifying blood biomarkers for mood disorders using convergent functional genomics.

There are to date no objective clinical laboratory blood tests for mood disorders. The current reliance on patient self-report of symptom severity and on the clinicians' impression is a rate-limiting step in effective treatment and new drug development. We propose, and provide proof of principle for, an approach to help identify blood biomarkers for mood state. We measured whole-genome gene expression differences in blood samples from subjects with bipolar disorder that had low mood vs those that had high mood at the time of the blood draw, and separately, changes in gene expression in brain and blood of a mouse pharmacogenomic model. We then integrated our human blood gene expression data with animal model gene expression data, human genetic linkage/association data and human postmortem brain data, an approach called convergent functional genomics, as a Bayesian strategy for cross-validating and prioritizing findings. Topping our list of candidate blood biomarker genes we have five genes involved in myelination (Mbp, Edg2, Mag, Pmp22 and Ugt8), and six genes involved in growth factor signaling (Fgfr1, Fzd3, Erbb3, Igfbp4, Igfbp6 and Ptprm). All of these genes have prior evidence of differential expression in human postmortem brains from mood disorder subjects. A predictive score developed based on a panel of 10 top candidate biomarkers (five for high mood and five for low mood) shows sensitivity and specificity for high mood and low mood states, in two independent cohorts. Our studies suggest that blood biomarkers may offer an unexpectedly informative window into brain functioning and disease state.

Renin inhibition: a new approach to cardiovascular therapy.

The renin-angiotensin system (RAS) functions as a primary regulator in the short-term and long-term control of blood pressure. Pharmacologic inhibition of the RAS with angiotensin-converting enzyme (ACE) inhibition is effective for treating systemic hypertension and congestive heart failure. As a more specific therapy, the development of renin inhibitors has evolved through various approaches: specific renin antibodies, peptides developed from prosegments of renin precursor, oligopeptides related to pepstatin a universal inhibitor of aspartyl proteinase enzyme, and analogs of angiotensinogen (the renin substrate). Angiotensinogen analogs are promising as therapeutic agents because of high potency, metabolic stability, and good oral bioavailability. Ongoing research is directed towards the application of renin inhibition, the treatment of various cardiovascular disorders, and as a biological probe for understanding the role of the RAS in control of blood pressure and blood volume.

Spectrum of musculo-skeletal disorders in sickle cell disease in Lagos, Nigeria.

BACKGROUND: Sickle cell anemia (SCA) is a common genetic disease in Nigeria. Past studies from West Africa focused on isolated aspects of its medical and surgical presentations. To the best of our knowledge, the musculo-skeletal presentations amongst Nigerians with SCA have not been documented in a single all encompassing study. This work aims to prospectively document the musculo-skeletal disease burden among SCA patients. METHODS: In a prospective study of 318 consecutive patients with genotype-confirmed SCA at the Lagos University Teaching Hospital (LUTH), the musculo-skeletal pathologies, anatomic sites, grade of disease, age at presentation and management outcome were recorded over a one-year period. Data obtained were analyzed using Epi-Info software version 6.0. Data are presented as frequencies (%) and mean values (SD) as appropriate. RESULTS: The HbSS genotype occurred in 296 (93.0%), while 22 (7.0%) were HbSC. 100 (31.4%) patients with average presenting haemoglobin concentration of 8.2 g/100 ml in the study group, presented with 131 musculo-skeletal pathologies in 118 anatomic sites. Osteomyelitis 31 (31%) and septic arthritis 19 (19%) were most commonly observed in children less than 10 years. Skin ulcers and avascular necrosis (AVN) occurred predominantly in the older age groups, with frequencies of 13 (13.0%) and 26 (26.0%) respectively. 20 (71.5%) of diagnosed cases of AVN presented with radiological grade 4 disease. The lower limbs were involved in 84 (71.1%) of sites affected. Lesions involving the spine were rare 11 (0.9%). Multiple presentations occurred in 89 (28.0%) of patients; 62 (69.7%) of which were children below 10 years. CONCLUSIONS: Musculo-skeletal complications are common features of sickle cell anaemia seen in 31.4%. Infectious aetiologies predominate with long bones and joints of lower limbs more commonly affected by osteomyelitis and septic arthritis. Healthcare providers managing SCA should be aware of the potential morbidity and mortality of these conditions to ensure early diagnosis and adequate management.