Publications by authors named "Richard A Hickman"

18 Publications

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COVID-19 neuropathology at Columbia University Irving Medical Center/New York Presbyterian Hospital.

Brain 2021 Apr 15. Epub 2021 Apr 15.

Department of Pathology and Cell Biology, Division of Neuropathology, Vagelos College of Physicians and Surgeons, Columbia University Irving Medical Center, and the New York Presbyterian Hospital, New York, NY, 10032, USA.

Many patients with SARS-CoV-2 infection develop neurological signs and symptoms, though, to date, little evidence exists that primary infection of the brain is a significant contributing factor. We present the clinical, neuropathological, and molecular findings of 41 consecutive patients with SARS-CoV-2 infections who died and underwent autopsy in our medical center. The mean age was 74 years (38-97 years), 27 patients (66%) were male and 34 (83%) were of Hispanic/Latinx ethnicity. Twenty-four patients (59%) were admitted to the intensive care unit (ICU). Hospital-associated complications were common, including 8 (20%) with deep vein thrombosis/pulmonary embolism (DVT/PE), 7 (17%) patients with acute kidney injury requiring dialysis, and 10 (24%) with positive blood cultures during admission. Eight (20%) patients died within 24 hours of hospital admission, while 11 (27%) died more than 4 weeks after hospital admission. Neuropathological examination of 20-30 areas from each brain revealed hypoxic/ischemic changes in all brains, both global and focal; large and small infarcts, many of which appeared hemorrhagic; and microglial activation with microglial nodules accompanied by neuronophagia, most prominently in the brainstem. We observed sparse T lymphocyte accumulation in either perivascular regions or in the brain parenchyma. Many brains contained atherosclerosis of large arteries and arteriolosclerosis, though none had evidence of vasculitis. Eighteen (44%) contained pathologies of neurodegenerative diseases, not unexpected given the age range of our patients. We examined multiple fresh frozen and fixed tissues from 28 brains for the presence of viral RNA and protein, using quantitative reverse-transcriptase PCR (qRT-PCR), RNAscope, and immunocytochemistry with primers, probes, and antibodies directed against the spike and nucleocapsid regions. qRT-PCR revealed low to very low, but detectable, viral RNA levels in the majority of brains, although they were far lower than those in nasal epithelia. RNAscope and immunocytochemistry failed to detect viral RNA or protein in brains. Our findings indicate that the levels of detectable virus in COVID-19 brains are very low and do not correlate with the histopathological alterations. These findings suggest that microglial activation, microglial nodules and neuronophagia, observed in the majority of brains, do not result from direct viral infection of brain parenchyma, but rather likely from systemic inflammation, perhaps with synergistic contribution from hypoxia/ischemia. Further studies are needed to define whether these pathologies, if present in patients who survive COVID-19, might contribute to chronic neurological problems.
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http://dx.doi.org/10.1093/brain/awab148DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8083258PMC
April 2021

Pathogenic Huntingtin Repeat Expansions in Patients with Frontotemporal Dementia and Amyotrophic Lateral Sclerosis.

Neuron 2021 02 26;109(3):448-460.e4. Epub 2020 Nov 26.

Molecular Markers Laboratory, IRCCS Istituto Centro San Giovanni di Dio Fatebenefratelli, Brescia 25125, Italy; MAC Memory Clinic, IRCCS Istituto Centro San Giovanni di Dio Fatebenefratelli, Brescia 25125, Italy.

We examined the role of repeat expansions in the pathogenesis of frontotemporal dementia (FTD) and amyotrophic lateral sclerosis (ALS) by analyzing whole-genome sequence data from 2,442 FTD/ALS patients, 2,599 Lewy body dementia (LBD) patients, and 3,158 neurologically healthy subjects. Pathogenic expansions (range, 40-64 CAG repeats) in the huntingtin (HTT) gene were found in three (0.12%) patients diagnosed with pure FTD/ALS syndromes but were not present in the LBD or healthy cohorts. We replicated our findings in an independent collection of 3,674 FTD/ALS patients. Postmortem evaluations of two patients revealed the classical TDP-43 pathology of FTD/ALS, as well as huntingtin-positive, ubiquitin-positive aggregates in the frontal cortex. The neostriatal atrophy that pathologically defines Huntington's disease was absent in both cases. Our findings reveal an etiological relationship between HTT repeat expansions and FTD/ALS syndromes and indicate that genetic screening of FTD/ALS patients for HTT repeat expansions should be considered.
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http://dx.doi.org/10.1016/j.neuron.2020.11.005DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7864894PMC
February 2021

Gonadotroph tumours with a low SF-1 labelling index are more likely to recur and are associated with enrichment of the PI3K-AKT pathway.

Neuropathol Appl Neurobiol 2021 04 20;47(3):415-427. Epub 2020 Dec 20.

Department of Medicine, Columbia University Medical Center, New York, NY, USA.

Aims: The gonadotroph tumour (GT) is the most frequently resected pituitary neuroendocrine tumour. Although many symptomatic GT are successfully resected, some recur. We sought to identify histological biomarkers that may predict recurrence and explore biological mechanisms that explain this difference in behaviour.

Methods: SF-1 immunohistochemistry of 51 GT, a subset belonging to a longitudinal prospective cohort study (n = 25), was reviewed. Four groups were defined: Group 1-recently diagnosed GT (n = 20), Group 2-non-recurrent GT with long-term follow up (n = 11), Group 3-initial resections of GT that recur (n = 7) and Group 4-recurrent GT (n = 13). The percentage of SF-1 immunolabelling in the lowest staining fields (SF-1 labelling index (SLI)) was assessed and RNA sequencing was performed on 5 GT with SLI <80% and 5 GT with SLI >80%.

Results: Diffuse, strong SF-1 immunolabelling was the most frequent pattern in Groups 1/2, whereas patchy SF-1 staining predominated in Groups 3/4. There was a lower median SLI in Groups 3/4 than 1/2. Overall, GT with SLI <80% recurred earlier than GT with SLI >80%. Differential expression analysis identified 89 statistically significant differentially expressed genes (FDR <0.05) including over-expression of pituitary stem cell genes (SOX2, GFRA3) and various oncogenes (e.g. BCL2, ERRB4) in patchy SF-1 GT. Gene set enrichment analysis identified significant enrichment of genes involved in the PI3K-AKT pathway.

Conclusions: We speculate that patchy SF-1 labelling in GT reflects intratumoural heterogeneity and are less differentiated tumours than diffusely staining GT. SF-1 immunolabelling patterns may have prognostic significance in GT, but confirmatory studies are needed for further validation.
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http://dx.doi.org/10.1111/nan.12675DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7987644PMC
April 2021

Authors' replies to the comments of Koga et al. on "Movement disorders rounds: A case of missing pathology in a patient with LRRK2 Parkinson's disease".

Parkinsonism Relat Disord 2020 Sep 5. Epub 2020 Sep 5.

Department of Neurology, Columbia University College of Physicians and Surgeons, Columbia University Medical Center, 710 West 168th Street, New York, NY, 10032, USA. Electronic address:

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http://dx.doi.org/10.1016/j.parkreldis.2020.08.037DOI Listing
September 2020

Neuronophagia and microglial nodules in a SARS-CoV-2 patient with cerebellar hemorrhage.

Acta Neuropathol Commun 2020 08 26;8(1):147. Epub 2020 Aug 26.

Department of Pathology and Cell Biology, Vagelos College of Physicians and Surgeons, Columbia University Irving Medical Center and the New York Presbyterian Hospital, New York, NY, USA.

We document the neuropathologic findings of a 73-year old man who died from acute cerebellar hemorrhage in the context of relatively mild SARS-CoV2 infection. The patient developed sudden onset of headache, nausea, and vomiting, immediately followed by loss of consciousness on the day of admission. Emergency medical services found him severely hypoxemic at home, and the patient suffered a cardiac arrest during transport to the emergency department. The emergency team achieved return of spontaneous circulation after over 17 min of resuscitation. A chest radiograph revealed hazy bilateral opacities; and real-time-PCR for SARS-CoV-2 on the nasopharyngeal swab was positive. Computed tomography of the head showed a large right cerebellar hemorrhage, with tonsillar herniation and intraventricular hemorrhage. One day after presentation, he was transitioned to comfort care and died shortly after palliative extubation. Autopsy performed 3 h after death showed cerebellar hemorrhage and acute infarcts in the dorsal pons and medulla. Remarkably, there were microglial nodules and neuronophagia bilaterally in the inferior olives and multifocally in the cerebellar dentate nuclei. This constellation of findings has not been reported thus far in the context of SARS-CoV-2 infection.
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http://dx.doi.org/10.1186/s40478-020-01024-2DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7447601PMC
August 2020

Primary Age-Related Tauopathy (PART): Addressing the Spectrum of Neuronal Tauopathic Changes in the Aging Brain.

Curr Neurol Neurosci Rep 2020 07 14;20(9):39. Epub 2020 Jul 14.

Departments of Neurology, Pathology and Psychiatry, Center for Cognitive Neurology, NYU School of Medicine, Science Building, Rm 1017, 435 East 30th Street, New York, NY, 10016, USA.

Purpose Of Review: Primary age-related tauopathy (PART) was recently proposed as a pathologic diagnosis for brains that harbor neurofibrillary tangles (Braak stage ≤ 4) with little, if any, amyloid burden. We sought to review the clinicopathologic findings related to PART.

Recent Findings: Most adult human brains show at least focal tauopathic changes, and the majority of individuals with PART do not progress to dementia. Older age and cognitive impairment correlate with increased Braak stage, and multivariate analyses suggest that the rate of cognitive decline is less than matched patients with Alzheimer disease (AD). It remains unclear whether PART is a distinct tauopathic entity separate from AD or rather represents an earlier histologic stage of AD. Cognitive decline in PART is usually milder than AD and correlates with tauopathic burden. Biomarker and ligand-based radiologic studies will be important to define PART antemortem and prospectively follow its natural history.
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http://dx.doi.org/10.1007/s11910-020-01063-1DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7849162PMC
July 2020

Meningomyeloencephalitis secondary to Mycobacterium haemophilum infection in AIDS.

Acta Neuropathol Commun 2020 05 19;8(1):73. Epub 2020 May 19.

Department of Pathology & Cell Biology, Columbia University Irving Medical Center, New York, NY, 10032, USA.

Infections by opportunistic non-tuberculous mycobacteria (NTM) are rising in global incidence. One emerging, slowly growing NTM is Mycobacterium haemophilum, which can cause skin, lung, bone, and soft tissue infections in immunocompromised patients as well as lymphadenitis in immunocompetent individuals. Detection of this microorganism is difficult using conventional culture-based methods and few reports have documented involvement of this pathogen within the central nervous system (CNS).We describe the neuropathologic autopsy findings of a 39-year-old man with AIDS who died secondary to M. haemophilum CNS infection. He initially presented with repeated bouts of pyrexia, nausea and vomiting, and altered mental status that required numerous hospitalizations. CSF infectious workups were consistently negative. His most recent admission identified hyperintensities within the brainstem by MRI and despite antibiotic therapies for suspected CNS infection, he died. Autopsy revealed a swollen brain with marked widening of the brainstem. Microscopic examination of the brain and spinal cord showed focal lymphohistiocytic infiltrates, gliosis and neuronal loss that were associated with acid-fast bacilli (AFB). The brainstem was the most severely damaged and AFB were found to congregate along arterial territories lending support to the notion of hematogenous spread as a mechanism for the organisms' dissemination. 16S rRNA sequencing on formalin-fixed paraffin-embedded tissue enabled post-mortem identification of M. haemophilum. This sequencing methodology may permit diagnosis on CSF intra-vitam.
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http://dx.doi.org/10.1186/s40478-020-00937-2DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7236527PMC
May 2020

Presenting Features in 269 Patients With Clinically Nonfunctioning Pituitary Adenomas Enrolled in a Prospective Study.

J Endocr Soc 2020 Apr 18;4(4):bvaa021. Epub 2020 Feb 18.

Departments of Neurosurgery, Mount Sinai School of Medicine, New York, New York.

Context: Clinically nonfunctioning pituitary adenomas (CNFPAs) typically remain undetected until mass effect symptoms develop. However, currently, head imaging is performed commonly for many other indications, which may increase incidental discovery of CNFPAs. Since current presentation and outcome data are based on older, retrospective series, a prospective characterization of a contemporary CNFPA cohort was needed.

Objective: To determine the prevalence of incidental presentation and hypopituitarism and its predictors in a CNFPA cohort that spanned 6 to 9 mm micro- to macroadenoma included observational and surgical therapy.

Methods: At enrollment in a prospective, observational study, 269 patients with CNFPAs were studied by history, examination, blood sampling, and pituitary imaging analysis and categorized into incidental or symptoms presentation groups that were compared.

Results: Presentation was incidental in 48.7% of patients and due to tumor symptoms in 51.3%. In the symptoms and incidental groups, 58.7% and 27.4% of patients had hypopituitarism, respectively, and 25% of patients with microadenomas had hypopituitarism. Many had unappreciated signs and symptoms of pituitary disease. Most tumors were macroadenomas (87%) and were larger in the symptoms than incidental and hypopituitary groups than in the eupituitary groups. The patients in the incidental group were older, and males were older and had larger tumors in both the incidental and symptoms groups.

Conclusions: Patients with CNFPAs commonly present incidentally and with previously unrecognized hypopituitarism and symptoms that could have prompted earlier diagnosis. Our data support screening all large micro and macro-CNFPAs for hypopituitarism. Most patients with CNFPAs still have mass effect signs at presentation, suggesting the need for more awareness of pituitary disease. Our ongoing, prospective observation of this cohort will assess outcomes of these CNFPA groups.
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http://dx.doi.org/10.1210/jendso/bvaa021DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7101088PMC
April 2020

Rasmussen Encephalitis: An Update.

Semin Neurol 2020 Apr 17;40(2):201-210. Epub 2020 Mar 17.

Department of Neurology, Columbia University Irving Medical Center, New York, New York.

Rasmussen encephalitis (RE) is a rare, devastating, progressive pediatric epilepsy. First described 60 years ago, RE continues to present challenges in diagnosis and management. RE causes a unilateral focal epilepsy in children that typically becomes medically refractory, results in significant hemiparesis, and causes progressive cognitive decline. The etiology is a cell-mediated immune attack on one cerebral hemisphere, though the inciting antigen remains unknown. While the underlying histopathology is unilateral and RE is described as "unihemispheric," studies have demonstrated (1) atrophy of the unaffected hemisphere, (2) electroencephalographic abnormalities (slowing and spikes) in the unaffected hemisphere, and (3) cognitive decline referable to the unaffected hemisphere. These secondary contralateral effects likely reflect the impact of uncontrolled epileptic activity (i.e., epileptic encephalopathy). Hemispheric disconnection (HD) renders 70 to 80% of patients seizure free. While it has the potential to limit the influence of seizures and abnormal electrical activity emanating from the pathological hemisphere, HD entails hemiparesis and hemianopia, as well as aphasia for patients with dominant HD. With the recent expansion of available immunomodulatory therapies, there has been interest in identifying an alternative to HD, though evidence for disease modification is limited to date. We review what is known and what remains unknown about RE.
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http://dx.doi.org/10.1055/s-0040-1708504DOI Listing
April 2020

A rare case of anal carcinosarcoma with human papilloma virus infection in both biphasic tumor elements: An immunohistochemical, molecular and ultrastructural study.

Papillomavirus Res 2016 Dec 28;2:164-166. Epub 2016 Sep 28.

Department of Veterans Affairs New York Harbor Healthcare System, New York, NY 10010, USA.

Carcinosarcoma of the anus is rare and has yet to be reportedly associated with the keratinocyte-specific Human Papilloma Virus (HPV). We describe a case of anal carcinosarcoma with HPV infection in both the epithelial and mesenchymal components of the tumor by immunohistochemistry, chromogenic in-situ hybridization (CISH) and further supported by electron microscopy (EM). Microscopic examination of the tumor showed nests of poorly-differentiated invasive squamous cell carcinoma with basaloid features intermixed with a hypercellular, atypical spindle cell proliferation. Immunohistochemistry demonstrated that the epithelial component was positive for AE1/AE3, p63, CK5/6 and p16, whilst the mesenchymal component was positive for smooth muscle actin, vimentin, and focally positive for desmin and p16, consistent with carcinosarcoma. The tumor was negative for GATA-3, CK7 and CK20. CISH demonstrated that the tumor was positive for high risk HPV (subtype 16/18) in both tumor components. EM further supported the presence of intracellular virus particles (~50 nm) that is compatible with HPV infection. Infection of both epithelial and mesenchymal tumor components by HPV has not been previously observed in the gastrointestinal tract. This finding may represent initial epithelial HPV infection with subsequent divergent tumoral differentiation and suggests the presence of viral replication in both biphasic tumor components.
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http://dx.doi.org/10.1016/j.pvr.2016.09.002DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5467539PMC
December 2016

Proteomic differences in amyloid plaques in rapidly progressive and sporadic Alzheimer's disease.

Acta Neuropathol 2017 06 4;133(6):933-954. Epub 2017 Mar 4.

Department of Neurology, Center for Cognitive Neurology, NYU School of Medicine, New York, NY, USA.

Rapidly progressive Alzheimer's disease (rpAD) is a particularly aggressive form of Alzheimer's disease, with a median survival time of 7-10 months after diagnosis. Why these patients have such a rapid progression of Alzheimer's disease is currently unknown. To further understand pathological differences between rpAD and typical sporadic Alzheimer's disease (sAD) we used localized proteomics to analyze the protein differences in amyloid plaques in rpAD and sAD. Label-free quantitative LC-MS/MS was performed on amyloid plaques microdissected from rpAD and sAD patients (n = 22 for each patient group) and protein expression differences were quantified. On average, 913 ± 30 (mean ± SEM) proteins were quantified in plaques from each patient and 279 of these proteins were consistently found in plaques from every patient. We found significant differences in protein composition between rpAD and sAD plaques. We found that rpAD plaques contained significantly higher levels of neuronal proteins (p = 0.0017) and significantly lower levels of astrocytic proteins (p = 1.08 × 10). Unexpectedly, cumulative protein differences in rpAD plaques did not suggest accelerated typical sAD. Plaques from patients with rpAD were particularly abundant in synaptic proteins, especially those involved in synaptic vesicle release, highlighting the potential importance of synaptic dysfunction in the accelerated development of plaque pathology in rpAD. Combined, our data provide new direct evidence that amyloid plaques do not all have the same protein composition and that the proteomic differences in plaques could provide important insight into the factors that contribute to plaque development. The cumulative protein differences in rpAD plaques suggest rpAD may be a novel subtype of Alzheimer's disease.
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http://dx.doi.org/10.1007/s00401-017-1691-0DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5503748PMC
June 2017

"Nature versus Nurture" and the indigenous microbiome.

J Public Health Emerg 2017 Mar 16;1. Epub 2017 Mar 16.

New York University School of Medicine, New York, NY, USA.

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http://dx.doi.org/10.21037/jphe.2017.03.08DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6145807PMC
March 2017

Atypical Intraductal Cribriform Proliferations of the Prostate Exhibit Similar Molecular and Clinicopathologic Characteristics as Intraductal Carcinoma of the Prostate.

Am J Surg Pathol 2017 Apr;41(4):550-556

*Department of Pathology and Urology, New York University Langone Medical Center, New York, NY †Miraca Life Sciences, Dallas, TX.

Atypical intraductal cribriform proliferations of the prostate (AIP) are loose cribriform proliferations of luminal cells that exhibit greater architectural complexity and/or nuclear atypia than high-grade prostatic intraepithelial neoplasia (HGPIN), but lack the diagnostic criteria for intraductal carcinoma (IDC). The significance of AIP has not been formally established. We compared the clinical, morphologic, and immunohistochemical characteristics of AIP with classic IDC in 310 radical prostatectomy specimens that were received over an 18-month period. Of the 310 cases, 46 cases had AIP only (n=10), IDC only (n=6), or AIP coexisting with IDC (n=30). The ERG status of all 46 AIP/IDC cases was identical to the nearby acinar carcinoma, contrasted to just 3 cases of HGPIN (7%, P<0.01). The degree of uniform phosphatase and tensin homolog (PTEN) loss in 34 selected cases was identical in AIP and IDC (66.7%). No foci of HGPIN showed uniform PTEN loss; there was only 38% concordance of PTEN expression pattern between HGPIN and the nearby acinar carcinoma, unlike AIP and IDC (77% and 81%, respectively, P<0.01). AIP-associated and/or IDC-associated carcinoma (n=46) showed a higher stage and grade compared with acinar-only carcinoma (n=264, P<0.01). AIP-associated carcinoma had similar clinicopathologic features as IDC-associated carcinoma, including preoperative prostate-specific antigen, Gleason score, extraprostatic extension, seminal vesicle invasion, and lymph node metastasis (n=36, P>0.05). In conclusion, AIP shares similar ERG/PTEN immunoprofiles and exhibits similar clinical behavior as IDC, warranting immediate repeat biopsy when AIP is identified on biopsy, as is recommended in the most recent WHO Classification of Tumours of the Urinary System and Male Genital Organs, 2016.
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http://dx.doi.org/10.1097/PAS.0000000000000794DOI Listing
April 2017

Alzheimer Disease and Its Growing Epidemic: Risk Factors, Biomarkers, and the Urgent Need for Therapeutics.

Neurol Clin 2016 11 4;34(4):941-953. Epub 2016 Aug 4.

Department of Pathology, The Center for Cognitive Neurology, New York University School of Medicine, Alexandria ERSP, 450 East 29th Street, New York, NY 10016, USA; Department of Neurology, The Center for Cognitive Neurology, New York University School of Medicine, Alexandria ERSP, 450 East 29th Street, New York, NY 10016, USA; Department of Psychiatry, The Center for Cognitive Neurology, New York University School of Medicine, Alexandria ERSP, 450 East 29th Street, New York, NY 10016, USA. Electronic address:

Alzheimer disease (AD) represents one of the greatest medical challenges of this century; the condition is becoming increasingly prevalent worldwide and no effective treatments have been developed for this terminal disease. Because the disease manifests at a late stage after a long period of clinically silent neurodegeneration, knowledge of the modifiable risk factors and the implementation of biomarkers is crucial in the primary prevention of the disease and presymptomatic detection of AD, respectively. This article discusses the growing epidemic of AD and antecedent risk factors in the disease process. Disease biomarkers are discussed, and the implications that this may have for the treatment of this currently incurable disease.
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http://dx.doi.org/10.1016/j.ncl.2016.06.009DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5116320PMC
November 2016

Inflammatory myofibroblastic tumour of the testis with confirmed anaplastic lymphoma kinase gene rearrangement.

Histopathology 2016 Jun 19;68(7):1109-11. Epub 2016 Jan 19.

Department of Pathology, NYU School of Medicine, NYU Langone Medical Center, New York, NY, USA.

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http://dx.doi.org/10.1111/his.12888DOI Listing
June 2016

Causes and management of infertility in systemic lupus erythematosus.

Rheumatology (Oxford) 2011 Sep 7;50(9):1551-8. Epub 2011 Jun 7.

Rheumatology Research Group, School of Immunity and Infection, College of Medical and Dental Sciences, University of Birmingham, Birmingham, UK.

SLE is a multi-system, autoimmune condition that can influence both male and female fertility. Inability to conceive may be attributed to several factors that may act singly or in combination: (i) older age in patients with SLE compared with healthy controls; (ii) disease-related infertility; and (iii) infertility through gonadotoxic treatments. In addition, psychosocial factors related to the disease may lower fecundity and may be associated with apparent infertility. Many therapeutic avenues are open to counteract reproductive damage in the management of SLE and to assist conception once infertility is diagnosed. These treatments can include the administration of gonadotrophin-receptor hormone analogues while receiving CYC treatment, the use of assisted reproductive technologies, such as in vitro fertilization and psychosocial intervention to promote a healthier relationship with their partner. Knowledge of how these reproductive problems occur and its prevention/treatment in SLE patients should avert irreversible infertility as well as give hope to SLE patients with infertility.
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http://dx.doi.org/10.1093/rheumatology/ker105DOI Listing
September 2011