A complicated pulmonary hydatid cyst resembling a tumour in an adult on PET scan: a case report

xloma.fota13 shared this article with you from Inoreader A complicated pulmonary hydatid cyst resembling a tumour in an adult on PET scan: a case report Via Journal of Surgical Case Reports - current issue Abstract Complicated pulmonary cysts have a wide range of possible diagnoses with different approaches as they can be benign or malignant. They can resemble malignancies in symptoms and imaging, mainly on positron emission tomography (PET) scan, which can increase the false positivity. We present an infected hydatid cyst resembling a malignancy as it presented with weight loss in a smoker and had necrosis and malignance features on computed tomography and PET scans. However, serology tests and fine needle aspiration were suggestive of a hydatid cyst, which made this case quite unique. Other diagnoses should always be suspected even if the malignancy was highly likely due to other lesions can resemble malignancies. View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.

Scalp mass: an atypical presentation of multiple myeloma

xloma.fota13 shared this article with you from Inoreader Scalp mass: an atypical presentation of multiple myeloma Via Journal of Surgical Case Reports - current issue Abstract A 64-year-old male with no histor y of trauma presented to the general surgery clinic with a 6-month history of an asymptomatic left parietal scalp mass. The differential included benign etiologies such as lipoma or sebaceous cyst. At surgery, a hemorrhagic soft tissue mass with underlying defect in the parietal calvarium was noted. The initial attempt at resection was abandoned and neurosurgical consultation was requested. Magnetic resonance imaging demonstrated an enhancing scalp mass with a lytic lesion of the parietal calvarium with no intradural extension. Craniectomy with mass resection and mesh cranioplasty were performed. Pathology confirmed plasma cell neoplasm; serum protein electrophoresis and lytic skull lesions confirmed multiple myeloma. This rare presentation of multiple myeloma serves as a call for providers to maintain a broad differential when evaluating a seemingly benign mass, consider rare etiologies when appropriate and maintain vigilance for abnormal findings during any procedure. View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.

Unusual disseminated Talaromyces marneffei infection mimicking lymphoma

xloma.fota13 shared this article with you from Inoreader Unusual disseminated Talaromyces marneffei infection mimicking lymphoma in a non-immunosuppressed patient in East China: a case report and review of the literature Via BMC Infectious Diseases - Latest Articles Talaromyces marneffei infection is an important opportunistic infection associated with acquired immune deficiency syndrome (AIDS). However, it is unusual in patients with non-AIDS and other non-immunosuppressed ... View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.

Hypoxia induces transcriptional and translational downregulation of the type I interferon (IFN) pathway in multiple cancer cell types

xloma.fota13 shared this article with you from Inoreader Hypoxia induces transcriptional and translational downregulation of the type I interferon (IFN) pathway in multiple cancer cell types Via Cancer Research Online First Articles Hypoxia is a common phenomenon in solid tumors and is strongly linked to hallmarks of cancer. Recent evidence has shown that hypoxia promotes local immune suppression. Type I IFN supports cytotoxic T lymphocytes by stimulating the maturation of dendritic cells (DC) and enhancing their capacity to process and present antigens. However, little is known about the relationship between hypoxia and the type I interferon (IFN) pathway, which comprises the sensing of double-stranded RNA and DNA (dsRNA/dsDNA) followed by IFNα/β secretion and transcriptional activation of IFN-stimulated genes (ISG). In this study, we determined the effects of hypoxia on the type I IFN pathway in breast cancer and the mechanisms involved. In cancer cell lines and xenograft models, mRNA and protein expression of the type I IFN pathway were downregulated under hypoxic conditions. This pathway was suppressed at each level of signaling, from the dsRNA sensors RIG-I and MDA5, the adaptor MAVS, transcription factors IRF3, IRF7, and STAT1, and several ISG including RIG-I, IRF7, STAT1, and ADAR-p150. Importantly, IFN secretion was reduced under hypoxic conditions. HIF1α- and HIF2α-mediated regulation of gene expression did not explain most of the effects. However, ATAC-seq data revealed in hypoxia that peaks with STAT1 and IRF3 motifs had decreased accessibility. Collectively, these results indicate that hypoxia leads to an overall downregulation of the type I IFN pathway due to repressed transcription and lower chromatin accessibility in a HIF1/2α-independent manner, which could contribute to immunosuppression in hypoxic tumors. View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.

Chromatin Looping Shapes KLF5-dependent Transcriptional Programs in Human Epithelial Cancers

xloma.fota13 shared this article with you from Inoreader Chromatin Looping Shapes KLF5-dependent Transcriptional Programs in Human Epithelial Cancers Via Cancer Research Online First Articles Activation of transcription factors is a key driver event in cancer. We and others have recently reported that the Krüppel-like transcription factor KLF5 is activated in multiple epithelial cancer types including squamous cancer and gastrointestinal adenocarcinoma, yet the functional consequences and the underlying mechanisms of this activation remain largely unknown. Here we demonstrate that activation of KLF5 results in strongly selective KLF5 dependency for these cancer types. KLF5 bound lineage-specific regulatory elements and activated gene expression programs essential to cancer cells. HiChIP analysis revealed that multiple distal KLF5 binding events cluster and synergize to activate individual target genes. Immunoprecipitation-mass spectrometry assays showed that KLF5 interacts with other transcription factors such as TP63 and YAP1, as well as the CBP/EP300 acetyltransferase complex. Furthermore, KLF5 guided the CBP/EP300 complex to increase acetylation of H3K27, which in turn enhanced recruitment of the bromodomain protein BRD4 to chromatin. The 3D chromatin architecture aggregated KLF5-dependent BRD4 binding to activate Polymerase II (POL2) elongation at KLF5-target genes, which conferred a transcriptional vulnerability to proteolysis-targeting chimera (PROTAC)-induced degradation of BRD4. Our study demonstrates that KLF5 plays an essential role in multiple epithelial cancers by activating cancer-related genes through 3D chromatin loops, providing an evidence-based rationale for targeting the KLF5 pathway. View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.

Chemotherapy-Induced Upregulation of Small Extracellular Vesicle-Associated PTX3 Accelerates Breast Cancer Metastasis

xloma.fota13 shared this article with you from Inoreader Chemotherapy-Induced Upregulation of Small Extracellular Vesicle-Associated PTX3 Accelerates Breast Cancer Metastasis Via Cancer Research Online First Articles Although neoadjuvant chemotherapy is a standard component of breast cancer treatment, recent evidence suggests that chemotherapeutic drugs can promote metastasis through poorly-defined mechanisms. Here we utilize xenograft mouse models of triple-negative breast cancer to explore the importance of chemotherapy-induced tumor-derived small extracellular vesicles (sEV) in metastasis. Doxorubicin (DXR) enhanced tumor cell sEV secretion to accelerate pulmonary metastasis by priming the pre-metastatic niche. Proteomic analysis and CRISPR/Cas9 gene editing identified the inflammatory glycoprotein PTX3 enriched in DXR-elicited sEV as a critical regulator of chemotherapy-induced metastasis. Both genetic inhibition of sEV secretion from primary tumors and pharmacologic inhibition of sEV uptake in secondary organs suppressed metastasis following chemotherapy. Taken together, this research uncovers a mechanism of chemotherapy-mediated metastasis by which drug-induced upregulation of sEV sec retion and PTX3 protein cargo primes the pre-metastatic niche and suggests that inhibition of either sEV uptake in secondary organs or secretion from primary tumor cells may be promising therapeutic strategies to suppress metastasis. View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.

Circ_0001421 facilitates glycolysis and lung cancer development by regulating miR-4677-3p/CDCA3

xloma.fota13 shared this article with you from Inoreader Circ_0001421 facilitates glycolysis and lung cancer development by regulating miR-4677-3p/CDCA3 Via Diagnostic Pathology - Latest Articles Lung cancer (LC) is a malignant tumor originating in the bronchial mucosa or gland of the lung. Circular RNAs (circRNAs) are proved to be key regulators of tumor progression. However, the regulatory effect of ... View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.

Distinct Genomic Alterations in Prostate Tumors

xloma.fota13 shared this article with you from Inoreader Distinct Genomic Alterations in Prostate Tumors Derived from African American Men Via Molecular Cancer Research Online First Articles We aim to understand, from acquired genetic alterations in tumors, why African American (AA) men are more likely to develop aggressive prostate cancer. By analyzing somatic mutations in 39 genes using deeper next-generation sequencing with an average depth of 2,522 reads for tumor DNA and genome-wide DNA copy-number alterations (CNA) in prostate cancer in a total of 171 AA/black men and comparing with those in 860 European American (EA)/white men, we here present several novel findings. First, >35% of AA men harbor damaging mutations in APC, ATM, BRCA2, KDM6A, KMT2C, KMT2D, MED12, ZFHX3, and ZMYM3, each with >1% of mutated copies. Second, among genes with >10% of mutated copies in tumor cells, ZMYM3 is the most frequently mutated gene in AA prostate cancer. In a patient's tumor with >96% frameshift mutations of ZMYM3, we find allelic imbalances in 10 chromosomes, including losses of five and gains of another four chr omosomes, suggesting its role in maintaining genomic integrity. Third, when compared to prostate cancer in EA/white men, a higher frequency of CNAs of MYC, THADA, NEIL3, LRP1B, BUB1B, MAP3K7, BNIP3L and RB1, and a lower frequency of deletions of RYBP, TP53, and TMPRSS2-ERG are observed in AA/black men. Finally, for the above genes with higher frequency of CNAs in AA than in EA, deletion of MAP3K7, BNIP3L, NEIL3 or RB1, or gain of MYC significantly associates with both higher Gleason grade and advanced pathologic stage in AA/black men. Deletion of THADA associates with advanced pathologic stage only. Implications: A higher frequency of damaging mutation in ZMYM3 causing genomic instability along with higher frequency of altered genomic regions including deletions of MAP3K7, BNIP3L, RB1, and NEIL3, and gain of MYC appear to be distinct somatically acquired genetic alterations that ma y contribute to more aggressive prostate cancer in AA/black men. View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.

Irrespective of the degree of hyperlactatemia, similar lactate levels were associated with a lower mortality rate in metformin users compared with non-users: beware of confounders!

xloma.fota13 shared this article with you from Inoreader Irrespective of the degree of hyperlactatemia, similar lactate levels were associated with a lower mortality rate in metformin users compared with non-users: beware of confounders! Via Annals of Intensive Care - Latest Articles View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.

Effect of continuous positive airway pressure on gastroesophageal reflux in patients with obstructive sleep apnea: a meta-analysis

xloma.fota13 shared this article with you from Inoreader Effect of continuous positive airway pressure on gastroesophageal reflux in patients with obstructive sleep apnea: a meta-analysis Via Latest Results for Sleep and Breathing Abstract Purpose Gastroesophageal reflux disease (GERD) often occurs in patients with obstructive sleep apnea (OSA). Although continuous positive airway pressure (CPAP) is considered to be the preferred treatment for OSA, the effect of CPAP therapy on reflux events remains controversial. In this study, we utilized meta-analysis to investigate whether or not CPAP treatment reduces the incidence of reflux. Methods Two independent reviewers obtained the data sources from the database of PubMed, Elsevier, Cochrane library, and CNKI using search terms, and then filtered the target articles based on the inclusion and exclusion criteria. RevMan (version 5.3) and STATA (version 12.0) were used for data synthesis. The effect of CPAP treatment on GERD was studied by calculating the weighted mean difference (WMD) and standard deviation (SD) before and after CPAP treatment. Results Ten studies involving a total of 272 participants were included in this study. The results showed that the total of WMD before and after CPAP was − 17.68 (95% CI − 30.67 to − 4.69) for percentage time pH < 4, − 24.66 (95% CI − 36.15 to − 13.18) for the longest reflux duration, − 27.53 (95% CI − 49.53 to − 5.52) for number of reflux events, − 49.76 (95% CI − 60.18 to − 39.35) for DeMeester score, − 1.85 (95% CI − 3.00 to − 0.71) for reflux diseases questionnaire (RDQ) score, and − 8.95 (95% CI − 16.00 to − 1.89) for reflux symptom index (RSI). The subgroup analysis demonstrated that the improvement of reflux symptoms was more obvious with the extension of treatment time. Conclusions This meta-analysis showed that CPAP treatment significantly reduces the incidence of reflux events in patients with OSA. View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.

Degos disease

xloma.fota13 shared this article with you from Inoreader Message: Wiki Loves Monuments: Photograph a monument, help Wikipedia and win! Learn more Degos disease From Wikipedia, the free encyclopedia Jump to navigationJump to search Degos disease Other names Köhlmeier-Degos disease Degos-disease.jpg Skin lesions in a person with Degos disease Specialty Cardiology, dermatology Edit this on Wikidata Degos disease, also known as Köhlmeier-Degos disease or malignant atrophic papulosis, is an extremely rare condition caused by blockage of arteries and veins. Individuals with this condition will develop papules. Those diagnosed with this disease may also develop complications due to impairment of internal organs. The exact underlying mechanism is still unknown, and an effective treatment is still being developed.[1] There are fewer than 50 living patients presently known worldwide, and fewer than 200 reported in medical literature. However, many individuals may go undiagnosed due to rarity of the disease.[2][3] Most individuals develop symptoms between the ages of 20–50; however, cases outside of this age range have been reported as well.[1] Contents 1 Symptoms and signs 2 Causes 3 Mechanism 4 Diagnosis 5 Treatment 6 Recent research 7 History 8 References 8.1 Notes 8.2 Further reading 9 External links Symptoms and signs The characteristic symptom of Degos disease is the development of papules. Initially, individuals may have skin lesions or rashes, but they will proceed to develop distinct bumps, or papules.[4] Papules are circular in shape, have a porcelain-white center and red border. As papules age, the white centers will skin in and only the border will remain raised. Typically, papules range from 0.5 to 1 cm in width. Papules appear on the trunk and upper extremities and are not found on the individual's palms, soles, scalp, or face.[1] Symptoms vary, depending on whether an individual has the benign variant or malignant variant of the disease. Both the benign and malignant forms have development of the characteristic papules. Individuals with the benign form will have the typical papules persisting anywhere from a few years to throughout their whole lives. In the benign form, no inner organs are affected. If an individual develops the malignant form, it means that not only are the papules present, but inner organs are involved. Most malignant cases involve problems of the gastrointestinal tract leading to small intestine lesions, abdominal pain, diarrhea, and bowel perforation. If the central nervous system is involved, symptoms can include headaches, dizziness, seizures, paralysis of cranial nerves, weakness, stroke, damage to small areas of the brain due to artery blockage (cerebral infarcts, and cerebral hemorrhage). Additional organs commonly impacted include the heart, lungs, and kidneys. Symptoms that may dev elop from damage to these organs include double vision (diplopia), clouding of lenses of eyes, swelling of the optic disc (papilledema), partial loss of vision, shortness of breath, chest pain, epilepsy, and thickening of pericardium.[3][4] Someone with the benign form may suddenly develop symptoms of the malignant form.[1] Symptoms can last anywhere from a few weeks to several years. Onset of symptoms typically begins to manifest between the ages of 20–50.[5] A few cases of this condition in newborns have also been described.[6] Causes The papules characteristic for this disease develop due to infarctions, or blockages in small-medium arteries and veins. The underlying cause is unknown for this disease.[1] Though not confirmed, some cases have shown signs of inheritance between first-degree relatives. It has been suggested that the disease has a familial inheritance pattern; it is thought to be an autosomal dominant disorder. In most cases of familial inheritance, the benign variant of the disease has been present.[4][7][8] Due to the lack of knowledge of the pathomechanism for this condition prevention strategies are not known. However, in order to prevent worsening of symptoms, consistent evaluations should be conducted by a physician.[1] Mechanism Although this disease has been known for around 70 years, the pathomechanism underlying it is still unknown.[1] Several hypotheses have been developed regarding the underlying mechanism for Degos disease. One theory suggests that inflammation of blood vessels may trigger the condition. Another theory has to do with Degos disease as a coagulopathy. Development of a thrombus and resulting reduction of blood flow is common in this condition. A reduction in blood flow throughout the body can lead to damaged endothelial cells and may perhaps lead to the formation of the characteristic papules. Another hypothesis suggests that abnormal swelling and proliferation of the vascular endothelium can lead to intestinal and central nervous system thrombosis, and ultimately lead to development of symptoms associated with Degos disease. Overall, individuals with Degos disease have abnormal blockages in their arteries and veins; however, the cause of these blockages is unknown.[1] Diagnosis Clinical evaluation and identification of characteristics papules may allow a dermatologist to diagnose Degos disease.[4] The papules have a white center and are bordered with a red ring. After lesions begin to appear, the diagnosis for Degos disease can be supported by histological findings. Most cases will show a wedge-shaped connective tissue necrosis in the deep corium. This shape is due to the blockage/occlusion of small arteries.[1] Individuals may be diagnosed with the benign form if only the papules are present. However, an individual may be diagnosed with the malignant form if involvement of other organs like the lungs, intestine and/or central nervous system occurs. The malignant, or systematic form of this condition may suddenly develop even after having papules present for several years. In order to quickly diagnose this shift to the malignant variant of the disease, it is important for individuals to have consistent follow-up evaluations. In these evaluations, depending on which organs are suspected to be involved, the following procedures and tests may be conducted: skin inspection, brain magnetic resonance tomography, colonoscopy, chest X-ray, and/or abdominal ultrasound.[1] Treatment Due to the lack of knowledge around the underlying mechanism of malignant atrophic papulosis, an effective treatment method has not been developed.[1][1] Treatment for this condition is symptomatic.[4] However, several treatment methods have been tested and are still being developed as more information regarding the condition is found. Fibrinolytic and immunosuppressive therapeutic regimens were tested and found to be mostly unsuccessful as treatment methods.[1][8] After treating conditions comorbid with Degos disease, physicians have recently found improvement in symptoms with the use of eculizumab and treprostinil.[9][10] Discovered by dermatopathologist, Cynthia Magro, response to eculizumab is often immediate and dramatic, but has been of limited duration and is expensive, needing to be infused every 14 days.[9] Treprostinil use has been reported to result in clearing of gastrointestinal and central nervous system findings as well as clearing of cutaneous lesions, but reports are limited. Treprostinil may be more effective than other vasodilators because it may also increase the population of circulating endothelial cells, allowing angiogenesis.[1] Recent research A 46-year-old male patient was diagnosed with the malignant, systemic form of the disease and was severely ill. The diagnosing dermatopathologist, Cynthia Magro MD, identified the presence of C5b-9 complexes in the involved vessels of the skin biopsy. For treatment of the thrombotic microangiopathy in this patient, she suggested the use of eculizumab, a humanized monoclonal antibody drug developed by Alexion Pharmaceuticals and approved by the Food and Drug Administration for treatment of Paroxysmal nocturnal hemoglobinuria. The patient experienced a dramatic improvement in his condition.[9] Lee Shapiro MD and Aixa Toledo-Garcia MD at Albany Medical College learned of the success with the adult patient, and became the first physicians to successfully treat a pediatric Degos patient with eculizumab.[10] Dr. Shapiro later observed the resolution of Degos skin lesions in an adult patient with an overlap syndrome involving systemic lupus, systemic sclerosis, and Degos disease who was treated with treprostinil for her pulmonary hypertension. His pediatric Degos patient was developing significant complications despite treatment with eculizumab, so Dr. Shapiro's group became the first to treat a Degos patient with treprostinil.[10] To this point, all known long-term survivors of systemic Degos disease are being treated with a combination of eculizumab and treprostinil.[9][10] History In 1941, this disease was first described by Kohlmeier. However, it was not until 1942 that the disease was recognized as a new clinical entity by Robert Degos. Initially the condition was referred to as Degos Disease or Kohlmeier-Degos disease. However, Degos himself subsequently suggested the name "papulose atrophiante maligne," translated as malignant atrophic papulosis.[11] References Notes Theodoridis, Athanasios; Makrantonaki, Evgenia; Zouboulis, Christos C. (2013-01-14). "Malignant atrophic papulosis (Köhlmeier-Degos disease) - A review". Orphanet Journal of Rare Diseases. 8: 10. doi:10.1186/1750-1172-8-10. ISSN 1750-1172. PMC 3566938. PMID 23316694. "Degos Disease: Background, Pathophysiology, Epidemiology". 2017-02-07. De Breucker S, Vandergheynst F, Decaux G (2008). "Inefficacy of intravenous immunoglobulins and infliximab in Degos' disease". Acta Clin Belg. 63 (2): 99–102. doi:10.1179/acb.2008.63.2.007. PMID 18575050. S2CID 34148667. "Degos Disease - NORD (National Organization for Rare Disorders)". NORD (National Organization for Rare Disorders). Retrieved 2017-12-13. Snow, J. L.; Muller, S. A. (June 1995). "Degos syndrome: malignant atrophic papulosis". Seminars in Dermatology. 14 (2): 99–105. doi:10.1016/S1085-5629(05)80004-5. ISSN 0278-145X. PMID 7640203. Torrelo, A.; Sevilla, J.; Mediero, I.g.; Candelas, D.; Zambrano, A. (2002-05-01). "Malignant atrophic papulosis in an infant". British Journal of Dermatology. 146 (5): 916–918. doi:10.1046/j.1365-2133.2002.04677.x. ISSN 1365-2133. PMID 12000397. Katz, Sara K.; Mudd, Leslie J.; Roenigk, Henry H. (1997). "Malignant atrophic papulosis (Degos' disease) involving three generations of a family". Journal of the American Academy of Dermatology. 37 (3): 480–484. doi:10.1016/s0190-9622(97)70151-8. PMID 9308565. Powell; Bordea; Wojnarowska; Farrell; Morris (1999-09-01). "Benign familial Degos disease worsening during immunosuppression". British Journal of Dermatology. 141 (3): 524–527. doi:10.1046/j.1365-2133.1999.03050.x. ISSN 1365-2133. PMID 10583060. Magro, CM; Poe, JC; Kim, C; Shapiro, L; Nuovo, G; Crow, MK; Crow, YJ (2011). "Degos disease: A C5b-9/interferon-α-mediated endotheliopathy syndrome". Am J Clin Pathol. 135 (4): 599–610. doi:10.1309/ajcp66qimfarlzki. PMID 21411783. Shapiro, LS; Toledo-Garcia, AE; Farrell, JS (April 4, 2013). "Effective treatment of malignant atrophic papulosis (Köhlmeier-Degos disease) with treprostinil--early experience". Orphanet J Rare Dis. 8: 52. doi:10.1186/1750-1172-8-52. PMC 3636001. PMID 23557362. Degos R.; Delort J.; Tricot R. (1942). "Dermatite papulosquameuse atrophiante". Bulletin de la Société Française de Dermatologie et de Syphiligraphie et de Ses Filiales. 49: 148–150. Further reading Scheinfeld N (September 2007). "Malignant atrophic papulosis". Clin. Exp. Dermatol. 32 (5): 483–7. doi:10.1111/j.1365-2230.2007.02497.x. PMID 17692056. Fazio S (June 13, 2014). "Rash, Myalgia, and Weakness". Now@NEJM. External links Classification D ICD-9-CM: 447.8OMIM: 602248MeSH: D054853DiseasesDB: 29425 External resources eMedicine: derm/931 vte Cardiovascular disease (vessels) Categories: Rare diseasesDisorders causing seizures Navigation menu Not logged inTalkContributionsCreate accountLog in ArticleTalk ReadEditView historySearch Search Wikipedia Main page Contents Current events Random article About Wikipedia Contact us Donate Contribute Help Learn to edit Community portal Recent changes Upload file Tools What links here Related changes Special pages Permanent link Page information Cite this page Wikidata item Print/export Download as PDF Printable version In other projects Wikimedia Commons Languages العربية Čeština Deutsch Español Français Italiano Polski Português Edit links This page was last edited on 24 September 2020, at 15:34 (UTC). Text is available under the Creative Commons Attribution-ShareAlike License; additional terms may apply. By using this site, you agree to the Terms of Use and Privacy Policy. Wikipedia® is a registered trademark of the Wikimedia Foundation, Inc., a non-profit organization. Privacy policyAbout WikipediaDisclaimersContact WikipediaMobile viewDevelopersStatisticsCookie statementWikimedia FoundationPowered by MediaWiki Degos disease: a case report and review of the literature Via Journal of Medical Case Reports - Latest Articles Degos disease is a very rare syndrome with multisystem vasculopathy of unknown cause. It can affect the skin, gastrointestinal tract, and central nervous system. However, other organs such as the kidney, lungs... View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.