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FindZebra
Datensatz: duchenne:25714938
Quellenstand: f262dbc3a1d234f500d9173f9ebf8d19996b03ba
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11 angezeigte Datensätze · Seite 1 · Publikationszuordnung geprüft. Dieselbe Publikation kann in beiden Sammlungen vorkommen.
Nur Publikationshinweis. Kein zur Wiederverwendung freigegebener Textauszug in HealthOS.
FindZebra
Datensatz: duchenne:25714938
Quellenstand: f262dbc3a1d234f500d9173f9ebf8d19996b03ba
Nur Publikationshinweis. Kein zur Wiederverwendung freigegebener Textauszug in HealthOS.
FindZebra
Datensatz: duchenne:21784636
Quellenstand: f262dbc3a1d234f500d9173f9ebf8d19996b03ba
Fabry disease (FD) is an X-linked lysosomal storage disorder caused by mutations of the GLA gene, followed by deficiency in α-galactosidase A (α-gal) activity. Nephrotic syndrome, as the renal phenotype of FD, is unusual. Here, we report the rare case of a patient with FD with nephrotic syndrome whose proteinuria disappeared by immunotherapy. A 67-year-old Japanese man was admitted to our hospital because of emesis, abdominal pain, and facial edema due to nephrotic syndrome. The patient was diagnosed with focal segmental glomerulosclerosis (FSGS) by renal biopsy before being diagnosed with FD, and immunotherapy was initiated. After treatment, the kidney biopsy results showed typical glycosphingolipid accumulation in the podocytes of this patient. The white blood cell α-gal activity was very low, and genetic analysis revealed a GLA gene variant (M296I), which is known as a late-onset genetic mutation of FD. Immunotherapy (steroids and cyclosporine A) dramatically improved the massive proteinuria. Currently, he has been undergoing enzyme replacement therapy, and his proteinuria has further decreased. There is the possibility that other nephrotic syndromes, such as minimal change nephrotic syndrome or FSGS, may co-exist in this patient. We experienced the rare case of a FD patient whose nephrotic syndrome disappeared by immunotherapy. These findings suggest that immunosuppressive treatment may be considered if nephrotic syndrome develops, even in patients with FD.
Auszug in der Originalsprache. Fujisawa H, Nakayama Y, Nakao S, Yamamoto R, Kurokawa Y, Nakamura N, Nagata A, Tsukimura T, Togawa T, Sakuraba H, Fukami K. · Lizenz: cc by. Für den vollständigen Kontext die Originalpublikation öffnen.
FindZebra
Datensatz: fabry:31847900
Quellenstand: f262dbc3a1d234f500d9173f9ebf8d19996b03ba
Hereditary angioedema (HAE) is a potentially life-threatening group of conditions that is often underdiagnosed or misdiagnosed. As HAE is typically diagnosed by detecting C1 inhibitor deficiency, there is a critical need for methods that can identify affected individuals with normal C1 inhibitor. The recent discovery of associations between PLG K330E and ANGPT1 A119S and HAE of unknown genetic cause (HAE-U), has raised the possibility that genetic evaluation could be used to diagnose HAE-U in patients with unexplained angioedema or non-confirmatory laboratory testing. We analyzed genome sequences from a generally healthy population cohort of 2820 adults and identified PLG K330E in one individual. Subsequent review of this participant's medical history revealed symptoms clinically attributed to allergy of unknown etiology but that are consistent with published descriptions of HAE patients carrying the PLG K330E variant. The participant, a 31 year old female, reported lip and tongue angioedema, without wheals, which did not respond to treatment with steroids or antihistamines. The genotype-first approach demonstrated that detection of PLG K330E in undiagnosed or misdiagnosed individuals can identify patients actually affected with HAE-U. The genetic diagnosis will facilitate selection of appropriate treatment, discontinuation of therapies ineffective for this condition, and timely diagnosis of affected family members. The results support a role of PLG K330E in the pathogenesis of HAE and suggest that genetic testing be considered as an approach to diagnose patients with unexplained angioedema.
Auszug in der Originalsprache. Bodian DL, Vilboux T, Hauser NS. · Lizenz: cc by. Für den vollständigen Kontext die Originalpublikation öffnen.
FindZebra
Datensatz: hae:31131012
Quellenstand: f262dbc3a1d234f500d9173f9ebf8d19996b03ba
Nur Publikationshinweis. Kein zur Wiederverwendung freigegebener Textauszug in HealthOS.
PMOA-TTS
Datensatz: PMC10006705
Quellenstand: 01b59ac92489cd65efef92899d2e53b9ffe80327
Nur Publikationshinweis. Kein zur Wiederverwendung freigegebener Textauszug in HealthOS.
FindZebra
Datensatz: hae:25650214
Quellenstand: f262dbc3a1d234f500d9173f9ebf8d19996b03ba
Melkersson-Rosenthal syndrome (MRS) is a rare, neuro-mucocutaneous disease which presents as orofacial swelling, facial palsy and fissured tongue. These symptoms may occur simultaneously or, more frequently, with a oligosymptomatic or monosymptomatic pattern. Swelling, that is the most common initial finding, may mimic hereditary or acquired angioedema, a disorder caused by histamine or bradykinin-mediated plasma-leakage affecting subcutaneous and/or submucosal tissue. The differential diagnosis of MRS includes also chronic inflammatory and infective diseases characterized by granulomatous infiltration, as well as rosacea, contact dermatitis, allergic reactions and Bell's palsy. A 71-year old, non-allergic female patient with no familial and personal history of angioedema presented, a few days after a possible herpes simplex or varicella-zoster virus infection, with monolateral facial paraesthesia and lower lip edema. After temporary remission of symptoms on oral steroids and antihistamines, she showed swelling recurrence refractory to valaciclovir therapy and a subsequent course of antihistamines. The clinical picture and a previous history of non-Hodgkin lymphoma prompted us to rule out an acquired form of paraneoplastic, C1-inhibitor (C1-INH) deficiency: C1q and both antigen and functional C1-INH tested normal, whilst we found low plasma levels of C3 and C4 possibly related to the parallel detection of antiphospholipid antibodies. Thus, we hypothesized a non-histaminergic, idiopathic form of angioedema and planned further therapy with tranexamic acid and the leukotriene receptor antagonist montelukast. Treatment failure with both drugs finally suggested a Melkersson-Rosenthal syndrome, which was confirmed by histologic findings of non caseating granulomas on lip biopsy. Melkersson-Rosenthal syndrome may occur with rather non-specific symptoms and overlap with alternative conditions, including recurrent angioedema. No specific biomarkers for MRS exist and clinical
Auszug in der Originalsprache. Cancian M, Giovannini S, Angelini A, Fedrigo M, Bendo R, Senter R, Sivolella S. · Lizenz: cc by. Für den vollständigen Kontext die Originalpublikation öffnen.
FindZebra
Datensatz: hae:30622569
Quellenstand: f262dbc3a1d234f500d9173f9ebf8d19996b03ba
Nur Publikationshinweis. Kein zur Wiederverwendung freigegebener Textauszug in HealthOS.
FindZebra
Datensatz: duchenne:30167630
Quellenstand: f262dbc3a1d234f500d9173f9ebf8d19996b03ba
Hereditary angioedema (HAE) due to a C1-esterase inhibitor(C1-INH) deficiency is a rare and potentially life-threatening disorder. It is characterized by an episodic and self-limiting increase in vascular permeability. The condition manifests itself as recurrent attacks of swelling in any part of the body. The angioedema can cause the involvement of the respiratory tract, skin, and gastrointestinal tract. Laryngeal involvement can make the condition life-threatening. It does not respond well to conventional angioedema therapy of steroids, adrenaline, and antihistamines. The targeted therapy for HAE consists of plasma-derived or recombinant C1-INH, ecallantide, and icatibant or bradykinin receptor antagonist. In the absence of these therapies, it becomes difficult to manage this condition effectively. We present a case of hereditary angioedema, who presented with life-threatening laryngeal edema, causing asphyxia, leading to cardiac arrest. Due to a lack of availability of C1-INH concentrate, he was given fresh frozen plasma (FFP). His condition gradually improved, and he was successfully extubated after three days. This is the first time we are reporting a case from Pakistan in which the patient was successfully treated with FFP for an acute attack of hereditary angioedema.
Auszug in der Originalsprache. Sabeen Ahmed A, Fayyaz S. · Lizenz: cc by. Für den vollständigen Kontext die Originalpublikation öffnen.
FindZebra
Datensatz: hae:32923264
Quellenstand: f262dbc3a1d234f500d9173f9ebf8d19996b03ba
Angioedema secondary to C1 inhibitor deficiency has been rarely reported to be associated with systemic lupus erythematosus. A genetic defect of C1 inhibitor produces hereditary angioedema, which is usually presented with cutaneous painless edema, but edema of the genital area, gastrointestinal and laryngeal tracts have also been reported. In lupus patients, angioedema may be the result of an acquired type of C1 inhibitor deficiency, most probably due to antibody formation directed against the C1 inhibitor molecule. Herein we report a new case of lupus nephritis that developed angioedema and a rapid course of disease progression with acute renal failure and alveolar hemorrhage without response to high dose steroid and plasmapheresis.
Auszug in der Originalsprache. Habibagahi Z, Ruzbeh J, Yarmohammadi V, Kamali M, Rastegar MH. · Lizenz: cc by. Für den vollständigen Kontext die Originalpublikation öffnen.
FindZebra
Datensatz: hae:26170526
Quellenstand: f262dbc3a1d234f500d9173f9ebf8d19996b03ba
Tension pneumocephalus is a rare condition that can be a life-threatening neurosurgical emergency. It usually results from head trauma, but there have been case reports of iatrogenic causes including on non-invasive mechanical ventilation. We report a case of pneumocephalus resulting from high mechanical ventilation pressures in a patient without prior head trauma. A 37-year-old male with Duchenne's muscular dystrophy who had been ventilator-dependent through tracheostomy was admitted for shortness of breath and intermittent fevers. The patient was found to have pneumonia, with left-lower lobe consolidation, and was started on linezolid given known Methicillin-resistant Staphylococcus aureus from previous sputum culture; he was later switched to vancomycin and piperacillin-tazobactam given persistent fevers to cover for hospital-acquired pneumonia. The patient went into septic shock requiring multiple pressors as well as stress steroids for persistent shock, with eventual improvement in hemodynamics. He developed further respiratory acidosis on his usual ventilator settings, and peak inspiratory pressures (PIPs) progressively increased to as high as 45-70 cm H2O during his hospital course. PIPs did not improve with suctioning or after bronchoscopy. On the 17th day of the patient's stay, he had acutely altered mental status with non-reactive fixed and dilated pupils and disconjugate gaze of the right eye on neurologic examination. CT of the head at that time revealed extensive pneumocephalus along the bifrontal convexities, suprasellar cisterns, and posterior fossa, with a possible fracture of the frontal skull base near the ethmoid roof. Mount Fuji sign was present on CT scan, indicative of "tension pneumocephalus". Neurosurgical consultation was obtained but the family declined intervention given his overall debilitated stated. Comfort measures were instituted, and the patient expired the following day. Pneumocephalus is the accumulation of air entry into the crani
Auszug in der Originalsprache. Kumar V, Oduwole A, Raminfard A, Barnes M, Le TH. · Lizenz: cc by. Für den vollständigen Kontext die Originalpublikation öffnen.
FindZebra
Datensatz: duchenne:33062510
Quellenstand: f262dbc3a1d234f500d9173f9ebf8d19996b03ba