scholarly journals SUN-192 Spontaneous Adrenal Hemorrhage in a Patient with Antiphospholipid Syndrome on Rivaroxaban: A Potentially Fatal Complication

2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Daniela Maria DiCenso ◽  
Carlos A Penaherrera ◽  
Alejandro Ayala
Keyword(s):  
Antiphospholipid Syndrome ◽  
Adrenal Glands ◽  
Oral Anticoagulants ◽  
Adrenal Hemorrhage ◽  
Post Contrast ◽  
Severe Fatigue ◽  
Bilateral Adrenal Hemorrhage ◽  
Intravenous Hydration ◽  
History Of ◽  
Contrast Ct

Abstract Introduction: Primary Adrenal insufficiency is an uncommon complication of antiphospholipid syndrome, with an incidence of 0.4% [2]. It is often secondary to bilateral adrenal hemorrhage. We present a case of bilateral adrenal hemorrhage in a patient with APLS on anticoagulation with rivaroxaban. Case: 46-year-old m with a history of antiphospholipid syndrome, recently transitioned from warfarin to rivaroxaban for anticoagulation, who presented to the ED after a syncopal episode following a prior episode of abdominal pain with an unremarkable work-up. He subsequently developed severe fatigue, dizziness, headaches, nausea and 15 lbs weight loss. On presentation, the patient was hypotensive(72/45 mmHg) and tachycardic. Intravenous hydration was started with minimal response. Initial laboratory testing showed serum sodium of 121mmol/L, potassium of 5.5mmol/L and random cortisol of 0.8mcg/dL. The patient was admitted to the intensive care unit where he was started on vasopressors and hydrocortisone 50 mg IV every 8 hours. A non-contrast CT of the abdomen and pelvis showed thickening of the adrenal glands with decreased attenuation. MRI of the abdomen showed hyper-intensity of the adrenal glands bilaterally (T1 images), without post-contrast enhancement suggestive of bilateral adrenal hemorrhage. His electrolytes normalized, and he was successfully discharged home on hydrocortisone and fludrocortisone replacement with outpatient follow-up. Discussion: Atraumatic bilateral adrenal hemorrhage is rare, but remains one of the most common endocrine-related complications of antiphospholipid syndrome (APLS). The venous anatomical configuration of the adrenal gland increases risk of thrombotic hemorrhagic infarction[1]. Patients with APLS are commonly anticoagulated to prevent thrombosis. The ideal anticoagulation regimen remains controversial. Only three other cases of spontaneous bilateral adrenal hemorrhage on patients with APLS using new oral anticoagulants (NOACs) were reported. The use of NOACs seem to increase the already-elevated risk of adrenal hemorrhage seen in patients with APLS. References: 1. Aldaajani, H. et al. Bilateral adrenal hemorrhage in antiphospholipid syndrome: Anticoagulation for the treatment of hemorrhage. Saudi Med J. 2018; 39(8): 829-833. 2. Cervera R, Piette JC, Font J, Khamashta MA, Shoenfeld Y, Camps MT, et al. Antiphospholipid syndrome: Clinical and immunologic manifestations and patterns of disease expression in a cohort of 1,000 patients. Arthritis Rheum. 2002;46:1019-27.

Catastrophic antiphospholipid syndrome with bilateral adrenal hemorrhage: a case report

2019 ◽  
Author(s):  
De Marchi Lucrezia ◽  
M K de Filette Jeroen ◽  
Sol Bastiaan ◽  
E Andreescu Corina ◽  
Kunda Rastislav ◽  
...  
Keyword(s):  
Case Report ◽  
Antiphospholipid Syndrome ◽  
Adrenal Hemorrhage ◽  
Catastrophic Antiphospholipid Syndrome ◽  
Bilateral Adrenal Hemorrhage

scholarly journals Bilateral Adrenal Hemorrhage in a Patient with Antiphospholipid Syndrome during Chronic Graft-versus-host Disease

2018 ◽  
Vol 57 (10) ◽  
pp. 1439-1444 ◽  
Author(s):  
Mariko Minami ◽  
Tsuyoshi Muta ◽  
Masahiro Adachi ◽  
Masakazu Higuchi ◽  
Kenichi Aoki ◽  
...  
Keyword(s):  
Antiphospholipid Syndrome ◽  
Graft Versus Host Disease ◽  
Adrenal Hemorrhage ◽  
Host Disease ◽  
Graft Versus Host ◽  
Bilateral Adrenal Hemorrhage

scholarly journals 123 Gemcitabine-related radiation recall as a cause of focal myositis and muscle necrosis

2019 ◽  
Vol 90 (e7) ◽  
pp. A40.1-A40
Author(s):  
Sean Byrnes
Keyword(s):  
Palliative Radiotherapy ◽  
Radiation Recall ◽  
Post Contrast ◽  
Immune Mediated ◽  
Cutaneous Tissue ◽  
Muscle Necrosis ◽  
History Of ◽  
Contrast Ct ◽  
Ct And Mri

IntroductionRadiation recall is a phenomenon in which chemotherapy triggers an inflammatory response in tissue previously subjected to radiation therapy. A wide variety of agents have been implicated. Cutaneous tissue is most frequently affected but other tissue can be involved; myositis has been associated with administration of gemcitabine in particular. Incidence has been estimated at less than 6% and the pathophysiology is not understood. We present a case report from Gosford Hospital, with the additional feature of positive SRP antibodies.CaseA 74 year old female presented with a one day history of left hip pain and inability to weight bear. She had been diagnosed with metastatic squamous cell carcinoma of the lung five months earlier and underwent palliative radiotherapy to a left acetabular metastasis. 12 days prior to presentation she completed her second cycle of chemotherapy with carboplatin and gemcitabine. Pre- and post-contrast CT and MRI demonstrated necrosis in left sartorius, with foci of myositis in other muscles of the thigh, and surrounding soft tissue oedema. Symptoms improved after chemotherapy was ceased. Myositis antibody studies subsequently revealed low level positive Ku and SRP antibodies.ConclusionRadiation recall should be considered in the differential diagnosis of myositis in oncology patients. The serum of our patient contained SRP antibodies, which are associated with immune mediated necrotising myopathy. A previous case study reported gemcitabine-induced radiation recall muscle necrosis associated with dermatomyositis. These findings hint that radiation recall myositis may occur in the setting of a predisposition to immune mediated myopathy.

Unusual case of antiphospholipid syndrome presenting as adrenal insufficiency

2020 ◽  
Vol 13 (3) ◽  
pp. e233631
Author(s):  
Sanval Ahmed Warriach ◽  
Mohamad Mustafa ◽  
Denis O'Keeffe ◽  
Michael Watts
Keyword(s):  
Adrenal Gland ◽  
Adrenal Insufficiency ◽  
Antiphospholipid Syndrome ◽  
Adrenal Glands ◽  
Pet Scan ◽  
Gland Size ◽  
Vein Thrombosis ◽  
Positron Emission ◽  
History Of ◽  
Synacthen Test

A 64-year-old man presented to the emergency department with generalised fatigue and dizzy spells. His background history includes a previous admission with right leg deep vein thrombosis, provoked by pneumonia. Laboratory results showed evidence of hyponatremia and hyperkalaemia. A synacthen test was performed that indicated hypoadrenalism. CT of his abdomen revealed enlarged adrenal glands bilaterally. Adrenal antibodies and positron emission tomography (PET) scan were performed to assess the cause of enlarged adrenals. PET scan showed no evidence of increased uptake. Adrenal antibodies were found to be negative. Tuberculous (TB) adrenalitis was the principle differential diagnosis. TB QuantiFERON was strongly positive. Following 9 months of TB treatment, surveillance CT scan indicated a significant reduction in adrenal gland size. However, subsequent events culminated in a retrospective review of CT scans questioning the initial clinical diagnosis and suggesting that the observed adrenal gland enlargement was secondary to bilateral adrenal infarction and haemorrhage. Equally, the subsequently observed marked reduction in adrenal gland size was not secondary to an assumed response to TB therapy, but rather the sequela of infracted atrophied adrenal glands, as a manifestation of the underlying antiphospholipid syndrome (APS). The case highlights the importance of recognising adrenal insufficiency in patients with a history of APS. It also illustrates the role of multidisciplinary meetings in the management of such complex cases.

scholarly journals Testosterone Use and Adrenal Hemorrhage

2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A160-A160
Author(s):  
Moin U Sattar ◽  
Priyanka L Mahali ◽  
Natalia Chamorro-Pareja ◽  
Nisha Suda ◽  
Noah Bloomgarden
Keyword(s):  
Adrenal Insufficiency ◽  
Antiphospholipid Syndrome ◽  
Immunoglobulin Therapy ◽  
Dehydroepiandrosterone Sulfate ◽  
International Normalized Ratio ◽  
Adrenal Hemorrhage ◽  
Critically Ill Patient ◽  
Primary Adrenal Insufficiency ◽  
Intravenous Immunoglobulin Therapy ◽  
History Of

Abstract Background: Testosterone supplementation has been associated with a variety of side effects, such as polycythemia, and can potentially increase the risk of cardiovascular disease. Testosterone use has also been associated with increased thrombotic events, especially in patients with underlying hypercoagulable state. Clinical Case: A 57-year-old man presented with abdominal pain and distention. He had history of previous intramuscular (IM) and oral testosterone use for ten years. For 8 weeks prior to initial presentation, he reported using weekly IM 500mg Testosterone injections. Computed Tomography (CT) of the abdomen and pelvis revealed multiple thrombi of the portal, splenic, superior mesenteric and inferior mesenteric veins. He was started on Warfarin and discharged home. A few weeks later, he presented with similar symptoms with labs now showing an International Normalized Ratio (INR) of 10.2. Repeat CT was significant for presence of bilateral adrenal hemorrhage, measuring 2.9cm on the right and 2.4cm on the left, which were not seen on previous imaging done one week prior. During the hospital course, he was found to be hypotensive with low platelet count so Intravenous Immunoglobulin therapy was initiated for suspected catastrophic antiphospholipid syndrome (CAPS). Morning cortisol was 5.82 ug/dL (6.2–29.0) so this critically-ill patient was started on stress dose hydrocortisone, which was subsequently tapered to physiological dose after clinical improvement. Cosyntropin stimulation test was performed after withholding the prior dose of hydrocortisone. The baseline cortisol was 0.88 ug/dL (6.20–29.00ug/dL), after administration of 250mcg of Cosyntropin 30- and 60-minute cortisol levels were 1.5 ug/dL (4.3–22.4ug/dL) and 1.6 ug/dL (4.3–22.4ug/dL) respectively. Baseline ACTH of 121.0 pg/mL (7.2–63.3pg/mL), consistent with primary adrenal insufficiency. Dehydroepiandrosterone Sulfate (DHEA-S) level was 15.7 ug/dL (80.0–560.0ug/dL). Hypercoagulability workup was significant for the presence of lupus anticoagulant and antibodies positive for heparin induced thrombocytopenia, so patient was diagnosed with Antiphospholipid syndrome. Conclusion: This is a case of hypercoagulability in a patient with history of anabolic steroid misuse who developed extensive intraabdominal venous thrombosis, adrenal hemorrhage, and primary adrenal insufficiency. Adrenal vein thrombosis and hemorrhage can be life threatening sequalae of testosterone misuse and should be considered in the differential for patients with history of testosterone misuse and adrenal insufficiency.

scholarly journals Definitive Adrenal Insufficiency Due to Bilateral Adrenal Hemorrhage and Primary Antiphospholipid Syndrome

1998 ◽  
Vol 83 (5) ◽  
pp. 1437-1439 ◽  
Author(s):  
Philippe Caron ◽  
Marie-Hélène Chabannier ◽  
Jean-Pierre Cambus ◽  
Françoise Fortenfant ◽  
Philippe Otal ◽  
...  
Keyword(s):  
Adrenal Insufficiency ◽  
Antiphospholipid Syndrome ◽  
Adrenal Hemorrhage ◽  
Primary Antiphospholipid Syndrome ◽  
Bilateral Adrenal Hemorrhage

scholarly journals Primary Adrenal Insufficiency Due to Bilateral Adrenal Hemorrhage-Adrenal Infarction in the Antiphospholipid Syndrome: Long-Term Outcome of 16 Patients

2013 ◽  
Vol 98 (8) ◽  
pp. 3179-3189 ◽  
Author(s):  
Isolde Ramon ◽  
Alexis Mathian ◽  
Anne Bachelot ◽  
Baptiste Hervier ◽  
Julien Haroche ◽  
...  
Keyword(s):  
Adrenal Insufficiency ◽  
Acute Phase ◽  
Antiphospholipid Syndrome ◽  
Adrenal Hemorrhage ◽  
Primary Adrenal Insufficiency ◽  
Term Outcome ◽  
Long Term Outcome ◽  
Bilateral Adrenal Hemorrhage ◽  
Adrenal Infarction

Context: Primary adrenal insufficiency due to bilateral adrenal hemorrhage-adrenal infarction is a rare and life-threatening manifestation of the antiphospholipid syndrome (APLS). Data on the long-term outcome are scarce. Objective: The aims of the present study were to analyze the long-term outcome related to APLS per se and to characterize the course of adrenal involvement. Design: We conducted a retrospective study of patients with bilateral adrenal hemorrhage-adrenal infarction secondary to APLS seen in the Department of Internal Medicine of Pitié-Salpêtrière Hospital in Paris (France) between January 1990 and July 2010. Results: Three patients died during the acute phase related to APLS manifestations. Sixteen patients (7 males; 9 females) were followed up during a median period of 3.5 years (range 0.3–28.1 years). Three episodes of recurrent thrombosis were noted. One patient died from cerebral hemorrhage 3 months after the onset of adrenal insufficiency. Repeated Synacthen tests showed complete absence of response in 8 of the 10 patients assessed; cortisol and aldosterone increased appropriately in one patient and to some extent in another one. Dehydroepiandrosterone levels and 24-hour urinary epinephrine levels remained abnormally low in all evaluated patients. Adrenal imaging performed more than 1 year after the initial event revealed completely atrophic glands in 9 of 11 patients. Conclusions: This particular subset of APLS patients who survive the acute phase has a rather favorable long-term outcome. Although adrenal dysfunction is generally irreversible, adrenocortical function may, at least partially, recover in rare cases. In this view, measurement of early morning cortisol during follow-up is indicated to detect these patients.

scholarly journals Management of Thrombotic Antiphospholipid Syndrome

2017 ◽  
Vol 44 (05) ◽  
pp. 419-426 ◽  
Author(s):  
Cecilia Chighizola ◽  
Maria Raimondo ◽  
Pier Meroni
Keyword(s):  
Antiphospholipid Syndrome ◽  
Vitamin K Antagonists ◽  
Oral Anticoagulants ◽  
Antiplatelet Agents ◽  
Coagulation Cascade ◽  
Moderate Intensity ◽  
Pregnancy Morbidity ◽  
Significant Burden ◽  
History Of

AbstractPersistent serum positivity for antiphospholipid antibodies (aPL) is required to diagnose antiphospholipid syndrome (APS), an autoimmune disease characterized by recurrent vascular thrombosis and/or pregnancy morbidity. The current therapeutic management of patients with thrombotic APS aims at preventing recurrences and long-term complications by attenuating the procoagulant state. There is overall consensus to reserve moderate-intensity anticoagulation to aPL-positive patients with a previous venous thrombosis; the therapeutic options for those with a history of arterial event comprise antiplatelet agents and high-intensity anticoagulation. Unfortunately, thrombotic occurrences might occur despite adequate anticoagulation, carrying a significant burden of morbidity and mortality. The management of refractory thrombotic APS and catastrophic APS is still not clear, warranting the issue of recommendations. Vitamin-K antagonists are limited by significant side effects, and a careful weighting of risks and benefits should be performed to reserve the optimal treatment to each patient. To overcome these limitations, novel oral anticoagulants have been introduced in the market, but their efficacy in thrombotic APS has still to be unraveled. The poor safety profile and the scarce efficacy of drugs acting on the coagulation cascade explain why novel therapeutic approaches are currently under investigation, to identify pharmacological tools specifically counteracting aPL-mediated prothrombotic effects.

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