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

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.

2013 ◽  
Vol 98 (8) ◽  
pp. 3179-3189 ◽  
Author(s):  
Isolde Ramon ◽  
Alexis Mathian ◽  
Anne Bachelot ◽  
Baptiste Hervier ◽  
Julien Haroche ◽  
...  

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.


2010 ◽  
Vol 9 (4) ◽  
pp. 217-221 ◽  
Author(s):  
Shigeki Shimada ◽  
Hideto Yamada ◽  
Tatsuya Atsumi ◽  
Takashi Yamada ◽  
Noriaki Sakuragi ◽  
...  

Author(s):  
Iza F R Machado ◽  
Isabel Q Menezes ◽  
Sabrina R Figueiredo ◽  
Fernando Morbeck Almeida Coelho ◽  
Debora R B Terrabuio ◽  
...  

Abstract Context Coronavirus disease 2019 (COVID-19) is a proinflammatory and prothrombotic condition, but its impact on adrenal function has not been adequately evaluated. Case report A 46-year-old woman presented with abdominal pain, hypotension, skin hyperpigmentation after COVID-19 infection. The patient had hyponatremia, serum cortisol <1.0 ug/dL, ACTH of 807 pg/mL and aldosterone <3 ng/dL. Computed tomography (CT) findings of adrenal enlargement with no parenchymal and minimal peripheral capsular enhancement after contrast were consistent with bilateral adrenal infarction. The patient had autoimmune hepatitis and positive antiphospholipid antibodies, but no previous thrombotic events. The patient was treated with intravenous hydrocortisone, followed by oral hydrocortisone and fludrocortisone. Discussion Among 115 articles, we identified nine articles, including case reports, of new-onset adrenal insufficiency and/or adrenal hemorrhage/infarction on CT in COVID-19. Adrenal insufficiency was hormonally diagnosed in five cases, but ACTH levels were measured in only three cases (high in one case and normal/low in other two cases). Bilateral adrenal non- or hemorrhagic infarction was identified in five reports (two had adrenal insufficiency, two had normal cortisol levels and one case had no data). Interestingly, the only case with well-characterized new-onset acute primary adrenal insufficiency after COVID-19 had a previous diagnosis of antiphospholipid syndrome. In our case, antiphospholipid syndrome diagnosis was established only after the adrenal infarction triggered by COVID-19. Conclusions Our findings support the association between bilateral adrenal infarction and antiphospholipid syndrome triggered by COVID-19. Therefore, patients with positive antiphospholipid antibodies should be closely monitored for symptoms or signs of acute adrenal insufficiency during COVID-19.


2018 ◽  
Vol 2018 ◽  
pp. 1-4
Author(s):  
Adele Latina ◽  
Massimo Terzolo ◽  
Anna Pia ◽  
Giuseppe Reimondo ◽  
Elena Castellano ◽  
...  

Adrenal insufficiency is a potentially life-threatening condition when it occurs acutely, as in adrenal hemorrhage. Generally it is not reversible and requires chronic replacement therapy. Acute intermittent porphyria (AIP) is a rare genetic disease characterized by alterations in heme biosynthesis that result in accumulation of precursors in tissues. A crisis can be triggered by many conditions such as surgery and infections. Symptoms are similar to those of acute hypoadrenalism. Moreover, both conditions are characterized by hyponatremia. We describe the case of a postmenopausal woman known to be affected by AIP who developed after surgery a primary adrenal insufficiency associated with adrenal enlargement; the latter completely reverted in six months.


2020 ◽  
Vol 48 (7) ◽  
pp. 030006052090365
Author(s):  
Katarina Mlekuš Kozamernik ◽  
Mojca Jensterle ◽  
Aleš Ambrožič ◽  
Marija Pfeifer

We herein report two cases of primary adrenal insufficiency (AI) associated with antiphospholipid syndrome (APS). In both patients, the main finding that led to the diagnosis was hyponatraemia. The major difference between the two cases was the time at which AI evolved during the course of APS. In the first patient, AI developed acutely along with other presenting features of APS. In the second patient, the AI was unmasked during a stressful situation induced by severe inflammation that occurred 7 years after the first APS manifestation and had probably evolved slowly during the previous few years. These cases emphasise the importance of considering AI in patients with either suspected or newly diagnosed APS as well as in patients who have long been known to have APS. The symptoms and signs alerting the clinician to possible AI are general abdominal complaints, fever, hypotension, and hyponatraemia. Conversely, patients with primary AI should be questioned about the signs and symptoms of APS.


2020 ◽  
Vol 13 (3) ◽  
pp. e233631
Author(s):  
Sanval Ahmed Warriach ◽  
Mohamad Mustafa ◽  
Denis O'Keeffe ◽  
Michael Watts

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.


2014 ◽  
Vol 2014 ◽  
pp. 1-7 ◽  
Author(s):  
Marianna Strakhan ◽  
Mariana Hurtado-Sbordoni ◽  
Nahun Galeas ◽  
Kamila Bakirhan ◽  
Karenza Alexis ◽  
...  

Catastrophic antiphospholipid syndrome (CAPS) is a rare but potentially life-threatening condition characterized by diffuse vascular thrombosis, leading to multiple organ failure developing over a short period of time in the presence of positive antiphospholipid antibodies (aPL). CAPS is a severe form of antiphospholipid syndrome, developing in about 1% of cases of classic antiphospholipid syndrome, manifesting as microangiopathy, affecting small vessels of multiple organs. It is acute in onset, with majority of cases developing thrombocytopenia and less frequently hemolytic anemia and disseminated intravascular coagulation. Lupus anticoagulant and anticardiolipin antibodies have been reported as predominant antibodies associated with CAPS. Treatment options often utilized in CAPS include anticoagulation, steroids, plasma exchange, cyclophosphamide therapy, and intravenous immunoglobulin therapy. Even though the reported incidence of this condition is considered to be low, the mortality rate is approaching 50%. The high rate of mortality should warrant greater awareness among clinicians for timely diagnosis and treatment of this life-threatening condition. Studies have shown that complement activation plays a key role in the pathogenesis of aPL mediated thrombosis in CAPS. We report a case of a 36-year-old female admitted with clinical and laboratory findings consistent with CAPS successfully treated with eculizumab, a terminal complement inhibitor.


2016 ◽  
Vol 118 ◽  
pp. 116
Author(s):  
Yoko Maesawa ◽  
Masashi Deguchi ◽  
Shinya Tairaku ◽  
Mayumi Morizane ◽  
Kenji Tanimura ◽  
...  

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