Rare Adrenal Bleeding Reveals Hidden Blood Clot Disorder in Young Man

When a 35-year-old man arrived at his hospital in Hebron, Palestine, with fever, abdominal pain, crushing fatigue, loss of appetite, and unexplained weight loss, his doctors could not have predicted that the trail of clues would end at a pair of small, fist-sized glands sitting atop his kidneys. A new case report published in BMC Endocrine Disorders describes how a dramatic adrenal hemorrhage turned out to be the very first sign of a serious autoimmune clotting disorder known as triple-positive antiphospholipid syndrome. The case, led by Murad Isaak Alshamisti of Al-Quds University and colleagues at Al-Ahli Hospital, offers a striking reminder that bleeding inside the body can paradoxically be caused by blood clots, and that recognizing this paradox can save a patient’s life.

The adrenal glands are small but vital endocrine organs that produce cortisol, aldosterone, and other hormones essential for blood pressure regulation, salt and water balance, and the body’s response to stress. Because of their exceptionally rich blood supply and their unusual venous drainage into a single central vein, the adrenal glands are surprisingly vulnerable to a rare but well-described catastrophe: thrombosis of the adrenal vein, which cuts off the outflow of blood, causes hemorrhagic infarction, and leads to bleeding into the gland itself. In other words, the hemorrhage that appears on a CT scan is not a simple bleed but the end result of a clot that choked off the gland’s circulation. This mechanism explains why adrenal hemorrhage is a recognized, if uncommon, complication of antiphospholipid syndrome, an autoimmune condition in which the immune system mistakenly produces antibodies against phospholipid-binding proteins in the blood.

What makes the Palestinian patient’s case so unusual is that the hemorrhage affected only one adrenal gland. Adrenal insufficiency, the clinical state that arises when the glands fail to produce enough cortisol, is far more commonly associated with bilateral adrenal involvement, because the remaining healthy gland can usually compensate when only one side is damaged. In this patient, however, a large right adrenal hematoma was accompanied by severe biochemical derangement, including a profoundly low serum sodium concentration and a morning serum cortisol level of just 2.8 micrograms per deciliter, a value far below the threshold expected in a critically ill patient. These findings raised immediate concern that the single damaged gland had left him functionally unable to mount a cortisol response, a condition that can rapidly become life-threatening if untreated.

The diagnostic journey began with computed tomography, which revealed the large right adrenal hematoma and effectively excluded other causes of the patient’s abdominal pain. But the laboratory workup added the crucial pieces of the puzzle. His platelet count was low, a finding known as thrombocytopenia that is common in antiphospholipid syndrome. More tellingly, his activated partial thromboplastin time, or aPTT, a standard measure of blood clotting, was markedly prolonged. In most clinical contexts, a prolonged aPTT suggests a bleeding tendency, and one might expect such a patient to hemorrhage more easily. Yet in antiphospholipid syndrome, the prolongation is a laboratory artifact caused by antibodies that interfere with the phospholipid reagents used in the test, even as the patient’s actual physiology is prothrombotic. This is the famous lupus anticoagulant paradox: a test that suggests poor clotting in a patient whose disease is defined by clotting.

To distinguish between a clotting factor deficiency and an inhibitor, the team performed a mixing study, in which the patient’s plasma is combined with normal pooled plasma. If the prolonged clotting time corrects with the addition of normal plasma, the problem is a missing factor; if it fails to correct, an inhibitor is present. In this patient, the mixing study failed to correct the aPTT, pointing squarely toward an inhibitor. Follow-up testing confirmed a positive lupus anticoagulant, and subsequent assays revealed high-titer anticardiolipin antibodies and high-titer anti-beta2-glycoprotein I antibodies. Together with the lupus anticoagulant, these three positive tests constitute the triple-positive antiphospholipid antibody profile, the highest-risk serological pattern in the syndrome, associated with the greatest likelihood of thrombotic events. The combination of adrenal hemorrhage, thrombocytopenia, and the characteristic coagulation abnormalities established the diagnosis of antiphospholipid syndrome presenting for the first time through its adrenal complication.

Once hematology specialists reviewed the case, they favored APS-associated thrombotic adrenal injury as the underlying mechanism, and treatment was initiated accordingly. The patient received therapeutic anticoagulation, first with enoxaparin, a low-molecular-weight heparin delivered by injection, and later transitioned to warfarin, an oral vitamin K antagonist that remains the mainstay of long-term anticoagulation in antiphospholipid syndrome. At the same time, the adrenal insufficiency was treated with hydrocortisone, a replacement glucocorticoid that restores the missing cortisol, and fludrocortisone, a mineralocorticoid that helps the body retain sodium and maintain blood pressure. This dual approach addressed both faces of the disease simultaneously: preventing further clots with anticoagulation while replacing the hormones the damaged gland could no longer produce.

The clinical course was encouraging. During follow-up, the patient showed progressive improvement in his symptoms, his laboratory values normalized, including his kidney function and electrolytes, and repeat imaging demonstrated a marked reduction in the size of the adrenal hematoma. The recovery underscores an important point about adrenal hemorrhage in the context of antiphospholipid syndrome: with prompt anticoagulation and appropriate hormone replacement, even a dramatic presentation can resolve substantially, and patients can return to good health. It also highlights the value of multidisciplinary care, since the case required coordinated input from internal medicine, endocrinology, hematology, and radiology to arrive at the correct diagnosis and treatment plan.

For the wider medical community, the authors argue that this case carries a clear message. When clinicians encounter a patient with unexplained adrenal hemorrhage, particularly when it is accompanied by thrombocytopenia, evidence of adrenal dysfunction, and a markedly prolonged aPTT, antiphospholipid antibody testing should be high on the differential. The alternative is a dangerous diagnostic delay, in which the hemorrhage is attributed to trauma or other causes and the underlying prothrombotic disorder goes untreated, leaving the patient exposed to further clots in the adrenal glands, the brain, the lungs, or the deep veins of the legs. Equally important is the early recognition of adrenal insufficiency itself, because untreated cortisol deficiency in a stressed, febrile patient can precipitate an adrenal crisis, a medical emergency characterized by hypotension, shock, and death if glucocorticoid replacement is not given immediately.

The case also illustrates the subtlety of the antiphospholipid syndrome’s laboratory signature. Lupus anticoagulant antibodies earned their name because they were first identified in patients with lupus and because they prolong clotting tests in a test tube, yet they are among the strongest laboratory predictors of thrombosis in the body. This inversion of expectations, in which a bleeding test predicts clotting, is one of the most counterintuitive phenomena in clinical medicine, and cases like this one, where the paradox plays out in a single organ, provide vivid teaching material for physicians in training. The triple-positive profile identified in this patient, with all three major antiphospholipid antibody tests positive at high titer, marks him as requiring careful, long-term anticoagulation management and monitoring for future thrombotic risk.

Published as an open-access report with the patient’s written informed consent, the study adds to the limited literature on unilateral adrenal hemorrhage as the initial manifestation of antiphospholipid syndrome. It demonstrates that clinically significant adrenal insufficiency can develop even when only one gland is visibly affected, that the hemorrhagic appearance of adrenal injury should not obscure its thrombotic origin, and that a simple mixing study followed by targeted antibody testing can unravel a diagnosis that might otherwise remain hidden. For a young man whose vague symptoms of fever, pain, and fatigue masked a rare autoimmune catastrophe, the systematic application of basic clinical reasoning, from CT imaging to coagulation studies to antibody panels, made the difference between a mysterious illness and a treatable disease with a clear path to recovery.

Subject of Research: Adrenal hemorrhage and adrenal insufficiency as the initial presentation of triple-positive antiphospholipid syndrome

Article Title: Unilateral adrenal hemorrhage and adrenal insufficiency as the initial presentation of triple-positive antiphospholipid syndrome: a case report

Article References: Alshamisti, M. I., Deeb, N., Almasalmah, A., Amayre, S., Kurdi, L., Atawnah, S. I., & Ibriwesh, M. (2026). Unilateral adrenal hemorrhage and adrenal insufficiency as the initial presentation of triple-positive antiphospholipid syndrome: a case report. BMC Endocrine Disorders. https://doi.org/10.1186/s12902-026-02609-z

Image Credits: AI Generated

DOI: 10.1186/s12902-026-02609-z

Keywords: adrenal hemorrhage, adrenal insufficiency, antiphospholipid syndrome, triple-positive antiphospholipid antibodies, lupus anticoagulant, thrombocytopenia, cortisol, anticoagulation, case report, endocrine disorders, hydrocortisone, warfarin