The concept at the heart of the paper is deceptively simple. An antinomic medical term is one whose literal meaning or surface logic directly contradicts the true pathophysiology or clinical behavior of the condition it names. The authors, led by Etienne Rivière of the Internal Medicine and Infectious Diseases unit at Haut-Lévêque Hospital, catalog a series of such paradoxes and explore why they persist, why they matter, and what could be done about them. Their argument is not merely semantic. They contend that misleading nomenclature imposes a real cognitive load on trainees and practicing physicians alike, forcing the brain to memorize exceptions rather than understand mechanisms, at a time when medical knowledge is already expanding at an overwhelming pace.

The flagship example is the lupus anticoagulant, a name that manages to be wrong twice over. First, the test detects antibodies that are strongly associated with thrombosis, not bleeding; the “anticoagulant” label arises only because the antibodies interfere with clotting tests in the laboratory, prolonging the activated partial thromboplastin time, or aPTT, in a test tube. In the body, the opposite happens: patients carrying these antibodies face an elevated risk of venous and arterial clots. Second, despite the name, many people who test positive have no connection whatsoever to systemic lupus erythematosus. The result is a term that can confuse students preparing for exams and, more worryingly, clinicians making rapid decisions about thrombosis workups, where misreading the meaning of a prolonged aPTT in the presence of these antibodies can lead to inappropriate management.

The authors extend the analysis to the rheumatology clinic. So-called connective tissue diseases, a category that includes systemic lupus erythematosus and related systemic autoimmune conditions, are named for the tissue type once thought to be their unifying pathological substrate. Yet the clinical manifestations of these diseases—rashes, kidney inflammation, joint disease, blood count abnormalities—are driven by immune dysregulation that is not confined to connective tissue, and histological findings frequently fail to match the label. Similarly, lupus pernio, a chronic skin manifestation associated with sarcoidosis, has nothing to do with lupus erythematosus; the name borrows the Latin word for wolf because of the violaceous, wolf-like appearance of the lesions, a historical accident that continues to send learners down the wrong diagnostic path.

Gastroenterology supplies one of the most vivid examples: paradoxical diarrhea, also described in the literature as fecal impaction seepage. In elderly, immobile, or constipated patients, a hard mass of stool obstructs the rectum, and only liquid stool can leak around the blockage, producing what looks like diarrhea. The intuitive response—give an antidiarrheal agent—would be exactly wrong, potentially worsening the impaction and its complications. The correct treatment is disimpaction. The authors argue that the term itself, while memorable, encodes the paradox rather than resolving it, and that a name built on the underlying mechanism, such as overflow diarrhea secondary to fecal impaction, would teach the pathophysiology instead of merely flagging the surprise.

The paper also ventures into cardiology and infectious disease, where naming problems take subtler forms. Heart failure with preserved ejection fraction, or HFpEF, is defined partly by a preserved pumping measurement, yet the symptomatic reality for patients is diastolic dysfunction and congestion; the authors discuss how the framing around ejection fraction can obscure the hemodynamic mechanisms that actually produce breathlessness and fluid retention. In the aftermath of infections, a proliferating zoo of labels—post-acute infection syndromes, post-treatment Lyme disease syndrome, post-infectious chronic syndromes—describes overlapping clinical realities with inconsistent terminology, a fragmentation the authors see as an obstacle both to research and to patients seeking recognition of their persistent symptoms. They also cite heparin-induced thrombocytopenia, a condition in which the drop in platelet count is accompanied, paradoxically, by an increased risk of thrombosis driven by antibodies against platelet factor 4, so that the most feared complication of a platelet-lowering drug is clotting.

Why do such terms survive? The authors point to the deep historical layers of medical language. Many names were coined before the mechanisms were understood, when a visible feature, a laboratory artifact, or a superficial resemblance seemed like the most salient characteristic. Once embedded in textbooks, examination syllabi, billing codes, and decades of literature, a term acquires inertia that is difficult to overcome. Renaming is costly: it disrupts literature searches, breaks continuity with older studies, and requires international consensus in fields where even the definitions of the diseases themselves are contested. The result is a kind of linguistic path dependence, in which each generation of students must learn not only the biology but also the archaeology of the words.

The cost of this inertia, the authors argue, is measured in cognitive overload. Medical education has long been criticized for privileging encyclopedic memorization over mechanistic understanding, and antinomic terms are a concentrated expression of that problem. A student who learns that the lupus anticoagulant causes clots despite its name has memorized a fact; a student who learns why the name exists—because of an in vitro artifact in the aPTT assay—has acquired a transferable insight into laboratory medicine and antibody biology. The authors advocate a pedagogical shift away from rote learning of archaic labels and toward teaching the underlying mechanisms first, with the historical names presented explicitly as fossils of earlier misunderstanding rather than as neutral descriptors.

Beyond the classroom, the authors emphasize the consequences for patients. Terms like lupus anticoagulant or paradoxical diarrhea are not merely confusing to laypeople; they can be actively frightening or misleading when a patient reads them in a laboratory report or discharge summary. A person told they have an “anticoagulant” in their blood may reasonably wonder whether they are at risk of bleeding, when the actual clinical concern is thrombosis. The authors call for a global, cross-disciplinary effort to simplify medical language, involving clinicians, educators, linguists, and patient representatives, with the goal of fostering clinical competence and genuine comprehension rather than the accumulation of opaque vocabulary. They propose specific improvements to current nomenclature, suggesting that the most misleading terms be critically re-examined and, where feasible, renamed in ways that reflect mechanism rather than historical accident.

The paper, published as an open-access debate article, is unlikely to settle the question on its own—renaming entrenched medical terms is a slow, collective enterprise—but it crystallizes a problem that many educators recognize and rarely name so directly. In an era when artificial intelligence tools can retrieve facts instantly, the authors suggest, the value of medical education lies increasingly in deep mechanistic reasoning, and language that contradicts mechanism is a tax on that reasoning. Whether the community chooses to reform its most paradoxical terms or simply to teach them more honestly, the underlying message stands: in medicine, the name of a disease should illuminate the disease, not conceal it, and every term that belies the biology it describes is a small, persistent obstacle between knowledge and understanding.

Subject of Research: Misleading antinomic terminology in medical nomenclature and its impact on clinical reasoning and medical education

Article Title: Medical antinomy: when the name belies the disease

Article References: Rivière, E., Mathé, A., Rivière, P., Bonnet, G., James, C., & Guy, A. (2026). Medical antinomy: when the name belies the disease. BMC Medicine. https://doi.org/10.1186/s12916-026-05220-0

Image Credits: AI Generated

DOI: 10.1186/s12916-026-05220-0

Keywords: medical education, nomenclature, lupus anticoagulant, connective tissue diseases, paradoxical diarrhea, heparin-induced thrombocytopenia, post-acute infection syndromes, clinical reasoning, cognitive overload, systemic lupus erythematosus, BMC Medicine, medical language

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