| { |
| "predictor.predict": { |
| "traces": [], |
| "train": [], |
| "demos": [ |
| { |
| "augmented": true, |
| "summary_text": "A 36-year-old female with ulcerative colitis (well controlled on sulfasalazine, ferrous fumarate, and intermittent prednisone for flares) presented with 1 week of progressive oppressive precordial pain associated with dyspnea and neurovegetative symptoms. On admission, the ECG was in sinus rhythm with ST-segment elevation in the inferior wall. She endorsed a 6-month history of general malaise, fatigue, and night sweats, and had experienced exertional precordial pain that progressed to occur at rest. Physical examination revealed no murmurs or peripheral pulse abnormalities.\n\nEmergency coronary angiography demonstrated severe 2-vessel coronary disease: a severe 90% ostial lesion in the left coronary trunk (left main) and a severe 99–100% subocclusive ostial lesion in the right coronary artery (culprit vessel). Primary angioplasty of the right coronary artery was performed with successful placement of a drug-eluting stent. The hemodynamicist noted possible aortitis given arch involvement and vessel friability during balloon advancement and recommended an inflammatory/etiologic evaluation prior to definitive management of the left main lesion.\n\nLaboratory testing showed mild anemia (hemoglobin 11.6 g/dL), mild leukocytosis (13,800/mm3), elevated ESR 42 mm/h, CRP 4.9 mg/L (normal <1), and elevated high-sensitivity troponin. Autoimmunity panel: normal complement C3/C4, negative ANA, anti-DNA, and ENA profile; non-reactive VDRL. Cardiac MRI with contrast demonstrated acute non-transmural infarction of the left ventricular inferior wall and subendocardial ischemia in the anteroseptoapical region at rest, with mild aortic and mitral insufficiency and preserved biventricular systolic function.\n\nComputed tomographic angiography of the chest/abdomen/pelvis showed periaortic fibrotic wall thickening involving the aortic root, arch, and abdominal aorta, with severe left coronary trunk stenosis, mild left subclavian and left vertebral artery stenoses, and severe inferior mesenteric artery stenosis. The differential included IgG4-related disease versus Takayasu arteritis. Total IgG was 1,600 mg/dL (ref 700–1,600) with IgG1 1,024 mg/dL (elevated) and normal IgG2 456 mg/dL, IgG3 98.8 mg/dL, and IgG4 13.6 mg/dL, findings not supportive of IgG4-related aortitis. Takayasu arteritis was diagnosed clinically and by imaging.\n\nImmunosuppression was initiated with prednisone 60 mg daily and methotrexate 20 mg weekly (parenteral) with folic acid 1 mg daily. After 3 weeks of therapy, she underwent myocardial revascularization surgery using the left internal mammary artery graft to the descending anterior artery (LAD) and an aortocoronary bypass to the circumflex artery. Intraoperatively, the aortic root and ascending aorta appeared healthy. She was discharged home in good general condition and remains under ambulatory follow-up.\n\nContext: Takayasu arteritis is a large-vessel granulomatous vasculitis affecting the aorta and its major branches that can produce aorto-ostial coronary lesions (as in this case, involving the left main and right coronary ostia), leading to myocardial ischemia/infarction. The mildly elevated inflammatory indices, periaortic fibrotic thickening, and multifocal arterial stenoses on CTA are characteristic, and the lack of IgG4 elevation argues against IgG4-related aortitis. The staged approach—urgent culprit-vessel PCI followed by immunosuppression and delayed CABG—is consistent with management principles aiming to control vascular inflammation before definitive surgical revascularization.", |
| "reasoning": "The summary uses extensive medical jargon and acronyms (e.g., ECG, ST-segment elevation, PCI, RCA/LAD/left main, drug‑eluting stent, aortitis, ESR/CRP, ANA/ENA/VDRL, MRI/CTA, non‑transmural infarction, subendocardial ischemia, periaortic fibrotic thickening, stenosis, IgG subclasses, Takayasu arteritis, immunosuppression, CABG). Sentences are long and information-dense, with detailed imaging, lab values, and procedural nuances (e.g., “aorto‑ostial,” “culprit vessel,” “hemodynamicist,” dosing regimens). It assumes familiarity with cardiology, vascular immunology, and surgical management, offering minimal lay explanations. Overall complexity and terminology require advanced medical literacy.", |
| "label": "proficient_health_literacy" |
| }, |
| { |
| "summary_text": "A 23-year-old man came to the emergency department with a sudden severe headache, nausea, vomiting, and chest heaviness. His initial vital signs showed high blood pressure and a fast breathing rate. An emergency ECG showed a heart attack pattern (STEMI), so he was urgently sent for percutaneous coronary intervention; the angiogram revealed normal coronary arteries. Further evaluation with a brain CT identified a cisternal subarachnoid hemorrhage (bleeding around the brain). Despite coordinated care by multiple teams, his condition rapidly worsened, leading to cardiac arrest and death.", |
| "label": "intermediate_health_literacy" |
| }, |
| { |
| "summary_text": "A 36-year-old woman had trouble swallowing.\n\nTests showed she was born with an unusual shape of the large blood vessel that carries blood from the heart (the aorta). Instead of curving to the left like most people, it curves to the right.\n\nMost people with this do not have symptoms. Symptoms can happen if the aorta presses on nearby tubes in the chest. This pressure can squeeze the food tube (esophagus) or the breathing tube (trachea).\n\nSurgery may be needed if the pressure is severe, if the aorta becomes weak and bulges, if there is a tear in the aorta, or if there is a pouch on the aorta that is larger than 2 cm.\n\nThere is no single best treatment for everyone. Care depends on the person’s symptoms and body shape. This patient did not get treatment.", |
| "label": "low_health_literacy" |
| }, |
| { |
| "summary_text": "A 23-year-old man went to the emergency room because he suddenly got a very bad headache.\n\nHe also felt sick, threw up, and felt heavy pressure in his chest.\n\nHis blood pressure was high and he was breathing fast.\n\nA heart test (ECG) first made doctors think he might be having a major heart attack.\n\nHe was rushed for a procedure to look at the blood vessels of his heart, but they were normal.\n\nA head scan (CT) then showed bleeding around his brain.\n\nEven with care from a team of doctors, he got worse, had cardiac arrest, and died.", |
| "label": "low_health_literacy" |
| }, |
| { |
| "summary_text": "A 69-year-old man with prior coronary bypass surgery presented with two months of severe shortness of breath with mild activity (NYHA class III). He was diagnosed with heart failure due to ischemia after failure of a saphenous vein graft to the right coronary artery. This was supported by an abnormal ECG, elevated NT-proBNP, and a coronary angiogram; echocardiography also showed reduced pumping function. The team reopened a chronic total occlusion in the native right coronary artery using a retrograde approach through septal channels (septal surfing). To enable that route, they first re-opened the totally occluded left coronary artery. After the procedure, his dyspnea improved before discharge, and at 6 months he had no recurrence of shortness of breath.", |
| "label": "intermediate_health_literacy" |
| }, |
| { |
| "summary_text": "A 23-year-old male with a 23 pack-year smoking history, no alcohol use, and no illicit drug use presented with 2 hours of sudden severe frontal headache, nausea, vomiting, and chest heaviness. He was distressed but alert and oriented. Vitals: BP 178/103 mmHg, RR 26/min, T 38.9°C, HR 87/min, SpO2 94%. Exam: normal vesicular breath sounds; cardiovascular and abdominal exams inconclusive; neurological exam notable for neck stiffness, dilated but light-reactive pupils, normal plantar reflexes, and no focal deficits. ECG showed ST-segment elevation >2 mm in V2–V5, consistent with STEMI; he received a 300 mg aspirin load and was urgently transferred for PCI. Troponin was elevated at 1.48 mg/dl (normal <0.16 mg/dl). Femoral-access coronary angiography demonstrated normal coronary arteries with TIMI 3 flow. Post-angiography ECG showed normal sinus rhythm with LVH; echocardiography revealed normal ventricular function without RWMA. Subsequent workup found lymphocytosis and mildly elevated CRP. Non-contrast CT brain demonstrated a cisternal subarachnoid haemorrhage with extension anterior to the right temporal lobe. Abdominal ultrasound was negative for polycystic kidney disease; cerebral CT angiography was planned to exclude aneurysm. Nimodipine 60 mg q4h was initiated with a BP target of 160/100 mmHg. On day 2, he acutely deteriorated with cardiac arrest; after CPR, GCS was 6, and he was intubated and mechanically ventilated in the ICU. Owing to instability, repeat CT brain and planned cerebral CTA were not performed. He received multidisciplinary ICU care with NG feeding, IV fluids, antibiotics, a proton pump inhibitor, and nimodipine. On day 8, he developed ventricular fibrillation and, despite CPR and more than five defibrillation attempts, could not be resuscitated and died.", |
| "label": "proficient_health_literacy" |
| }, |
| { |
| "summary_text": "A 20‑year‑old woman had been followed since age eight for idiopathic nephrotic syndrome (NS) inaugurated by cerebral venous thrombosis extended to the right jugular vein with a massive pulmonary embolism, without sequelae and without personal or family thrombotic history. Kidney biopsy was deferred because there was no kidney failure, gross hematuria, hypertension, or extra‑renal signs suggestive of secondary NS at presentation. She was treated with an oral vitamin K antagonist and oral corticosteroids with good evolution. Subsequently, she had multiple steroid‑dependent relapses and was started on mycophenolate mofetil (MMF) as background therapy to spare corticosteroids and ensure normal growth. An exhaustive thrombophilia assessment was negative: homocysteine, fibrinogen, protein C, protein S, antithrombin III, factor V Leiden, JAK‑2, cryoglobulins, anticardiolipin antibodies, lupus anticoagulant, and anti‑β2‑glycoprotein I antibodies were all normal. Anticoagulation was stopped after nine years. Several relapses occurred but were controlled with oral corticosteroids. NS remission was documented from 2017; MMF was gradually discontinued in 2019, and she remained asymptomatic without relapse.\n\nOne year later, she presented to the emergency department with acute intense diffuse abdominal pain without irradiation, associated with postprandial vomiting and bilateral lower‑limb edema for six hours. Examination showed intense epigastric tenderness with normal vital signs (BP 120/70 mm Hg, HR 83 bpm, SpO2 100% on room air) and no fever or neurological impairment. Urinalysis detected proteinuria. Hemogasanalysis showed metabolic acidosis with respiratory compensation. Labs revealed hypoalbuminemia, hypercholesterolemia, prothrombin time 90%, elevated D‑dimer, LDH, and creatine phosphokinase, with inflammatory markers (CRP 37 mg/L) and leukocytosis (26.4 × 10^3/µL); renal and liver function were normal. Urgent abdominal ultrasound showed a low‑to‑moderate intra‑abdominal effusion. Contrast‑enhanced CT demonstrated acute thrombosis of the superior mesenteric artery with acute mesenteric ischemia. She underwent emergency laparotomy: intraoperative exploration confirmed mesenteric ischemia with extensive necrosis of almost the entire small bowel, rendering resection incompatible with life. She died 48 hours later.\n\nThis case illustrates catastrophic arterial thrombosis in the setting of NS despite a negative thrombophilia work‑up. NS is a hypercoagulable state with multifactorial mechanisms, including urinary loss of anticoagulant proteins (e.g., antithrombin III, protein S), increased fibrinogen, hemoconcentration, dyslipidemia, and systemic inflammation. While venous thromboembolism is more common in NS, superior mesenteric artery thrombosis is rare but often fatal, underscoring the need for high clinical suspicion and rapid imaging when severe acute abdominal pain occurs in patients with active or relapsing NS.", |
| "label": "proficient_health_literacy" |
| }, |
| { |
| "summary_text": "A 20-year-old woman had a long-term kidney problem that made protein leak into her urine.\n\nWhen she was 8, she got serious blood clots in the veins of her brain and a clot in her lungs. Doctors treated her with blood-thinner medicine and steroid medicine. Later, she also took a medicine (mycophenolate) to help control the kidney problem.\n\nTests did not find an inherited reason for blood clots.\n\nOver the years, her kidney problem flared up several times, but steroids helped. After 2017, she did not have more flare-ups, so her doctors stopped the blood thinner and the other immune medicine.\n\nOne year later, she suddenly had very bad belly pain all over, threw up after eating, and had swelling in both legs. Tests showed her kidney problem had come back.\n\nA CT scan showed a new blood clot blocking a main artery that carries blood to the intestines. During surgery, doctors found that a large part of her small intestine had died. She died 48 hours later.", |
| "label": "low_health_literacy" |
| }, |
| { |
| "summary_text": "A 62-year-old North African woman was diagnosed in 2021 with Von Hippel–Lindau (VHL) disease, a condition that can cause tumors in different organs. She had several VHL-related tumors, including a tumor near the left ear bone, a tumor in the left adrenal gland (pheochromocytoma), kidney cancer on the left side, a right kidney with many cysts, and growths in the pancreas. She was treated with radiation for the ear-bone tumor and had surgeries to remove the left adrenal gland, the left kidney, and part of the pancreas. During follow-up scans (ultrasound and MRI), doctors found a solid-and-cystic mass near the left ovary/fallopian tube area. A laparoscopy then showed cystic tumors on both sides in tissue next to the fallopian tubes (mesosalpinx). She had surgery to remove the uterus and both ovaries/fallopian tubes. Lab testing of the tissue showed benign tumors called clear-cell papillary cystadenomas on both sides, in the mesosalpinx and broad ligament, which fit with VHL disease.", |
| "label": "intermediate_health_literacy" |
| }, |
| { |
| "summary_text": "A 20‑year‑old woman had a 12‑year history of idiopathic nephrotic syndrome that initially presented with extensive cerebral venous thrombosis and pulmonary embolism. She was treated with anticoagulation and oral corticosteroids, then mycophenolate mofetil as a steroid‑sparing agent. A comprehensive thrombophilia work‑up was negative. She experienced multiple relapses controlled with steroids until 2017, then remained in remission; anticoagulation and MMF were discontinued. One year later, she developed sudden diffuse abdominal pain with postprandial vomiting and bilateral leg edema. Laboratory tests confirmed a relapse of nephrotic syndrome. Abdominal CT showed acute superior mesenteric artery thrombosis causing acute mesenteric ischemia. At surgery, there was extensive small‑bowel necrosis not compatible with survival. She died 48 hours later.", |
| "label": "intermediate_health_literacy" |
| }, |
| { |
| "summary_text": "This is about a 13-year-old boy. He has had wart-like growths in his throat since he was 2 years old. He came to the hospital because he was having trouble breathing. Doctors found many small growths that were narrowing his voice box and windpipe. A chest scan also showed several small air pockets (cysts) in his lungs. Doctors removed the growths and made a small breathing opening in his neck (a tracheostomy) to help him breathe. He got one dose of a medicine called bevacizumab (400 mg) through a vein and did breathing therapy. He got better, and the problem did not come back during follow-up.", |
| "label": "low_health_literacy" |
| }, |
| { |
| "summary_text": "A 65-year-old male presented with six months of swelling and boutonniere deformity of the right digit III following a motorcycle accident on January 1, 2023. He initially self-managed with analgesics and did not seek care. He reported inability to fully extend the right middle finger. Examination demonstrated edema and a boutonniere posture (PIP flexion, DIP hyperextension). Active PIP ROM was 45–110 degrees, with passive PIP ROM within normal limits. Radiographs of the right hand (AP/lateral) revealed no osseous pathology, supporting a soft-tissue etiology consistent with a central slip injury. \n\nSurgical technique: Central slip defect reconstruction was performed using the partial ulnar slip of the flexor digitorum superficialis (FDS) tendon. Under anesthesia and tourniquet control in the supine position, a midlateral incision was made on the ulnar aspect of the middle phalanx centered at the PIP joint with dorsal oblique extension, and a transverse incision was made over the MCP flexion crease proximal to the A1 pulley. The ulnar digital neurovascular bundle was identified and protected. Full-thickness dorsal flaps were elevated to expose the central slip and extensor mechanism to the PIPJ. Scar and pseudotendinous tissue were excised. The central slip was not amenable to primary repair; therefore, the ulnar slip of the FDS was selected for reconstruction. The ulnar neurovascular bundle was mobilized to visualize the periosteal insertion of the A3 pulley. The extensor tendon was mobilized and tenolyzed; the dorsal PIP capsule was incised with removal of interposed tissue. The A3 pulley periosteal insertion and the volar capsule of the PIP joint were incised longitudinally. A 2–0 non-absorbable monofilament suture was placed around the ulnar FDS slip at the PIP level. Through the proximal incision, the flexor sheath and A1 pulley were incised longitudinally to expose the FDS; the ulnar slip was isolated and transected, preserving the radial slip. The previously placed 2–0 suture facilitated delivery of the distally based ulnar FDS slip distally. A 2.8‑mm dorsal-to-volar bone tunnel was drilled at the base of the middle phalanx; an elevator protected the FDP, volar plate, and volar structures. With the PIP reduced in full extension, the FDS slip was passed through the tunnel and routed through the intact proximal segment of the central slip/extensor tendon. A tendon weaver completed a Pulvertaft weave under appropriate tension with the PIP in full extension and reduction, secured with 3–0 non-absorbable suture. The capsule and central slip reconstruction margins were approximated; adhesions were released and lateral bands mobilized. Tenodesis effect, posture, stability, and motion were assessed. Wounds were irrigated, the tourniquet deflated, hemostasis obtained, and capillary refill confirmed. Skin was closed with horizontal mattress sutures. A sterile dressing and a well-padded PIP extension splint were applied to allow early DIP and MCP motion.\n\nPostoperative course: First wound check at postoperative day 4; the patient received meloxicam 7.5 mg PO BID and doxycycline 100 mg PO BID for 3 days. A second wound visit occurred 3 days later. At 2 weeks, the back slab and external sutures were removed, and active and passive PIP ROM exercises were initiated. By 3 weeks, the wound had healed and PIP ROM was 0–90 degrees. At 1 month, PIP ROM improved to 0–100 degrees, with continued functional gains. After 7 weeks of rehabilitation, he returned to work with PIP ROM 0–110 degrees. Overall function improved substantially, with the DASH score decreasing from 50 to 4.2.\n\nInterpretation: Clinical and radiographic findings were concordant with a chronic central slip injury producing boutonniere deformity (PIP flexion, DIP hyperextension due to dorsal apparatus disruption and volar migration of lateral bands). Reconstruction using an ulnar FDS slip via bone tunnel and Pulvertaft weave restored PIP extension and yielded progressive ROM gains and marked functional recovery.", |
| "label": "proficient_health_literacy" |
| }, |
| { |
| "summary_text": "A 78-year-old man in Ethiopia had a heart pacemaker to help his heart beat normally. He needed prostate surgery.\n\nBefore surgery, the doctors recommended changing the pacemaker setting to lower the chance of heart problems during the operation. The man could not afford this change. He decided to have the surgery anyway.\n\nHe agreed to the plan and signed a consent form. After the surgery, he also agreed that doctors could write about his case.\n\nFor the operation, the doctors used medicine to numb his lower body with an injection in his lower back. They watched his heart and blood pressure closely. His vital signs stayed stable. His blood pressure stayed okay with IV fluids.\n\nAfter surgery, he went to the recovery area. He got pain medicine about 4 hours later and extra pain medicine through the back tube. About 6 hours after surgery, he moved to the regular hospital ward in stable condition.\n\nHe continued getting pain control this way for 72 hours. He went home about 88 hours after surgery in stable condition.", |
| "label": "low_health_literacy" |
| }, |
| { |
| "summary_text": "A 59-year-old Japanese man with a 28-year history of type 1 diabetes on intensive multiple-dose insulin therapy (BMI 18.4 kg/m2, undetectable C‑peptide, HbA1c ~9.0%) and remote, asymptomatic chronic severe (grade III) aortic regurgitation (diagnosed 16 years earlier without subsequent follow‑up) presented with acute decompensated heart failure. He had never undergone surgery or prosthetic device implantation and had no history of immunosuppressive therapies.\n\nEight days after a routine visit, he developed dyspnea and fever >38℃. On arrival: BP 192/82 mmHg, HR 118/min, orthopnea, SpO2 80%. Exam: Levine 3/6 systolic murmur; no Osler nodes, Janeway lesions, or conjunctival petechiae. Labs: WBC 20,800/μL, CRP 6.06 mg/dL, CK‑MB 6.0 IU/L, troponin T negative. CXR showed pulmonary congestion with cardiomegaly (CTR 55%). ECG had ST elevation in V1–V4, but emergent echocardiography showed no systolic dysfunction. He was diagnosed with acute heart failure due to valvular disease and treated with non‑invasive positive pressure ventilation and nitrates.\n\nTransthoracic echocardiography demonstrated severe aortic regurgitation and severe mitral regurgitation with a mobile mitral vegetation. Transesophageal echocardiography identified a 16.5×6‑mm mobile vegetation on the anterior leaflet of the mitral valve and an 11.2×5‑mm nonmobile vegetation on the noncoronary cusp of the aortic valve, raising strong suspicion for native valve endocarditis (NVE). Head CT and MRI showed no cerebral infarction or hemorrhage.\n\nRetrospective review revealed subtle abnormalities starting four months pre‑admission: mildly elevated WBC, albumin decreased to 3.0 g/dL the following month, and gradual hemoglobin decline over two months, with a 4‑kg weight loss. EGD and whole‑body CT were unrevealing. He partially regained weight and labs nearly normalized except for a CRP of 0.54 mg/dL. At the last pre‑admission visit (8 days prior), WBC was 9,300/μL, Hb 13.1 g/dL, Alb 3.0 g/dL, CRP 4.18 mg/dL, and diastolic BP had fallen; he remained afebrile and asymptomatic aside from weight loss.\n\nEmpiric antibiotics were initiated with ampicillin–sulbactam 12 g/day plus gentamicin 120 mg/day. Three admission blood culture sets all grew Staphylococcus warneri, a coagulase‑negative staphylococcus (CoNS) and resident skin flora (MICs: ABPC/S ≤8 μg/mL; GM ≤1 μg/mL; CEZ ≤2 μg/mL), confirming S. warneri IE. Per Japanese Circulation Society guidance, emergency surgery is generally recommended for NYHA III–IV heart failure or urgent surgery for NVE with mobile vegetation >10 mm and severe valve dysfunction. Because heart failure improved rapidly and appropriate antibiotics were started (reducing embolic risk), and given poorly controlled type 1 diabetes increasing operative risk, elective surgery was planned after stabilization of infection and glycemia. Antibiotics were narrowed to cefazolin 6 g/day; dental evaluation showed no periodontitis.\n\nAfter four weeks of antibiotics, surgery revealed a bicuspid aortic valve with intact aortic and mitral annuli and no abscess. Large vegetations were exenterated, and both valves were replaced with mechanical prostheses. The postoperative course was uneventful; he was discharged on postoperative day 22 without apparent embolism and has remained recurrence‑free for over two years. This case represents NVE due to the resident CoNS S. warneri in a patient without prosthetic material or immunosuppression, with prodromal laboratory abnormalities and weight loss evident up to four months before presentation.", |
| "label": "proficient_health_literacy" |
| }, |
| { |
| "summary_text": "A 36-year-old woman with ulcerative colitis developed a week of worsening chest pressure with autonomic symptoms (such as sweating and nausea). Her electrocardiogram showed ST-segment elevation in the inferior leads, consistent with an inferior-wall heart attack. She also reported several months of fatigue and night sweats.\n\nUrgent coronary angiography found severe two-vessel coronary artery disease. The right coronary artery was the culprit lesion and was opened successfully with a stent. Because the interventional team suspected inflammation of the aorta (aortitis), additional workup was done. Inflammatory markers were mildly elevated, and CT angiography showed fibrotic thickening around the aorta with significant narrowing in multiple arteries, pointing to Takayasu arteritis.\n\nShe started treatment with prednisone and methotrexate. After stabilization, she underwent delayed coronary bypass surgery and did well.", |
| "label": "intermediate_health_literacy" |
| } |
| ], |
| "signature": { |
| "instructions": "Judge the health literacy level of a generated medical summary.\nIdentify if the language is suitable for a layperson (low) or requires medical expertise (proficient).", |
| "fields": [ |
| { |
| "prefix": "Summary Text:", |
| "description": "The generated medical summary to be analyzed." |
| }, |
| { |
| "prefix": "Reasoning:", |
| "description": "Analysis of jargon, acronyms, and sentence complexity." |
| }, |
| { |
| "prefix": "Label:", |
| "description": "${label}" |
| } |
| ] |
| }, |
| "lm": null |
| }, |
| "metadata": { |
| "dependency_versions": { |
| "python": "3.11", |
| "dspy": "3.1.0", |
| "cloudpickle": "3.1" |
| } |
| } |
| } |
|
|
