The stakes are high because AGASACA behaves in a paradoxical way. Although the primary tumor at the anal sac can be small at diagnosis, metastatic lymph nodes in the sublumbar region can grow large enough to partially obstruct the rectum, creating life-threatening consequences from disease that started in a gland the size of a pea. The disease also tends to progress relatively slowly compared with many other malignancies, which means that long-term locoregional control, rather than a rapid strike against distant spread, is the single most important goal for a successful outcome. Late in the disease course, metastases can also appear in distant organs such as the lungs, but it is the pelvic battlefield where most treatment decisions are won or lost.

Surgery has long been considered the first line of defense. Yet the review makes clear that the surgical landscape is more complicated than many clients realize. Local recurrence of the primary tumor after resection has been reported in anywhere from 4 to 44 percent of cases, with a median time to recurrence ranging from 140 to 374 days. When surgeons attempt to remove metastatic iliosacral lymph nodes, recurrence within the lymphocentrum has been documented in between roughly 12 and 59 percent of cases, sometimes within just six months of the operation. Perioperative complications occur in 12 to 39 percent of patients, and the most feared complication, hemorrhage during lymph node extirpation, affects up to 18 percent of dogs, with mortality reaching 2.2 percent. Critically, the risk of complications climbs sharply when lymph nodes exceed 4.5 centimeters in size, a threshold that should prompt especially careful conversations between veterinarians and owners.

Patterns of treatment failure tell a coherent story across studies. In one investigation of 34 dogs with early-stage disease treated with surgery alone, 21 percent developed local recurrence of the primary tumor at a median of 354 days, and 26 percent developed locoregional metastases at a median of 589 days. A larger study of 161 dogs stratified patients by surgical margins, using the familiar R0, R1, and R2 classification system, and found that only the presence of lymphovascular invasion and an R1 resection, in which tumor cells extend to the cut edge of the specimen, were statistically associated with recurrence. In dogs with massive primary tumors greater than 5 centimeters, none of the stage 2 patients developed lymph node metastasis, while more than half of those presenting with stage 3 disease progressed further. The unifying message is that disease stage at initial treatment mediates the risk of relapse, which implies that adjuvant therapies should be deployed on a risk-based basis rather than universally.

This is where radiation therapy enters the picture, and where the review offers its most nuanced analysis. Conventionally fractionated definitive radiotherapy, or CFDRT, aims to deliver the highest possible dose to residual tumor cells while respecting the tolerance of surrounding normal tissues, typically in 16 to 20 fractions of 2.5 to 3 Gy for total doses of 48 to 50 Gy. The problem is that its clinical role in microscopic AGASACA after surgery remains poorly defined. In a study of 113 variably treated dogs, adjuvant radiation did not produce a significant improvement in survival time, though the small number of irradiated patients and the slow natural history of the tumor may have masked a real effect. Meanwhile, dogs undergoing CFDRT develop moderate to severe acute side effects in organs at risk including the rectum, colon, urinary bladder, skin, and spinal cord, with recovery from acute toxicity taking 23 to 36 days after onset. The therapeutic index, the ratio of benefit to harm, may simply not be favorable enough for this approach in every patient.

The most striking finding in the review concerns hypofractionated radiotherapy for advanced disease. In a study comparing hypofractionated radiation against surgical extirpation of iliosacral lymph nodes in dogs with stage 3b AGASACA, radiation produced significantly longer outcomes: a median progression-free interval of 347 days versus 159 days for surgery, and a median survival time of 447 days versus 182 days. The authors offer a compelling technical explanation rooted in the geometry of radiation planning. When radiation oncologists contour a CT scan, they delineate all visible gross disease as the gross tumor volume, then add margins for subclinical microscopic extension to create the clinical target volume, and finally add further margin for setup uncertainty to create the planning target volume. This means radiation can treat the entire iliosacral lymphocentrum, including microscopic disease threading through the lymphatic network, in a way that no surgeon’s hands can match. Surgery removes individual enlarged nodes; radiation can sterilize the whole nodal basin.

Even the terminology of palliative care may need revision for this disease. Protocols delivering 20 Gy in five daily 4 Gy fractions, often labeled palliative because of their low total dose, have produced median progression-free survival of 289 to 347 days and median survival times of 329 to 447 days in AGASACA patients. For comparison, across a broad range of other tumor types treated with the same 4 Gy by 5 protocol, median progression-free survival was only 4.4 months. AGASACA appears roughly twice as responsive as expected, suggesting the tumor may harbor a low alpha-beta ratio, the radiobiological parameter that determines sensitivity to large fraction sizes, consistent with its slowly proliferating nature. The authors argue that defining treatment intent purely by fraction size and number may be inappropriate when a so-called palliative regimen delivers a year of disease control with mostly mild, grade 1 to 2 gastrointestinal side effects.

Not every advanced technique earns endorsement. Stereotactic body radiotherapy, which delivers ablative doses of 6 to 10 Gy per fraction over 3 to 5 fractions, showed promising survival numbers in small studies, with one report of a 991-day median survival in five dogs. But the largest SBRT study to date, involving 25 dogs treated for metastatic sublumbar lymph nodes, revealed a sobering safety signal: 48 percent of dogs developed late-onset changes in gait and hind limb lameness, including ataxia, paraparesis, weakness, and pain. The authors recommend reserving SBRT for macroscopic disease rather than microscopic tumor beds, and focusing treatment on the nodal region while addressing the primary site surgically. Chemoradiotherapy fares even worse in the evidence hierarchy. The largest dataset, 15 dogs treated with concurrent mitoxantrone, produced a 93 percent rate of severe moist desquamation and a 53 percent rate of clinically relevant late effects, including two dogs euthanized for chronic colorectal toxicity. The review concludes there is insufficient evidence to recommend routine chemoradiotherapy in this disease.

One further clinical pearl concerns hypercalcemia of malignancy, a paraneoplastic syndrome affecting 27 to 34 percent of AGASACA patients that can become an emergency when total calcium exceeds 16 mg/dL. Hypofractionated radiation resolved hypercalcemia in about 31 percent of cases alone, rising to 77 percent when combined with steroids or bisphosphonates, offering a non-surgical route to controlling this dangerous metabolic derangement. Looking forward, the authors call for prospective trials comparing fractionation schemes, systematic imaging-based assessment of response rates, and rigorous studies of patterns of failure. Modern technology, including intensity-modulated radiation therapy and cone beam CT image guidance, should theoretically reduce both acute and late toxicities compared with the older two-dimensional planning used in much of the published literature, though no study has yet confirmed this. For now, the review’s practical bottom line is clear: surgery remains the cornerstone for the primary tumor, radiation deserves serious consideration, and may even be preferred, for advanced nodal disease, and the humble five-fraction protocol may deserve a better name than palliative.

Subject of Research: The role of radiotherapy in treating canine apocrine gland anal sac adenocarcinoma

Article Title: Role of radiotherapy in canine apocrine gland anal sac adenocarcinoma: a review

Article References: Murakami, K., & Rancilio, N. (2025). Role of radiotherapy in canine apocrine gland anal sac adenocarcinoma: a review. Veterinary Oncology, 2(1), Article 12. https://doi.org/10.1186/s44356-025-00028-1

Image Credits: AI Generated

DOI: 10.1186/s44356-025-00028-1

Keywords: canine cancer, AGASACA, radiotherapy, veterinary oncology, hypofractionated radiation, SBRT, iliosacral lymph nodes, hypercalcemia, chemoradiotherapy, surgical oncology, dogs, radiation side effects

The clinical stakes are considerable. In children, hypercalcemia can present anywhere along a spectrum from an incidental laboratory finding to vomiting, dehydration, lethargy, hypertension, arrhythmia, acute kidney injury, nephrocalcinosis, or failure to thrive. While primary hyperparathyroidism and malignancy dominate the adult landscape, the causes in neonates, infants, and toddlers skew differently: nutritional excess, vitamin D metabolic disorders, renal phosphate-handling defects, calcium-sensing pathway disorders, subcutaneous fat necrosis, and syndromic disease all demand earlier consideration. The editorial is explicitly framed as an expert-informed triage aid rather than a formal guideline, and its authors stress that outcome-validated studies are still needed.

The framework’s first decision point is deceptively basic: is this really hypercalcemia, and how severe is it? Confirmation and severity assessment should proceed in parallel with stabilization. Total calcium must be interpreted alongside serum albumin, and corrected or ionized calcium may be needed—particularly when albumin is abnormal, acid–base disturbance is present, or the child is critically ill. The authors emphasize that pediatric calcium reference intervals are age-dependent, and that adult-derived ranges may misclassify infants and young children. As practical severity prompts, albumin-adjusted total calcium above 10.5 mg/dL (2.60 mmol/L) or ionized calcium above 5.25 mg/dL (1.32 mmol/L) supports true hypercalcemia, while values approaching or exceeding 12–14 mg/dL (3.00–3.50 mmol/L), rapidly rising calcium, or hypercalcemia accompanied by dehydration, altered mental status, arrhythmia, severe vomiting, renal dysfunction, or nephrocalcinosis should trigger immediate supportive care while the diagnostic workup continues.

That initial evaluation should include serum albumin, iPTH, phosphate, magnesium, alkaline phosphatase, creatinine, 25-hydroxyvitamin D, and a spot urinary calcium-to-creatinine ratio (UCa/UCr). During acute management, calcium, phosphate, magnesium, creatinine, fluid balance, urine output, and clinical status should be reassessed serially, with electrocardiographic monitoring when hypercalcemia is moderate to severe or when symptoms, arrhythmia, renal dysfunction, or relevant electrolyte abnormalities are present. A focused history matters too: calcium or exogenous vitamin D exposure, formula preparation, parenteral nutrition, medications, immobilization, malignancy, renal or transplant history, and family history can all reshape the differential. Renal ultrasonography is useful when hypercalcemia persists, hypercalciuria or renal impairment is present, nephrolithiasis or nephrocalcinosis is suspected, or onset is in infancy.

On the treatment side, isotonic saline is usually first-line for significant or symptomatic hypercalcemia, restoring intravascular volume and promoting renal calcium excretion—though fluid overload must be watched in children with renal or cardiac disease. Notably, the authors caution against routine loop diuretics; if used, they should follow volume restoration and close electrolyte monitoring, and are mainly reserved for fluid overload after euvolemia is achieved. Calcitonin acts rapidly but briefly; glucocorticoids are most useful for vitamin D-mediated or granulomatous disease; and bisphosphonates offer more sustained effects but carry risks of delayed onset, hypocalcemia, renal toxicity, and prolonged skeletal retention in children. In potentially transient infantile conditions such as subcutaneous fat necrosis, bisphosphonates should generally be reserved for severe, prolonged, or persistent hypercalcemia refractory to aggressive hydration and calcitonin. Dialysis remains a last resort for life-threatening or refractory cases, particularly with renal failure or fluid intolerance. Importantly, the authors note that improvement after hydration does not establish dehydration as the underlying cause.

The framework’s central biochemical hinge is iPTH, and the authors deliver a memorable warning: in true hypercalcemia, parathyroid hormone should be suppressed, so a value reported as “normal” may actually be inappropriate if calcium is elevated. Suppressed iPTH points toward iPTH-independent hypercalcemia—vitamin D intoxication or impaired vitamin D catabolism, malignancy, granulomatous disease, immobilization, subcutaneous fat necrosis, medication-related causes, and selected genetic or syndromic disorders. A non-suppressed, inappropriately normal, or elevated iPTH raises concern for iPTH-dependent disease, including primary hyperparathyroidism, familial hypocalciuric hypercalcemia, neonatal severe hyperparathyroidism, multiple endocrine neoplasia-related disease, and tertiary hyperparathyroidism. If the phenotype and iPTH result are discordant, repeat testing after stabilization is reasonable, since biotin exposure, assay differences, renal dysfunction, and sampling after treatment can all complicate interpretation.

Age then becomes the lens through which iPTH-independent causes are prioritized. In neonates, infants, and young toddlers, clinicians should first revisit intake and exposure, because excess vitamin D or calcium is reversible and easily missed. If exposure does not explain the picture, inherited or syndromic disease should be considered early—especially when hypercalcemia is persistent, recurrent, or accompanied by hypercalciuria, hypophosphatemia, nephrocalcinosis, or a positive family history. CYP24A1- and SLC34A1-related disease and Williams–Beuren syndrome are highlighted as important examples. A subtle technical point carries real weight here: a normal 25-hydroxyvitamin D level does not exclude impaired vitamin D catabolism, and 1,25-dihydroxyvitamin D results may not be available when early inpatient decisions must be made. Once available, elevated or inappropriately normal 1,25-dihydroxyvitamin D despite suppressed iPTH supports vitamin D-mediated hypercalcemia and may point toward impaired catabolism, renal phosphate-handling defects, or extrarenal 1α-hydroxylase activity.

In older children and adolescents with suppressed iPTH, acquired causes move to the fore: malignancy, immobilization, iatrogenic or drug-induced hypercalcemia, granulomatous infection or inflammation, vitamin A excess, thiazides, and endocrine disorders including thyrotoxicosis and adrenal insufficiency. In children with chronic kidney disease or after transplantation, the iPTH pattern and treatment exposure should guide classification, because treatment-related hypercalcemia may be iPTH independent while persistent or tertiary hyperparathyroidism is iPTH dependent. Parathyroid hormone-related peptide testing may help when malignancy is suspected, though assay and age-related interpretation require caution.

The third pillar—urinary calcium—exists to prevent one of the most consequential errors in this field: misclassifying familial hypocalciuric hypercalcemia (FHH) as primary hyperparathyroidism. FHH is usually mild, lifelong, and often familial, and parathyroidectomy is usually ineffective. Relative hypocalciuria for age and context should therefore prompt family calcium testing and consideration of CASR, GNA11, and AP2S1 genetic testing before localization imaging or surgery. The authors stress that urinary calcium indices are supportive, not diagnostic, and that a spot urine sample for UCa/UCr should be collected within the same clinical time frame as serum calcium and iPTH whenever feasible—asynchronous sampling during hydration, diuretic use, or rapid calcium fluctuation can mislead. Infants normally have higher UCa/UCr than older children, and hydration, sodium intake, renal function, diuretics, and vitamin D status all alter results. Conversely, primary hyperparathyroidism can sometimes appear relatively hypocalciuric, especially with renal dysfunction, low calcium intake, vitamin D deficiency, or thiazide exposure. In neonates with severe hypercalcemia and non-suppressed iPTH, neonatal severe hyperparathyroidism or CASR-related disease should be considered urgently.

Finally, the framework calls for earlier but selective genetic testing. Not every transient mild episode warrants sequencing, but infantile onset, persistent or recurrent hypercalcemia, nephrocalcinosis or nephrolithiasis, family history, syndromic features, or discordant results after common causes are excluded should all accelerate testing. Infantile hypercalcemia with suppressed iPTH supports a panel or exome strategy including vitamin D metabolism and renal phosphate-handling genes such as CYP24A1 and SLC34A1, while non-suppressed iPTH with relative hypocalciuria supports calcium-sensing pathway testing. Dysmorphism, congenital heart disease, developmental delay, or multisystem involvement may require chromosomal microarray or syndrome-directed testing, and early-onset primary hyperparathyroidism, multigland disease, recurrence, parathyroid carcinoma, jaw tumor features, or family history should raise concern for MEN1-, CDC73-, RET-, or CDKN1B-related disease. Variants of uncertain significance, the authors caution, should not be treated as diagnostic without biochemical and segregation support. Because pediatric inpatient hypercalcemia is uncommon, the authors frame their proposal as a starting point, calling for multicenter studies or registry-based audits to test whether structured use of iPTH, age, and urinary calcium genuinely improves diagnostic timeliness, treatment escalation, renal outcomes, avoidance of inappropriate surgery, and hospital stay.

Subject of Research: Triage of pediatric inpatient hypercalcemia using intact parathyroid hormone, age, and urinary calcium

Article Title: Pediatric inpatient hypercalcemia: triage using intact parathyroid hormone, age, and urinary calcium

Article References: Lin, H., Fu, J.-F., & Dong, G.-P. (2026). Pediatric inpatient hypercalcemia: triage using intact parathyroid hormone, age, and urinary calcium. World Journal of Pediatrics. https://doi.org/10.1007/s12519-026-01102-w

Image Credits: AI Generated

DOI: 10.1007/s12519-026-01102-w

Keywords: hypercalcemia, pediatrics, parathyroid hormone, urinary calcium, familial hypocalciuric hypercalcemia, CYP24A1, SLC34A1, vitamin D metabolism, neonatal severe hyperparathyroidism, genetic testing, calcium-sensing pathway, World Journal of Pediatrics

The clinical picture on admission was dominated by neurological deficits. Physical examination revealed diminished knee reflexes and profound motor weakness, with muscle strength graded just 1 out of 5 in the upper extremities and 2 out of 5 in the lower extremities. The straight-leg-raise test was positive on both sides, and the patient displayed bilateral digital clubbing, a finding often associated with chronic pulmonary disease. Lumbar tenderness was present at the L4 to L5 level, yet strikingly, there were no external signs of inflammation such as redness or swelling over the affected area. Electromyography and nerve conduction studies pointed to chronic bilateral L5-S1 radiculopathy along with moderate C5-C6 root involvement, and the pattern initially raised suspicion for an underlying paraneoplastic process, sending the diagnostic workup in a direction that would soon prove misleading.

Magnetic resonance imaging of the central nervous system became the turning point. Brain MRI was unremarkable, but cervical and lumbar imaging told a different story. The scans revealed an epidural abscess at the L5-S1 level causing severe spinal canal stenosis, a paravertebral abscess, and destruction of the vertebral endplates and anterior portions of the vertebral bodies accompanied by bone marrow edema at the S1-S2 level, findings consistent with spondylodiscitis. The absence of local inflammatory signs suggested a so-called cold abscess, a classic feature of tuberculous infection of the spine, also known as Pott’s disease. Given the characteristic imaging, the patient’s history of smoking and methadone use, and his recent migration from Afghanistan, a country where tuberculosis remains endemic, spinal tuberculosis moved to the top of the differential diagnosis. Surgeons recommended urgent decompression and abscess drainage, but the patient declined operative intervention and opted for conservative management, a decision that would shape the entire course of his hospitalization.

The search for the source of infection quickly extended to the chest. A plain radiograph revealed bilateral diffuse patchy opacities suggestive of active pulmonary tuberculosis, predominantly involving the upper lobes and perihilar regions. High-resolution computed tomography went further, demonstrating diffuse micronodular and interstitial infiltrates consistent with miliary tuberculosis, the disseminated form of the disease in which tiny seedlings of infection spread throughout both lungs. Supporting evidence accumulated rapidly: a purified protein derivative skin test produced an induration of 30 millimeters, and sputum smear microscopy was positive for acid-fast bacilli. After informed consent was obtained, surgical aspiration of the spinal abscess was performed, and polymerase chain reaction analysis of the aspirated material confirmed the presence of Mycobacterium tuberculosis. Standard four-drug anti-tuberculosis therapy, combining isoniazid, rifampin, pyrazinamide, and ethambutol, was initiated for the intensive two-month phase of treatment. Following aspiration and the start of therapy, the patient’s neurological status improved, and he regained the ability to walk with assistance.

But the story did not end there. During hospitalization, the patient experienced recurrent episodes of fever and agitation, prompting a sepsis workup. Follow-up imaging revealed new pulmonary lesions, and auscultation detected diminished breath sounds with expiratory wheezing. A low procalcitonin level of 0.196 nanograms per milliliter argued against bacterial sepsis, so the existing antimicrobial regimen was continued. Because chronic pulmonary aspergillosis was suspected, a serum galactomannan assay was performed and returned a positive result. Histopathological examination of the aspirated abscess material had already demonstrated septate hyaline hyphae, morphologically suggestive of Aspergillus species. In response, the treatment regimen was expanded to include liposomal amphotericin B, voriconazole at 200 milligrams every twelve hours, and adjunctive antibiotics. The diagnostic picture, however, remained incomplete: no fungal culture or molecular identification was obtained, so the aspergillosis could not be confirmed with certainty, a limitation the authors openly acknowledge.

The most dramatic and therapeutically stubborn feature of this case was the patient’s blood calcium. On the first day of admission, serum calcium measured 12.08 milligrams per deciliter, already well above the normal range, and it climbed to 13.24 within twelve hours. The usual suspects were systematically excluded. Primary hyperparathyroidism, the most common cause of hypercalcemia in outpatient practice, was ruled out by a suppressed parathyroid hormone level of 1.66 picograms per milliliter alongside a phosphorus level of 4.26 milligrams per deciliter. Malignancy, the dominant cause among hospitalized patients, was considered but computed tomography revealed no evidence of an underlying neoplastic process. The patient’s symptoms, including constipation and myalgia, were attributed to the elevated calcium, and electrocardiography showed ST-segment depression and prominent U waves, electrocardiographic changes consistent with the metabolic disturbance, though no immediate cardiac intervention was required.

What followed defied the typical behavior of tuberculosis-associated hypercalcemia. In most reported cases, hypercalcemia in tuberculosis is mild and asymptomatic, detected incidentally on routine laboratory testing, and it generally resolves as the underlying infection is treated. Studies cited in the report suggest that roughly 88 percent of tuberculosis patients with hypercalcemia experience only mild elevations, and even in the setting of granulomatous disease and bone destruction, serum calcium rarely exceeds 13 milligrams per deciliter. This patient’s calcium, by contrast, continued to rise despite aggressive intravenous hydration, reaching a peak of 18.01 milligrams per deciliter on the eighth day of hospitalization, a level associated with risk of life-threatening cardiac, renal, and neurological complications. The mechanism believed to underlie granulomatous hypercalcemia involves activated macrophages within granulomas ectopically producing 1,25-dihydroxyvitamin D3, the hormonally active form of vitamin D, which drives increased intestinal calcium absorption. Both tuberculosis and certain fungal infections are recognized causes of this pathway, and local bone destruction from vertebral infection may have contributed further.

Treatment escalation became necessary. Three liters of normal saline over twenty-four hours followed by one liter every six hours failed to control the rising calcium. Calcitonin, administered in both injectable and intranasal formulations, also proved inadequate. After consultation with the nephrology team, only liposomal amphotericin B was continued among the antifungal agents to minimize the risk of electrolyte disturbances. When the serum calcium still failed to decline significantly, intravenous pamidronate, a bisphosphonate that inhibits osteoclast-mediated bone resorption, was administered at 90 milligrams on two consecutive days. Only then did the calcium begin a gradual decline, reaching a corrected level of 11.12 milligrams per deciliter by discharge. The patient was sent home with instructions to continue treatment on an outpatient basis and to attend close follow-up, but he never returned, and his ultimate clinical outcome could not be determined.

The case raises intriguing questions about why the hypercalcemia was so unusually severe. The authors note that risk factors for severe hypercalcemia in tuberculosis include elevated serum creatinine, renal failure, diuretic use, severe anemia, disseminated tuberculosis, diabetes mellitus, hypertension, and HIV infection. Of these, only disseminated tuberculosis and mild anemia were present in this patient, and crucially, HIV status was never assessed, an omission the authors identify as a significant limitation given that the World Health Organization strongly recommends HIV testing for all tuberculosis patients and that both HIV infection and invasive fungal infection raise the possibility of underlying immunosuppression. A comparable case reported by Spindel and colleagues in 1995 involved an HIV-positive patient with an opportunistic fungal infection and persistent hypercalcemia that ultimately normalized after roughly four weeks of intravenous hydration, underscoring how difficult these cases can be to manage.

Perhaps the most important takeaway from this report is epidemiological. The prevalence of tuberculosis-Aspergillus co-infection has been estimated at approximately 14.7 percent in Asia, and pulmonary tuberculosis is considered the single most important risk factor for chronic pulmonary aspergillosis, because cavitary lung damage and immune dysregulation create a favorable environment for Aspergillus fumigatus to colonize and proliferate. Despite this substantial overlap, routine screening for Aspergillus is not commonly incorporated into the diagnostic evaluation of tuberculosis patients. Whether a synergistic interaction between the two infections drove the extreme, treatment-resistant hypercalcemia in this patient cannot be determined with certainty, and the authors are careful not to overclaim. What the case does demonstrate is that in patients with disseminated tuberculosis, particularly when fungal co-infection is suspected, clinicians should monitor calcium levels closely, recognize that severe hypercalcemia can develop abruptly and resist standard therapy, and be prepared to escalate to bisphosphonates when hydration and calcitonin fall short.

Subject of Research: Hypercalcemia associated with spinal tuberculosis and Aspergillus co-infection

Article Title: Hypercalcemia in a Patient With Spinal Tuberculosis and Aspergillus Co‐Infection: A Case‐Report

Article References: Parsa, N., Amlelshahbaz, A., & Soltani, H. (2026). Hypercalcemia in a Patient With Spinal Tuberculosis and Aspergillus Co‐Infection: A Case‐Report. Immunity, Inflammation and Disease, 14(9), Article e70508. https://doi.org/10.1002/iid3.70508

Image Credits: AI Generated

DOI: 10.1002/iid3.70508

Keywords: tuberculosis, spinal tuberculosis, Pott's disease, Aspergillus, hypercalcemia, miliary tuberculosis, granulomatous disease, vitamin D metabolism, pamidronate, chronic pulmonary aspergillosis, case report, co-infection