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To analyze the clinical characteristics of patients with metastatic calcification undergoing maintenance dialysis. Patients diagnosed with metastatic calcification via 99mTc-MDP bone scintigraphy between June 2019 and March 2023 at our hospital were included in this study. All patients were followed from the time of diagnosis until death, loss to follow-up, or the study endpoint (July 2023). The primary endpoint was all-cause mortality. The cohort comprised 7 males and 3 females, with a mean age of (48.7 ± 11.1) years. The most common sites of metastatic calcification included the lungs, joints, and skin, while rarer sites involved the stomach, myocardium, and mandibular angle. Nine patients received treatment with sodium thiosulfate, with a mean duration of STS administration of 23.5 days (range: 13.25 to 56.5 days). The mean follow-up duration was 14 months (range: 10 to 20 months). One patient died, one was lost to follow-up, while 8 out of 10 patients survived, and 6 out of 10 patients were followed for more than one year. 99mTc-MDP bone scintigraphy demonstrates high sensitivity and specificity for detecting metastatic calcification. The most frequently affected sites are the lungs, joints, and skin, with less common sites being the stomach, myocardium, and mandibular angle. Eight patients (8/10) survived, and 6 patients (6/10) remained alive with over one year of follow-up. [ABSTRACT FROM AUTHOR]

IntroductionMyocardial calcifications (MC) represent a relatively rare pathological process, which may accompany different cardiovascular conditions and can be broadly categorized as dystrophic or metastatic. Myocardial infarction (MI) has been traditionally regarded as the main cause of MC overall; however, no updated comprehensive data on the relative incidence of different forms of MC is available. The purpose of this systematic review of the literature is to analyze the currently available evidence on MC in terms of pathophysiology, diagnosis, and clinical presentation.Methods and resultsA total of 241 studies including a total of 368 patients affected by extensive MC were included in the final review. The majority of patients (69.8%) presented with dystrophic MC. Endomyocardial fibrosis (EMF) represents the single most common etiology of MC (24.2%), while sepsis/acute systemic inflammatory syndrome (SIRS) and chronic kidney disease were identified as the second and third most common causes respectively. The relative incidence of etiologies also varies across the years, with MI being more represented before 1990, and sepsis/SIRS becoming the single most common cause of MC after 1990. Multimodality imaging was used in the work-up of MC in 42.7% of cases. The most commonly employed imaging modality overall was echocardiography (51.9%), while after 1990 computed tomography scan became the most widely used tool (70.1%).ConclusionThe present systematic review provides new insights into the pathophysiology of MC. Previously thought to be mainly a consequence of ischemic heart disease, our data indicate that other diseases, namely EMF and sepsis/SIRS, are indeed the main conditions associated with MC. The importance of multimodality imaging in the work-up of MC is also highlighted.

Metastatic calcification is an uncommon condition with underlying abnormal bone and calcium metabolism, leading to ectopic deposition of calcium in soft tissues. The lung is a common site of involvement, and can mimic pulmonary edema in radiographic findings, especially in clinical context of end-stage renal failure. Recognition of such condition is important to avoid unnecessary diuretic therapy and extra dialysis sessions and guides correct treatment of underlying metabolic disorder. This article, therefore, serves to illustrate such condition with emphasis to radiological and clinical features suggestive of such condition.

Non-uremic calciphylaxis is a rare, life-threatening condition characterized clinically by cutaneous necrosis and histologically by calcium deposition in small vessel walls. The etiology of non-uremic calciphylaxis remains the subject of ongoing speculation and debate. Herein we present a patient with calciphylaxis who had normal kidney function and numerous rheumatologic diseases, namely systemic lupus erythematosus (SLE), Sjogren syndrome (SS), and myasthenia gravis (MG). We review the pathophysiology, possible mechanisms, and management for non-uremic calciphylaxis.

This report describes cardiovascular and renal soft tissue mineralization and renal intratubular crystals in 13 out of 16 guinea pigs that were given very hard drinking water for 9 months. These animals, aged 14 to 20 months, were experimentally naïve. No clinical symptoms were observed, but 1 guinea pig was found dead in its cage. Necropsy did not reveal any gross findings; however, histologic examination revealed mineralization and crystal formations. Despite no known changes in the feed sourcing or formulation, the possibility that the incident was feed-related was considered. The most recent analysis of the feed obtained from the manufacturer during this period, which was conducted by an accredited laboratory authorized by the Ministry of Agriculture and Forestry, was appropriate. No similar lesions were reported at other centers using the same feed; however, drinking water analysis for total dissolved solids revealed extremely hard water, with elevated levels of calcium and calcium carbonate and low magnesium levels, due to a malfunctioning water treatment system. After installing a new system to balance calcium and magnesium, no new cases appeared over the next 2 years. It was determined that the mineralization and crystal formations were most likely caused by water hardness. This study demonstrates that mineralization typically attributed to feed in guinea pigs can also result from high calcium content in drinking water, highlighting the importance of water analysis in such cases., Competing Interests: Declaration of Conflicting InterestsThe author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

Petrified ears is an uncommon clinical entity. It describes auricular cartilage hardening, due usually to ectopic calcification or, less commonly, ossification. The most common causes are frostbite and mechanical trauma. However, endocrinopathies have also been reported to cause ectopic calcium deposition through an unknown mechanism. Addison’s disease is the systemic disease most frequently associated, but the exact pathogenesis remains unclear. Patients are usually asymptomatic, and the diagnosis is made incidentally when rigid helices are noted on palpation and can be confirmed by radiological imaging. A biopsy can also help to differentiate between calcification and ossification. The presence of this condition may be a useful clinical sign, which in some cases precedes the development of endocrinopathies by many years. We report on a case, and we review the current literature.

Extraosseous calcifications correspond to ubiquitous deposits of intra-tissue calcium salts leading to dysfunction of the affected tissue or organ. There are two types: metastatic calcifications and dystrophic calcifications. Their formation mechanism is by mimicking the physiological mineralization process with an "osteoblast-like" cell. The cause of extra-osseous calcification is variable and depends on risk factors. If the subject is young, you will have to think about a genetic syndrome!, (Copyright © 2024. Published by Elsevier Masson SAS.)

BackgroundCommon causes of hypercalcemia include primary hyperparathyroidism and paraneoplastic syndrome of malignancy. Because of this, physicians can easily miss extrinsic causes of hypercalcemia such as milk-alkali syndrome in patients with cancer. We successfully treated a case of acute kidney injury due to severe hypercalcemia caused by milk-alkali syndrome due to long-term milk drinking in a patient with colon cancer.Case DescriptionA 62-year-old man was referred to nephrology for hypercalcemia and azotemia that was found during preoperative evaluation for colon cancer surgery. The patient had experienced several months of dizziness and anorexia. We started hemodialysis because hypercalcemia and azotemia were not improved despite large amounts of hydration and diuretics. We suspected paraneoplastic syndrome because of concomitant colon cancer and low intact parathyroid hormone (PTH). Renal microcalcifications were observed on ultrasonography. Metastatic calcifications of the lung and stomach were present, but no malignant metastasis appeared on bone scans. There was no evidence of metastatic malignant lesions on chest or abdominal enhanced computed tomography. PTH-related peptide was not detected. Thus, other causes of hypercalcemia beyond malignancy were considered. On history-taking, the patient reported consuming 1,000 to 1,200 mL of milk daily for the prior 3 months. Hypercalcemia was due to chronic milk-alkali syndrome. We advised withdrawal of milk and nutritional pills. Hemodialysis was stopped after 2 weeks since azotemia and hypercalcemia were resolving. Acute kidney injury was improved, and mild hypercalcemia remained when he underwent hemicolectomy after 1 month. Thereafter, serum calcium and creatinine remained normal at discharge and follow-up for 1 year in the outpatient clinic. However, lung calcifications still remained on bone scan after 1 year.ConclusionsChronic milk-alkali syndrome is a rare condition resulting from excessive calcium and alkali intake through various routes, like milk, nutritional supplements, and medicines for osteoporosis. Therefore, early management for hypercalcemia should include precise history taking including diet, previous diagnoses, and current medications.

Petrified ears is an uncommon clinical entity. It describes auricular cartilage hardening, due usually to ectopic calcification or, less commonly, ossification. The most common causes are frostbite and mechanical trauma. However, endocrinopathies have also been reported to cause ectopic calcium deposition through an unknown mechanism. Addison's disease is the systemic disease most frequently associated, but the exact pathogenesis remains unclear. Patients are usually asymptomatic, and the diagnosis is made incidentally when rigid helices are noted on palpation and can be confirmed by radiological imaging. A biopsy can also help to differentiate between calcification and ossification. The presence of this condition may be a useful clinical sign, which in some cases precedes the development of endocrinopathies by many years. We report on a case, and we review the current literature. [ABSTRACT FROM AUTHOR]

Metastatic calcification is the accumulation of calcium deposits in various tissues, especially in the lung, as a result of elevated serum calcium levels. Hyperparathyroidism secondary to chronic renal failure is the most common underlying cause. Although poorly defined nodular opacities can be seen on chest radiography, CT is more sensitive in demonstrating findings. Recognition of the imaging findings of the lesions is important to prevent unnecessary further interventional procedures and to plan the treatment. In this article, we aimed to present the imaging findings of metastatic calcification lesions in both lungs in a chronic renal failure patient. [ABSTRACT FROM AUTHOR]

Metastatic calcification relates to abnormal calcification resulting from hypercalcemia and can affect soft tissues, skeletal muscle, myocardium, lungs, stomach, kidneys, and blood vessels. We describe a case of metastatic pulmonary calcification in a 71-year-old male, images with 18F-fluorodeoxyglucose (FDG) PET/CT and 99mTc- methylene diphosphonate (MDP) bone scan.

A 48-year-old male with known tubercular osteomyelitis of the left elbow and chronic renal failure presented with PTH independent hypercalcemia and underwent F-18 fluorodeoxyglucose positron emission tomography/computed tomography (PET/CT) to look for any underlying malignancy that might be causing his hypercalcemia. The PET/CT did not reveal any malignancy, but extensive metastatic calcification of small- and medium-sized arteries was noted throughout the body with relative sparing of large vessels. Alkaline tissue such as lungs, gastric mucosa, and kidneys that are usually involved in metastatic calcification were also spared. The underlying pathology for this kind of metastatic calcification was most likely chronic granulomatous disease, which was tubercular osteomyelitis in this patient. We present the PET/CT scan images of this unusual case of metastatic vascular calcification. [ABSTRACT FROM AUTHOR]

99mTc-diphosphonates are a class of radiopharmaceuticals, used for bone scintigraphy, able to highlight all lesions characterised by altered osteogenesis. We report the case of a 47-year-old male with an end-stage mela - noma, presenting a multi-organ extraosseous activity. Patient underwent whole body scintigraphy using a dual head γ-camera, equipped with LEHR collimators. Images were obtained at 3 hours from i.v. injection of 700 MBq of 99mTc-HMDP. Radiochemical purity was 98.2%. The scan showed a decreased skeletal and urinary activity, as well as an intense extraosseous activity in the lungs (especially in the right one), in the stomach, in the liver and a bit lesser in the spleen. Unknown skeletal metastases were also identified. At the time of bone scan, the patient had hypercalcemia and an oliguric acute kidney injury caused by sepsis. Moreover, ultrasound and chest radiography showed the presence of hepatic metastases and radiographic signs of pneumonia in the right lung, respectively. Soft tissues calcifications can be classified in two groups: metastatic calcifications, where calcium sediments in normal tissues, and dystrophic calcifications, where this deposit occurs only in previously injured organs. Metastatic calcifications mainly occur in patients in hemodialytic treatment, since the hyperparathyroism and the acidosis, due to the interdialytic interval, induce an hypercalcemia. Moreover, the reduced glomerular filtration causes hyperphosphatemia and, consequently, increased calcium-phosphate products. On the other hand, dystrophic calcifications occur in injured tissues, even without increased serum calcium levels. Our patient had high levels of calcemia, but not a secondary hyperparathyroidism, so other causes must be researched. It's common knowledge that a high level of calcemia can be found in 10 to 20% of cases with advanced cancer. Indeed, the patient had bone metastases and malignant hypercalcemia. The 99mTc-HMDP uptake was different in the two lungs, with a greater intensity in the right one. This pattern is probably due to two causes: hypercalcemia (linked to the end-stage cancer), that explains the bilateral lungs uptake, and an injured tissue, for example in presence of an infection, that generates a greater uptake in the right lung. The increased uptake of 99mTc-HMDP in other patient's organs was probably due to some of mechanisms already involved in pulmonary calcifications. Moreover hepatic image showed a patchy activity, with some areas of more evident calcifications, probably due to the presence of malignant metastases. Malignant hypercalcemia depends on several causes, like the osteoclastic bone resorption and the secretion of parathyroid hormone related protein (PTHrP), and may be associated with extra-skeletal images at bone scintigraphy. A previous oxidant injury can contribute to more intense calcifications in the involved tissues. [ABSTRACT FROM AUTHOR]

Aims and Objectives: To determine the prevalence of visible calcifications in soft tissues of the orofacial region in digital panoramic radiographs. Materials and Methods: Panoramic radiographs of 1615 adult male and female dental outpatients who had visited the dental college for various dental treatments were scrutinized for calcifications. Soft tissue calcifications were recorded according to gender, age, and site. Results: Patients identified with soft tissue calcifications comprised 63.41% arteriosclerosis, 45.29% calcified atherosclerotic plaques, phlebolith in 11.7%, sialolith of submandibular salivary gland in 4.3%, calcified stylomandibular and stylohyoid ligament in 4.2%, tonsillolith in 3.2% and lymph node calcification in 2.1% of the radiographs. The association of presence of calcification with age was analyzed with the Chi-square test (P

Both leukocytoclastic vasculitis and metastatic pulmonary calcification are conditions that rarely occur during the course of multiple myeloma. We present a multiple myeloma patient that had severe dyspnea due to metastatic pulmonary calcinosis, and ulceronecrotic skin lesions caused by leukocytoclastic vasculitis. After 3 courses of standarddose chemotherapy all skin and pulmonary lesions disappeared. Autologous peripheral stem cell transplantation was performed and during 1 year of follow-up the patient was in complete remission; after 1 year, laboratory test results indicated disease relapse. Although the patient was treated with bortezomib and dexamethasone, the disease progressed. Non-myeloablative allogeneic stem cell transplantation was performed, but despite of all treatment the patient died due to disease progression.

Soft-tissue calcifications in the head and neck are relatively common and are the result of a wide variety of benign and malignant pathologies. They can present a diagnostic challenge given the broad range of underlying etiologies. Uremic tumoral calcinosis (UTC) is a rare complication of end-stage renal disease (ESRD) resulting from metastatic soft tissue calcification. Common sites include periarticular soft tissues of the shoulders, elbows, and hands (Pan and Chen, 2016). UTC can also affect the cervical spine and mimic osteosarcomas (Zhou et al., 2018). We present the case of a 71-year-old female with hypertension, left carotid artery stenosis, mitral valve prolapse, and ESRD secondary to diabetes mellitus type II (DMII) on peritoneal dialysis who was found to have large, heterogeneous, bilateral calcified neck masses. Given her clinical history, laboratory results, and imaging findings, she was diagnosed with UTC. In addition to this case, we provide an overview of tumoral calcinosis (TC) and a differential diagnosis for calcified lesions of the head and neck., Competing Interests: Conflicts of interest None to disclose., (Copyright © 2023 Elsevier Inc. All rights reserved.)

Background: Tumoral calcinosis is a rare manifestation of extraskeletal calcification, featuring large calcified cystic masses in the periarticular regions of large joints. In chronic kidney disease (CKD), this disorder is thought to evolve through a chronically elevated calcium-phosphorus solubility product leading to calcium precipitation in soft tissue. Treating tumoral calcinosis in these patients involves interventions to lower the calcium-phosphorus product such as reduction in vitamin D therapy and intensive hemodialysis regimens. Case Presentation: We report the case of a 54-year old woman with polycystic kidney disease on peritoneal dialysis with widespread tumoral calcinosis in the context of hypercalcemic tertiary hyperparathyroidism who had been on long-term alfacalcidol therapy. After withdrawal of the vitamin D analogue and initiation of daily hemodialysis, there was rapid dissolution of her tumoral calcium deposits with the abrupt onset of parathyroid hormone (PTH)-independent transient hypercalcemia that resolved once the soft tissue deposits disappeared. Conclusions: Resorption of soft tissue calcific deposits may result in transient parathyroid hormone (PTH)-independent hypercalcemia. In CKD patients, this hypercalcemia causes a decrease in the PTH level, distinguishing it from tertiary hyperparathyroidism, though PTH may not be totally suppressed, the way it is seen in PTH-independent hypercalcemia in non-CKD patients. [ABSTRACT FROM AUTHOR]

Hypercalcemia is a common paraneoplastic syndrome that may result in metastatic calcification. We report here on four autopsy cases with paraneoplastic hypercalcemia with metastatic calcification, to evaluate the clinicopathologic manifestations. All were males, aged 37-63 years old. Primary tumors included one transitional cell carcinoma of the urinary bladder, one multiple myeloma, and two squamous cell carcinomas of the esophagus. Calcium concentrations ranged from 3.3 to 5.9 mmol/L. Chronic hypercalcemia resulted in metastatic calcification. The kidney and stomach were the most vulnerable organs. Only case 1 presented with an increase in plasma calcium above 5 mmol/L (about twice the normal value); the metastatic calcification involved the capillary walls of his lungs, and he died of fulminant pulmonary edema. Our conclusion is that judicious treatment for paraneoplastic hypercalcemia is important with respect to the occurrence of pulmonary edema associated with metastatic calcification.

A commercial diet fed to a colony of inbred strain 13 guinea pigs for approximately 6 weeks was subsequently recalled for excessive levels of vitamin D. Twenty-one of 62 animals exhibited clinical signs, including anorexia, lethargy, and poor body condition. Nine affected and 4 clinically normal animals were euthanized for further evaluation, including serum chemistry, urinalysis, and gross and/or histopathology. Macroscopic findings included white discoloration in multiple organs in 8 animals, and microscopic evaluation confirmed multiorgan mineralization in tissues from 7 animals. Serum 25-hydroxyvitamin D levels were elevated in 10 animals. Serum inorganic phosphorus and alkaline phosphatase levels were increased in all exposed animals; however, total calcium and ionized calcium levels were not significantly higher in exposed animals than in control strain 13 guinea pigs from a different institution. The data support a diagnosis of hypervitaminosis D with metastatic calcification. Following the diet recall, the remaining guinea pigs increased their food intake and regained body condition. Diagnostic testing of 8 animals euthanized approximately 3 months after returning to a normal diet demonstrated that serum parathyroid hormone remained significantly lower, and ionized calcium and ionized magnesium were significantly higher, in recovered animals compared to controls and exposed animals. These results indicate that diagnostic tests other than serum calcium are necessary for a diagnosis of hypervitaminosis D in guinea pigs. [ABSTRACT FROM AUTHOR]

Calciphylaxis is a rare and potentially devastating condition also referred to as uremic gangrene syndrome, calcific uremic arteriolopathy, metastatic calcification, and uremic small-vessel disease that can present in patients with end stage renal disease. This article reports a case of a 38-year-old African-American female on peritoneal dialysis for six years with a known history of non-adherence with diet, medications, and prescribed peritoneal dialysis treatment regimen. At her monthly clinic visit, the patient complained of burning sensation in the fingers of both hands with limited fine motor movement due to edema and severe pain. A presumptive diagnosis of calciphylaxis led to hospital admission with confirmation by X-ray of her hands. The patient was switched to hemodialysis with low calcium dialysate, aggressive reduction in phosphorus, diet counseling, use of cinacalcet, and six weeks of intravenous sodium thiosulfate infusion with hemodialysis treatments. The patient's condition improved with resolution of symptoms. This case was chosen based on the rarity of a calciphylaxis presentation and paucity of knowledge regarding diagnosis and treatment. [ABSTRACT FROM AUTHOR]

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Background: Cutaneous calcification is an acquired disorder whereby insoluble, amorphous calcium salts deposit in the skin. Classically, cutaneous calcification is categorized as metastatic, dystrophic, idiopathic, or iatrogenic. Objective: The purpose of this study was to further elucidate the underlying pathogenic mechanism for cutaneous calcification. Methods: Three cases of cutaneous calcification, including clinical characteristics and associated histopathology, were reviewed. Previous reports of cutaneous calcification were searched for in the published literature and included. Results: Calcium is distributed within areas of underlying tissue damage (ie, locus minoris resistentiae), and in our cases, occurred specifically at sites of chronic actinic damage and intravenous extravasation tissue injury. Limitations: A small number of clinical cases and previously published reports were reviewed. Conclusion: We hypothesize that cutaneous calcification may preferentially occur at anatomic sites where tissue integrity has been compromised (ie, locus minoris resistentiae). We suggest one potential mechanism: that cutaneous calcification occurs within dermis that contains damaged elastic fibers. Pseudoxanthoma elasticum may serve as a possible genetic disease model for this process. [ABSTRACT FROM AUTHOR]

Abstract: Few autopsy cases of sudden death in renal transplant recipients have been reported in the literature. The present case was a 50-year-old female recipient of a living-related renal transplant, who died suddenly after a good post-transplant course of 14 years. The patient was admitted in December 2000 for detailed investigation for ascites, and died unexpectedly 1 month later. She complained of mild dyspnoea approximately 3 h before death. Detailed clinical and laboratory investigations after admission showed no malignant findings in the abdominal cavity. Postmortem pathological examination also showed no tumour in the abdominal cavity. Both lungs were pneumatized. Histopathological examinations revealed metastatic calcification. Calcification was observed in the heart, lungs, kidney graft and pancreas. Calcification in the heart was found in the central fibrous body surrounding the atrioventricular node and bundle of His, as well as in the origin of bifurcating bundle. In the myocardial fibres, fibre rupture and waviness were observed. Although these findings may indicate agonal changes, they might also be a consequence of sudden cardiac death. This patient was in a state of renal failure, which presumably caused metastatic calcification involving also the cardiac conduction system. This calcification might partially account for the sudden death. [ABSTRACT FROM AUTHOR]

Background. Disturbances of calcium‐phosphate (Ca‐P) metabolism in chronic renal insufficiency (CRI) play an important role not only in bone disease (renal osteodystrophy) but also in soft tissue calcification, with an increased risk of vascular calcification, arterial stiffness, and worsening of atherosclerosis. [ABSTRACT FROM PUBLISHER]

Calciphylaxis is a rapidly developing, fatal process of vascular calcium deposition with prominent cutaneous manifestation. We treated a long-term haemodialysis patient who developed an analogous disorder limited to the lungs. A 57-year-old man was admitted for initiation of peritoneal dialysis because limited cardiac reserve precluded further haemodialysis. He was treated successfully for pneumonia until hypoxia and progressive hypercalcaemia developed. [sup 99m] Tc-methylene disphosphonate scintigraphy showed diffusely increased pulmonary uptake. Death supervened despite aggressive and successful treatment of hypercalcaemia. Autopsy studies included immunohistochemistry and morphometric studies of bone. Alveolar capillary walls showed diffuse calcium deposition. Both gross and microscopical findings differed from those of typical metastatic calcification in dialysis patients. Immunoreactivity for parathyroid hormone-related protein was present in the lesions. Bone histomorphometry indicated mild osteitis fibrosa. Pneumonia is believed to have caused local synthesis of parathyroid hormone-related protein that, along with high calcium × phosphorus product, contributed to calcium deposition. By analogy with the cutaneous process we termed the deposition ‘pulmonary calciphylaxis’.Copyright © 2001 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

A patient with an intermediate state of human T lymphotropic virus type I (HTLV-l) infection and in whom autopsy showed multiple organ failure (MOF) associated with extensive metastatic calcification in systemic organs is described. A 56-year-old man presented with signs and symptoms of advanced cardiac insufficiency, respiratory disturbance and renal failure. Serologically, the anti-human T lymphotropic virus type I (HTLV-l) antibody titer and the levels of both calcium and parathyroid hormone-related peptide (PTHrP) were distinctly elevated. These data suggested a diagnosis of adult T cell lymphoma/leukemia (ATLL). However, examination of a peripheral blood sample revealed only a few atypical lymphoid cells (3%) associated with mild leukocytosis (white blood cell count, 13.7 x 103/mm3). Lymph node swelling was systemic but mild, with some nodes up to 10mm in diameter. The patient died of MOF. Adult T cell leukemia/lymphoma was unable to be diagnosed definitively because of the short duration of laboratory abnormalities and because of the discrepancy between the laboratory data and the magnitude of lymphoproliferation in both the lymph nodes and peripheral blood. At autopsy, the most conspicuous finding was extensive metastatic calcification in the multiple organs, including the heart, lungs, kidneys, tongue, liver, pancreas, spleen and systemic arterial walls. Very small numbers of medium-sized atypical lymphoid cells admixed with small reactive lymphocytes were identified in multiple organs, with no evidence of massive infiltration. Molecular analyses could not detect monoclonal integration of HTLV-l provirus DNA or monoclonality of T cell lineage cells. Parathyroid hormone-related peptide was demonstrated in the cytoplasm of the atypical lymphoid cells on immunohistochemical examination. The bone trabeculae generally showed distinct evidence of resorption associated with marked proliferation of osteoclasts. These findings suggested that the hypercalcemia in the present case was categorized as humoral hypercalcemia of malignancy rather than local osteolytic hypercalcemia. [ABSTRACT FROM AUTHOR]