Malakoplakia as a cause of severe hypercalcemia through ectopic 25-hydroxyvitamin D3 1-alpha-hydroxylase expression: A case report.

RATIONALE: Malakoplakia is a rare disease characterized by the presence of nongranulomatous macrophage infiltration. In most cases, it affects the urinary tract. Malakoplakia can cause acute kidney injury when it is localized in the kidneys. PATIENT CONCERNS: Here, we report the case of a 65-year-old female patient with renal malakoplakia responsible for hypercalcemia. During her initial assessment, she was also diagnosed 25-OH vitamin D insufficiency, for which she was prescribed oral cholecalciferol. Three months later, she developed severe hypercalcemia with normal 25-OH vitamin D and parathyroid hormone levels and high 1,25-dihydroxyvitamin D levels. DIAGNOSES: After a superimposed granulomatous disease was excluded, malakoplakia cells were suspected to be responsible for the abnormal 25-hydroxyvitamin D3 1-alpha-hydroxylase activity, which was confirmed by immunohistochemistry. INTERVENTIONS: Cholecalciferol was stopped, the patient was rehydrated with intravenous physiological saline, and prednisone was initiated to decrease the enzyme activity. OUTCOMES: Six months later, she displayed normal serum calcium, 25-OH vitamin D and 1,25-dihydroxyvitamin D levels. LESSONS: This case illustrates that malakoplakia may exhibit ectopic 25-hydroxyvitamin D3 1-alpha-hydroxylase activity and cause severe hypercalcemia upon vitamin D supplementation. Therefore, such supplementation should not be given in malakoplakia patients without an actual deficiency and requires careful monitoring of serum calcium.

[Ultrasonographic, serologic, and clinical characteristics of a case of prostatic malacoplakia]. / Caratteristiche ecografiche, sieriche e cliniche di un caso di malacoplachia prostatica.

An additional case of malakoplakia of the prostate in described to highlight its clinical, echographic and serum features. It's a rarest disease especially when prostate is involved, but well known in world literature. This case is reported to describe more accurately its echographic patterns and also for growing up precision in linguistical expressions used by echographists. We hope to contribute in collecting data about an uncommon pathology. At last we discuss about differential diagnosis when biopsy is negative for neoplasia and how it's possible to end further biopsies.

[Malakoplakia at 3 sites: the bladder, urethra and kidney. Isolation and ultrastructural study of blood monocytes]. / Malacoplasie à triple localisation: vésicale, urétérale et rénale. Isolement et étude ultrastructurale des monocytes sanguins.

We studied the blood mononuclear cells in a seventy-four-year old man who had urinary tract malacoplakia located to bladder, ureter and kidney. The blood mononuclear cells were isolated as described by Boyum [2] and studied by electron microscopy. They did not show bacilliform bodies or bacteria in the phagolysosomes. The microfilaments and the microtubules were not easily identifiable in the mononuclear cells of the patient. In the control, the internal skeleton of the mononuclear cells was normal. This ultrastructural finding may suggest that there is a relation between microfilaments and microtubules lesion and the low level of cyclic G.M.P. described by Abdou et al.

Leukocytic function in malakoplakia.

Leukocytic functions were studied in a patient with malakoplakia that involved the urinary tract and retroperitoneum in whom recalcitrant infections due to Escherichia coli developed. Polymorphonuclear leukocytic functions and monocytic chemotaxis were normal. Killing of E coli and Staphylococcus aureus by the patient's monocytes was impaired. This defect persisted after the infections were successfully treated and the treatment with antimicrobial agents was discontinued. Stimulated nitro blue tetrazolium reduction by the patient's monocytes was normal, suggesting that the microbicidal defect was not in the oxygen-dependent microbicidal system. Total lysozymal content of patient's monocytes was normal. Thus, the basis for this microbicidal defect is still undefined.