International Journal of Clinicopathological Correlation

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Objective: The objective of this study was to apply the newly recommended mandatory immunohistochemical (IHC) markers, isocitrate dehydrogenase (IDH) and ATRX, in addition to our previously applied panel of p53, epidermal growth factor receptor [EGFR], vascular endothelial growth factor [VEGF], MDM2, and Ki67 on histopathologically diagnosed thirty cases of glioblastoma. Their interrelationship and correlation with survival pattern were analyzed. Materials and Methods: A retrospective analysis of the histopathology records and clinical case files was done in thirty cases of glioblastoma (World Health Organization Grade IV). These cases were analyzed for certain defined clinical and histopathological parameters. IHC staining for IDH1-R132H and ATRX was done. IHC scores for p53, EGFR, VEGF, MDM2, and Ki67 were included from the previously published dataset. IHC labeling of all these markers was analyzed, and their interrelationship was studied and correlated with the survival pattern. Results: Cases were categorized as glioblastoma, IDH-wild type; glioblastoma, IDH-mutant; and glioblastoma, not otherwise specified (NOS). A total of 17 cases were categorized as glioblastoma, IDH-wild type and 10 cases were categorized as glioblastoma, IDH-mutant. Three cases in younger adults were categorized as glioblastoma, NOS. In glioblastoma, IDH-wild type, p53 expression was found in 7 cases, increased Ki67 expression was present in 12 cases, VEGF expression was found in 16 cases, MDM2 was expressed in 14 cases, while EGFR expression was present in 10 cases. In glioblastoma, IDH-mutant, p53 expression was found in 5 cases, increased Ki67 expression was present in 4 cases, VEGF expression was found in 9 cases, MDM2 was expressed in 5 cases, while EGFR expression was present in 3 cases. The mean overall survival in glioblastoma, IDH-wild type was 3.1 months and, in glioblastoma, IDH-mutant, the mean overall survival was 6.4 months. Conclusion: Survival pattern of glioblastoma, IDH-mutant, was better than glioblastoma, IDH-wild type.

Background: Leprosy is a chronic granulomatous disease caused by Mycobacterium leprae principally affecting the skin and peripheral nerves. M. leprae is an obligate intracellular bacillus (0.3–1 μ wide and 1–8 μ long) that is acid-fast. Leprosy exhibits a spectrum of clinical characteristics that correlate with the histopathological changes and the immunological status of the individual. There is a range of varied clinicopathologic manifestations, and the diagnosis is made from adequate clinical information combined with histopathology. The aim of the study was to classify leprosy according to the Ridley–Jopling classification and perform the clinicopathological correlation. Materials and Methods: A prospective study was conducted on 184 cases of skin biopsies clinically diagnosed with leprosy, received in the Department of Pathology, Government Medical College, Kota from July 2015 to July 2017. Adequate clinical history was taken and biopsies were stained with hematoxylin and eosin and modified Fite Faraco stain. The Ridley and Jopling classification was followed in both clinical and histopathological diagnosis. Results: This study included 184 patients diagnosed clinically with leprosy. Skin biopsy revealed evidence of leprosy in 158 cases. A maximum number of patients clinically belonged to indeterminate leprosy which constituted 57 (30.9%) cases followed by borderline tuberculoid (BT) 41 cases (22.2%). On the contrary, histologically, although indeterminate leprosy was the most common with 51 cases (32.2%), the second most common was borderline lepromatous (BL) with 28 cases (17.7%) cases. Twenty-six cases of clinically diagnosed leprosy showed no features of leprosy histologically. The clinical and histopathological correlation was seen in 158 cases (85.3%the). The correlation was highest in BL (89.2%) followed by lepromatous and BT leprosy. Fite-Farraco stain was positive in 85 cases (53.7%). Conclusion: The classification of leprosy requires attention to the histopathological criteria and correlation with clinical information and bacteriological examination to facilitate accurate therapy.

Adenomatoid odontogenic tumor (AOT) is considered to be an uncommon odontogenic tumor which occurs most commonly in an unerupted maxillary canine. Some investigators consider it to be a benign neoplasm, while others consider it to be a hamartomatous malformation due to its limited size and to the lack of recurrence in most of the cases. The specific stimulus that triggers proliferation of progenitor cells of AOT is unknown, as in case of all odontogenic tumors. As it is exclusively associated with an unerupted or impacted tooth and the cytological resemblance to the dental lamina and enamel organ, it can be considered as odontogenic in origin. The present case highlights the unusual presentation of AOT which is not associated with an impacted or unerupted tooth.

Phosphaturic mesenchymal tumor (PMT), while a rare entity, is nevertheless an important cause of oncogenic malacia/tumor-induced osteomalacia (TIO). We present a case of PMT. Our 47-year-old patient presented with unexplained osteomalacia refractory to medical therapy, associated with left subtrochanteric stress fracture. Further workup revealed the presence of a tumor in the left anterior inferior iliac spine, which was subsequently excised. Histopathology of the tumor showed the characteristic features of PMT, including grungy calcifications, osteoclast-type multinucleated giant cells, and bland round-to-spindled tumor cells. Following excision of the PMT, the patient's osteomalacia swiftly resolved. PMT is an important differential diagnosis in the context of oncogenic osteomalacia/TIO. As highlighted by our case report, PMT has fairly characteristic clinical and histopathologic features. However, given its rarity, an awareness of this entity is required for correct diagnosis and treatment.

Online since 19^th September, 2016