Carcinoma Cervix Leading to Ichthyosis Uteri: A Rare Case Report

Ichthyosis uteri is an exceedingly rare condition in which the entire surface of the endometrium is replaced by stratified squamous epithelium. It is a benign lesion and its association with benign and malignant conditions has been reported in the literature (Bewtra, Xie, Hunter, Jurgensen (Arch Pathol Lab Med 29:e124–e125, 2005)). Originally described as an endometrial response to iatrogenically introduced caustic substances, similar changes have since been described in association with a variety of inflammatory conditions of the endometrium. It is concluded that a squamous cell carcinoma of the cervix extended proximally into the endometrium (Bagga, Jaswal, Datta, Mahajan (Indian J Pathol Microbiol 51:267–268, 2008)). The possibility of significant cervical pathology should be considered when plaques of squamous epithelium with low-grade dysplastic changes are identified in an endometrial biopsy or curettage.

Isolated Splenic Metastases of Her2+++ Gastroesophageal Junction Adenocarcinoma

Isolated metastases from gastric adenocarcinoma to the spleen are very infrequent. Usually, there are multiple metastases from gastric cancer, and isolated splenic metastases are very rare [Lam and Tang: Arch Pathol Lab Med 2000;124:526-530] because of certain anatomical and physiological characteristics (e.g., angulation between the splenic artery and celiac trunk, paucity of afferent lymph flow toward the spleen, contractility of the spleen and major immune content). Here, we report 2 cases of isolated splenic metastases from an adenocarcinoma of the gastroesophageal junction, both with long-term survival outcome and overexpression of Her2.

ERRATUM

An abstract published in the September 2011 issue of the Archives (Murugan P et al. Tumor-to-Tumor Metastasis: A Rare Case of Cutaneous Melanoma Metastatic to a Parathyroid Adenoma [CAP abstract 109, session 100]. Arch Pathol Lab Med. 2011;135[9]:1132) contains incorrect data in line 10 when referring to the right inferior parathyroid gland that was removed. The weight of the gland should have been shown as “…1200-mg (normal, 30–70 mg)…”

ERRATUM

An article by Suryawanshi et al that appears in the August 2011 issue of the Archives (Suryawanshi P, Ramadwar M, Dikshit R, et al. A Study of Pathologic Risk Factors in Postchemoreduced, Enucleated Specimens of Advanced Retinoblastomas in a Developing Country. Arch Pathol Lab Med. 2011;135[8]:1017–1023) lists an incorrect e-mail address for the corresponding author. The correct e-mail address for Dr. Viswanathan is [email protected].

CORRECTION

Notice of Failure to Disclose Financial Interest: “Update on Fluorescence In Situ Hybridization in Melanoma: State of the Art” (Arch Pathol Lab Med. 2011;135[7]:830–837). Pedram Gerami, MD, has done consultant work for both NeoGenomics and Abbott Molecular Labs and has received honoraria from these companies.

CORRECTION

In the article by Younes et al that appeared in the April 2011 issue (The Significance of “Indefinite for Dysplasia” Grading in Barrett Metaplasia. Arch Pathol Lab Med. 2011;135[4]:430–432), the y-axis text in Figure 2, A and B, is shown as “Percent progression.” This text should have read “Percent Without Progression.”

CORRECTION

An abstract that appeared on page 1319 of the September 2010 issue (Ciarlini PD, Sandhaus LM, Kidric DM, O'Riordan M. Automated cerebrospinal fluid cell counts using the Sysmex XE-5000: Is it time for new reference ranges? [CAP abstract 30, session 200] Arch Pathol Lab Med. 2010;134[9]:1319) included a financial interest disclosure that Dr. Linda M. Sandhaus received honoraria from Sysmex America, Inc, in support of her work on this abstract. The speaker honoraria Dr. Sandhaus received from Sysmex America, Inc, did not support the study described in the abstract.

Unknown primary cancer (UPC): Accuracy of tissue of origin prediction by molecular profiling

11070 Background: Molecular profiling may be useful to identify the primary site and direct therapy for patients (pts) with UPC. Since most UPC pts never have a primary site identified, the accuracy of molecular profiling diagnoses are difficult to verify. We identified a group of UPC pts who had a primary site subsequently identified during their clinical course, and performed a 92-gene real time polymerase chain reaction (RT-PCR) assay (Arch Pathol Lab Med 130:465, 2006) on tissue from the initial diagnostic biopsy. We then compared the RT-PCR diagnosis with the subsequent clinical diagnosis. Methods: 38 of 501 UPC pts (7%) seen between 2000 and 2008 had their primary tumor subsequently identified during life. 24 of the 38 pts had tissue biopsies (excluding FNA cytology) and are the subject of this study. The RT-PCR assay was performed on unstained slides from the formalin-fixed, paraffin-embedded (FFPE) initial diagnostic biopsy, and the assay predictions were compared to the actual primary sites (found later). No clinical or pathologic data (other than sex, biopsy site, and 1 H&E stained slide) were used in the prediction of the primary site. Results: 16 of 24 assays were successful (8 had no tumor or RNA in the material). 11 of 16 predictions of the site of origin (68%) were correct, corresponding to the actual primary sites found 3–58 months (median 8.5 months) after the initial diagnosis of UPC. Primary sites correctly identified included breast 2, ovary/peritoneal 4, NSCLC 1, colorectal 2, gastric 1, melanoma 1. 3 predictions were inaccurate (colorectal, testicular, sarcoma) in patients with gastroesophageal, pancreas and NSCLC, respectively. 2 assays were unclassifiable. Conclusions: RT-PCR performed on FFPE initial diagnostic tissue was accurate in predicting the primary site of origin in 11 of 16 pts with UPC who eventually had their primary site identified clinically. These data provide a direct validation of the reliability of this RT-PCR assay in predicting the primary site in pts with UPC. When used in concert with clinical features and IHC stains, molecular profiling may provide the basis for more successful site-directed therapy for many of these pts. Prospective studies of RT-PCR in UPC are ongoing. [Table: see text]

A Cautionary Tale.

RV, a 62 year old caucasian male was admitted to LH from the ER for prolonged epistaxis. Ten months prior to admission he had appeared at the ER with the same complaint. At that time the patient’s Hb, Hmct, MCH and MCHC were 12.3 g/dL, 29.2 percent, 35.8 pg and 42 percent respectively. All hematological and chemical assays used instrumentation from Beckman-Coulter Inc.( Brea, CA). The patient’s epistaxis was attributed to anti-platelet therapy with aspirin and clopidogrel for coronary artery disease and he was subsequently lost to follow-up. At his most recent ER appearance his Hb, Hmct, MCH and MCHC were 11.8 g/dL, 22.9 percent, 42.5 pg and 51.6 percent respectively. The patient was admitted to allow evaluation by ENT because of difficulty controlling his epistaxis. Shortly after admission, a CBC revealed nearly identical hematological parameters to those seen in the ER and the pathologist was telephoned. Attempts at warming the patient’s specimen and even acquiring another specimen brought to the lab in a water bath resulted in only trivial changes in the patient’s CBC. If however, patient plasma was replaced by an equal volume of isotonic diluent supplied by the manufacturer, the Hb, Hmct, MCH and MCHC dropped to 6.5 g/dL, 19.4 percent, 23.1 pg and 33.5 percent respectively. Examination of a smear revealed numerous rouleaux. Serum protein and albumin assays revealed concentrations of 9.7 and 2.7 g/dL respectively suggesting an increase in the globulin fraction. Subsequent SPE, IFE and quantitative nephelometry assays performed at our reference lab (ARUP; Salt Lake City, UT) indicated the presence of an IgM-kappa monoclonal protein [6.99 g/dL]. A presumptive diagnosis of Waldenstrom’s macroglobulinemia was confirmed by bone marow biopsy. It has long been known that an MCHC greater than 36 percent should prompt a careful investigation of the data [Am J Clin Pathlol.83:218 (1985)]. In this case the elevated concentration of IgM resulted in increased turbidity and a spuriously elevated Hb [Arch Pathol Lab Med.124:616 (2000)]. Yet the clue went unrecoginized by laboratory personnel as well as ordering physicians leading to a probable delay of nearly one year in the diagnosis of the patient’s underlying hematologiclal disorder.