Malakoplakia, a medical, surgical, pathological and radiological enigma, is an infrequent chronic inflammatory condition that can affect many organ systems, including the gastrointestinal tract, integument, skeletal system and genitourinary tract. Review of the literature has shown that malakoplakia presents in paediatric as well as adult populations, and that it is associated with impaired immune function. Variable clinical manifestations as well as the sometimes non-specific radiological findings of malakoplakia can be misleading, making diagnosis quite difficult. We present a clinical case of renal malakoplakia mimicking a malignant renal carcinoma in a 62-year-old woman. This report highlights the importance of awareness of malakoplakia in the differential diagnosis for renal masses and renomegaly. This case can serve as a reminder that things are not always what they seem, and it reinforces the idea that unusual disease entities should be explored to aid in achieving a correct diagnosis and, thus, potentially avoid unnecessary treatment.
We report the case of a 67-year-old female who presented with a large renal mass. Gross examination of the nephrectomy specimen demonstrated a 6-cm renal mass that invaded into the renal sinus and perinephric fat. Histologic examination revealed two distinct tumor types. The first type was a conventional (clear cell) renal cell carcinoma that was of low nuclear grade and comprised the minority of the overall tumor. The second type was a high-grade collecting duct carcinoma with glandular/tubular differentiation and composed the majority of the tumor. Immunohistochemical studies demonstrated distinctive patterns of the two tumor types, thus confirming two distinct lineages. Five months postoperatively, the patient developed metastasis to the lungs and right hilar lymph node region. A fine needle aspiration of a lung nodule demonstrated a metastatic, poorly differentiated carcinoma, similar to the collecting duct carcinoma component in the kidney. Collision tumors of the kidney are rare with fewer than 10 cases reported in the literature. Our report further expands the spectrum of this rare phenomenon.
Mycetoma describes a heterogeneous group of cutaneous and subcutaneous infections caused by either fungi (eumycetomas) or bacteria (actinomycetomas). It is characterized by a triad of clinical symptoms: painless subcutaneous tumor-like swelling, multiple sinuses and fistulas, and discharged grains in pus. This predominantly affects the feet in more than 70% of patients. It is endemic in the “mycetoma belt” regions, including Africa, South America, and South Asia. Autochthonous mycetoma is rare in the United States of America (USA). We recently reported a Latin American immigrant with eumycetoma in the State of Maryland, USA. With millions of immigrants from endemic regions, the true number of mycetomas in the USA is most likely higher than currently recognized. With the aim to raise the awareness of clinicians about mycetoma, especially dermatologists and podiatrists, we update the development of the epidemiology, etiology, clinical presentations, pathogenesis, diagnosis, differential diagnosis, and treatment of mycetoma.
Prostaglandin D2 (PGD2) is a lipid mediator that promotes androgenic alopecia and inhibits wound-induced hair follicle neogenesis. Although the activation of its receptor, GPR44, has been implicated in this action, other mechanisms may exist as well. The role of testosterone and its reduced metabolite, dihydrotestosterone, as drivers of androgenic alopecia is well established. Our previous data showed that human keratinocytes treated with PGD2 upregulated the transcription of aldo-keto reductase 1C3 (AKR1C3), an enzyme that converts androstenedione (AD) a relatively weak androgen, to testosterone. We hypothesized that AKR1C3 upregulation in PGD2-treated keratinocytes increases their capacity to generate testosterone from AD. Our data suggest that testosterone production was elevated by PGD2-treated keratinocytes while another prostaglandin, PGE2, had no effect. Surprisingly, knock down of AKR1C3 by siRNA, or specific inhibition of its enzymatic activity, had no effect on PGD2-induced testosterone production. Thus, following preliminary findings, we speculated that PGD2 stimulation of testosterone synthesis occurs through ROS and changes in REDOX potential. We tested this assumption by using the ROS scavenger, n-acetyl-cysteine (NAC). Remarkably and consistent with our hypothesis, NAC completely blocked PGD2-induced testosterone increase. Attempting to identify genes involved in this response, we further investigated the effects of PGD2 on ROS-associated gene regulation using qPCR. Upregulation of a number of REDOX-associated genes was detected, including enzymes involved in GSH metabolism, ROS clearance, and NADPH synthesis. In ongoing experiments, we are testing the possible role of these genes to identify novel targets for the treatment of androgenic alopecia or other testosterone-driven skin pathologies.
Introduction: Appendiceal intussusception is an infrequent surgical disease that can present acutely, mimicking acute appendicitis, or chronically with intermittent right lower quadrant pain. Lead points are associated with appendiceal intussusceptions in slightly Ͼ70% of cases. Common lead points are endometriosis, mucinous neoplasm, adenoma, adenocarcinoma, and carcinoid. Surgical therapy is often required to manage the intussusception. In cases of nonreducible appendiceal intussusceptions or those that have a lead point, an appendectomy, ileocecectomy, or right hemicolectomy.
Case Description:We report a case of appendiceal intussusception with an intraoperative finding of a cystic mass and pathologic diagnosis of low-grade mucinous neoplasm in a healthy 23-year-old female patient. She underwent a laparoscopic ileocecectomy.Discussion: Appendiceal mucinous cystadenoma requires long-term follow-up after resection.
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