An arteriovenous malformation (AVM) is a vascular lesion most frequently encountered in the brain, lungs, colon, and soft tissues of the extremities. However, rarely, an AVM may develop in the uterus, where it can cause abnormal and even life-threatening uterine bleeding. Here, we present the case of a 41-year-old G6P6 woman with abnormal uterine bleeding which resulted in a hemoglobin level of 10.2 g/dL. On gross examination, the uterus was enlarged measuring 17.5 cm x 12.0 cm x 10.0 cm, with a pronounced globoid appearance and bogginess on palpation. The cut surface was hemorrhagic and notable for numerous tortuous dilated spaces of variable sizes. These hemorrhagic, cavernous spaces were grossly apparent throughout the entire myometrium, but were found to be most prominent in the lower uterine segment of the anterior wall. Microscopic examination revealed an admixture of malformed vasculature comprising arteries, venules, and capillaries. The vessels showed prominent dilation and tortuosity with abrupt variation in the thickness of the media and elastic lamina, as highlighted by Von Gieson stain. Unlike in many other organ systems where AVMs are often considered congenital lesions, uterine AVMs are more often acquired lesions that develop following iatrogenic uterine trauma, namely cesarean section or curettage. Upon review of our patient’s history, her final delivery was via cesarean section, after which she developed abnormal uterine bleeding. We present this case as a reminder to consider uterine AVM in cases of abnormal uterine bleeding, as it may be easily overlooked by even the most experienced pathologist.

Hemophagocytic lymphohistiocytosis (HLH) is a rare, potentially fatal, and systemic hyperinflammatory syndrome with exacerbated and uncontrolled activation of histiocytes and lymphocytes against mature cells. Secondary HLH can occur in association with a myriad of underlying infections or malignancies. Our patient is a 38-year-old male prisoner with poorly controlled diabetes and no known other medical conditions. He was referred to our emergency department with three-week history of worsening malaise, weight loss, fever, bruising, and shortness of breath; imaging showed pneumomediastinum, lung nodule, and adrenal mass. Biopsy of the lung nodule revealed acid-fast bacilli. Furthermore, bone marrow biopsy showed foci of necrosis with associated acid-fast bacilli and hemophagocytosis highlighted by CD163 stain; consequently, secondary HLH was suggested. Hence, lab results were reviewed and found to satisfy five of the eight secondary HLH criteria. Moreover, ferritin was >10,000ng/ml, which has been suggested to be highly suspicious for HLH. The patient was started on anti-MAC therapy. Unfortunately, the patients status declined rapidly; he developed multi-organ failure and succumbed to disease. Later, his culture confirmed Mycobacterium tuberculosis. In conclusion, we presented a rare and challenging case of secondary HLH associated with disseminated Mycobacterium tuberculosis. A high index of suspicion is required for early diagnosis and treatment, and pathologists should be aware of Mycobacterium tuberculosis association with secondary HLH.