A Case of Pituitary Apoplexy Following Leuprolide Injection for Prostate Cancer.

Pituitary apoplexy is a rare but potentially life-threatening complication of androgen deprivation therapy for prostate cancer. We present a case of a 70-year-old African American male with prostate cancer who developed symptoms of pituitary apoplexy, including hot flashes, nausea, vomiting, and cranial nerve III palsy, following the initiation of leuprolide therapy. Imaging revealed a pituitary adenoma with hemorrhage, and prompt multidisciplinary management was initiated. The patient was managed conservatively with improvement in symptoms. This case highlights the importance of recognizing the potential for pituitary apoplexy in patients receiving GnRH agonist therapy. We discuss the clinical presentation of GnRH agonist induced pituitary apoplexy, emphasizing that clinicians should maintain a high index of suspicion and promptly investigate any new neuro- ophthalmic symptoms in this group of patients. Ultimately, prompt diagnosis and treatment are crucial to mitigate the severity of this complication in patients with prostate cancer undergoing androgen deprivation therapy.

Gastrointestinal Stromal Tumor Complicated by Fistula Formation.

Gastrointestinal (GI) stromal tumors are mesenchymal tumors that may arise in any portion of the GI tract. Their clinical presentation and complications may vary but do not often present with fistulization. This case is of clinical interest because of the rarity of GI stromal tumor intestinal fistulas.

To Lick One's Wounds: A Case of Pasteurella canis oralis Osteomyelitis and Neisseria animaloris Infection from Canine Saliva.

The complications of wound infections caused by animal related trauma are well known and explored. Of the numerous polymicrobial etiologies, Neisseria animaloris and Pasteurella canis oralis have been reported only in a limited number of cases. This manuscript explores the rare finding of these species in the case of an 83-year-old male with a diabetic foot wound complicated by infection from the saliva of his pet dog. The case highlights the first instance of P. canis oralis without the setting of a penetrating animal bite, emphasizing the vulnerability of open lesions in patients whose comorbidities impair proper wound healing. These bacteria are susceptible to beta-lactams with beta-lactamase inhibitors and can be treated once identified. It is crucial to recognize rare pathogens and initiate appropriate treatment early, and to emphasize proper wound care, especially in the context of pet interactions.

Unbiased Quantification of Subplate Neuron Loss following Neonatal Hypoxia-Ischemia in a Rat Model.

BACKGROUND: Cellular targets of neonatal hypoxia-ischemia (HI) include both oligodendrocyte and neuronal lineages with differences in the patterns of vulnerable cells depending upon the developmental stage at which the injury occurs. Injury to the developing white matter is a characteristic feature of human preterm brain injury. Data are accumulating, however, for neuronal injury in the developing cerebral cortex. In the most widely used rodent model of preterm HI brain injury, conflicting data have been reported regarding the sensitivity of subplate neurons to early neonatal HI, with some reports of selective vulnerability and others that find no increased loss of subplate neurons in comparison with other cortical layers. Methods used to identify subplate neurons and quantify their numbers vary across studies. OBJECTIVE: To use recently developed cortical layer-specific markers quantified with definitive stereologic methods to determine the magnitude and specificity of subplate neuron cell loss following neonatal HI in a rodent model. METHODS: Postnatal day 2 (P2) rats underwent right common carotid artery coagulation followed by 2-3 h of hypoxia (5.6% oxygen). Categorically moderately injured brains were stained with subplate and cortical layer III-V markers (Complexin3 and Foxp1, respectively) at P8 and P21 (Foxp1 only). An Optical Fractionator was used to quantify subplate and middle/lower cortical neuronal numbers and these were compared across groups (naive control, hypoxia hemisphere, and HI hemisphere). RESULTS: Following HI at P2 in rats, the total Complexin3-expressing subplate neuron number decreases significantly in the HI hemisphere compared with naive controls or hypoxia alone (HI vs. control 26,747 ± 7,952 vs. 35,468 ± 8,029, p = 0.04; HI vs. hypoxia, 26,747 ± 7,952 vs. 40,439 ± 7,363, p = 0.003). In contrast, the total Foxp1-expressing layer III-V cell number did not differ across the 3 conditions at P8 (HI vs. control 1,195,085 ± 436,609 vs. 1,234,640 ± 178,540, p = 0.19; HI vs. hypoxia, 1,195,085 ± 436,609 vs. 1,289,195 ± 468,941, p = 0.35) and at P21 (HI vs. control 1,265,190 ± 48,089 vs. 1,195,632 ± 26,912, p = 0.19; HI vs. hypoxia, 1,265,190 ± 48,089 vs. 1,309,563 ± 41,669, p = 0.49). CONCLUSIONS: There is significant biological variability inherent in both the subplate neuron cell number and the pattern and severity of cortical injury following HI at P2 in rats. Despite this variability, the subplate neuron cell number is lower following P2 HI in animals with mild or moderate cortical injury, whereas the middle-to-lower-layer cortical neuronal number is unchanged. In more severe cases, neurons are lost from the lower cortical layers, suggesting a relative vulnerability of subplate neurons.