Rare and Complicated Overlap of Stevens-Johnson Syndrome and Acute Generalized Exanthematous Pustulosis.

Stevens-Johnson syndrome (SJS)/toxic epidermal necrolysis (TEN) and acute generalized exanthematous pustulosis (AGEP) are two separate pathological entities of severe cutaneous adverse reactions (SCARs) with different etiologies and treatment strategies. Diagnosis is, however, complicated by the similarity in their clinical presentation. Although there are few claims of AGEP-SJS/TEN overlap, a simultaneous true overlap of SJS/TEN and AGEP has rarely been described in the literature. Here, we report a case study of a 61-year-old female with a known allergy to sulfa drugs presenting with altered mental status, generalized weakness, and erythematous and excoriated purulent wounds. Based on initial workup and extensive consultation, the patient was diagnosed with severe sepsis secondary to diffuse purulent cellulitis, community-acquired pneumonia, and acute renal failure due to prerenal azotemia from dehydration. She was treated with several antibiotics, starting with vancomycin, piperacillin/tazobactam. Six days later, antibiotics were de-escalated to ceftriaxone and metronidazole because of the patient's improved status. The medications were withheld when the patient started developing extensive blistering on day 8. Blood cultures ruled out any bacterial etiology. Skin biopsy confirmed overlapping features of AGEP and SJS/TEN. Due to the uncontrolled progression of her rash, she was transferred to the burn unit of a higher care center. This is potentially the first histologically confirmed case of AGEP-SJS/TEN overlap in the United States. In this case study, a conclusive diagnosis would have never been made without a biopsy, especially because the condition presented clinically as SJS/TEN. We, therefore, recommend considering a potential overlap of multiple pathologies at each presentation or suspicion of a SCAR and performing an early skin biopsy in order to provide definitive diagnosis and treatment.

Cross-species withdrawal of MCL1 facilitates postpartum uterine involution in both the mouse and baboon.

A successful postpartum involution permits the postnatal uterus to rapidly regain its prepregnancy function and size to ultimately facilitate an ensuing blastocyst implantation. This study investigates the molecular mechanisms that govern the initiation of the involution process by examining the signaling events that occur as the uterus transitions from the pregnant to postnatal state. Using mouse and baboon uteri, we found a remarkable cross-species conservation at the signal transduction level as the pregnant uterus initiates and progresses through the involution process. This study originated with the observation of elevated levels of caspase-3 activation in both the laboring mouse and baboon uterus, which we found to be apoptotic in nature as evidenced by the concurrent appearance of cleaved poly(ADP-ribose) polymerase. We previously defined a nonapoptotic and potential tocolytic role for uterine caspase-3 during pregnancy regulated by increased antiapoptotic signaling mediated by myeloid cell leukemia sequence 1 and X-linked inhibitor of apoptosis. In contrast, this study determined that diminished antiapoptotic signaling in the postpartum uterus allowed for both endometrial apoptotic and myometrial autophagic episodes, which we speculate are responsible for the rapid reduction in size of the postpartum uterus. Using our human telomerase immortalized myometrial cell line and the Simian virus-40 immortalized endometrial cell line (12Z), we demonstrated that the withdrawal of antiapoptotic signaling was also an upstream event for both the autophagic and apoptotic processes in the human uterine myocyte and endometrial epithelial cell.