Catastrophic antiphospholipid syndrome: a case report and literature review.

Catatrophic antiphospholipid syndrome (CAPS), a rare variant of antiphospholipid syndrome (APS), is associated with rapid multiorgan failure. While APS is associated with single medium-to-large blood vessel occlusions, CAPS is most often associated with several, concurrent vascular occlusions of small vessels, commonly of the kidneys, heart, skin and brain. We present a case of a 21-year-old female patient with a history of immune thrombocytopenia purpura and APS, who eventually developed concurrent cerebral venous sinus thrombosis, diffuse alveolar haemorrhage, renal thrombotic microangiopathy, and a necrotic, vasculitic wound on her forearm. Despite hospitalisation and treatment, her condition worsened and the patient eventually died after succumbing to suspected CAPS.

Neuroendocrine Basis for Disrupted Ovarian Cyclicity in Female Mice During Chronic Undernutrition.

Chronic undernutrition is a type of metabolic stress that impairs reproduction in multiple species. Although energy balance and female reproductive capacity is recognized as tightly coupled, the neuroendocrine loci and molecular mechanisms that mediate ovarian cycle dysfunction during chronic undernutrition in adult females remain poorly understood. Here, we present a series of studies in which we tested the hypothesis that inhibition of kisspeptin (Kiss1) neurons, which are critical for controlling luteinizing hormone (LH) pulses and the preovulatory LH surge in females, underlies the impairment of the ovarian cycle by undernutrition. We first investigated the effect of chronic undernutrition (70% of unrestricted feed intake) on estrous cyclicity in intact female c57bl6 mice. Undernutrition caused a rapid cessation of ovarian cyclicity during the 2-week treatment, suppressing ovarian steroidogenesis and inhibiting ovulation. Using 2 well-defined estradiol-replacement paradigms, we directly tested the hypothesis that undernutrition inhibits Kiss1 neurons in the arcuate nucleus (ARCKiss1), which are required for LH pulses and in the anteroventral periventricular nucleus (AVPVKiss1), which are necessary for LH surge secretion. Undernutrition prevented LH pulses and impaired ARCKiss1 neuronal activation, using c-Fos as a marker, in ovariectomized females subcutaneously implanted with a pellet containing a diestrus-like level of estradiol. In addition, undernutrition completely blocked the estradiol-induced LH surge and diminished Kiss1 messenger RNA abundance, without decreasing estradiol receptor α (Erα), in micropunches of the AVPV. Collectively, these studies demonstrate that undernutrition disrupts ovarian cyclicity in females via impairment both of ARCKiss1 control of LH pulses and AVPVKiss1 induction of the LH surge.