RESUMEN
Sheehan's syndrome, first described in 1937, is characterised by postpartum haemorrhage, pituitary necrosis, lactational failure and hypopitutarism. Presentation is variable and late presentations are not unusual due to partial ischaemic injury of the pituitary and gradual loss of endocrine function. A history of postpartum haemorrhage is usual but in some cases it is not elicited. Presentations such as malaise, fatigue, hypoglycaemia, decline in cognition, hyponatraemia, pancytopoenia, osteoporosis, secondary infertility, confusion and coma have all been reported. Two interesting cases of Sheehan's syndrome are presented that were diagnosed in the eighth decade; one due to atypical presentation of recurrent hyponatraemia and confusion, another from hypoglycaemic coma and symptoms of malaise and lethargy.
Asunto(s)
Hipopituitarismo/diagnóstico , Corticoesteroides/uso terapéutico , Anciano , Diagnóstico Tardío , Diagnóstico Diferencial , Femenino , Humanos , Hipopituitarismo/tratamiento farmacológico , Imagen por Resonancia Magnética , Tiroxina/uso terapéuticoRESUMEN
Catastrophic antiphospholipid syndrome (APS) is caused by thrombotic vascular occlusions that affect both small and large vessels, producing ischaemia in the affected organs. The "catastrophic" variant of the antiphospholipid syndrome (cAPS) develops over a short period of time. Although patients with cAPS represent <1% of all patients with APS, they are usually life threatening with a 50% mortality rate. A strong association with concomitant infection is thought to act as the main trigger of microthromboses in cAPS. Several theories have been proposed to explain these physiopathological features. Some of them suggest the possibility of molecular mimicry between components of infectious microorganisms and natural anticoagulants, which might be involved in the production of cross-reacting antiphospholipid antibodies. We present a case of catastrophic cerebral APS characterised by massive temporal lobe infarction and subsequent haemorrhagic transformation after sudden withdrawal of warfarin.
RESUMEN
Toxic epidermal necrolysis (TEN) is a rare but life threatening skin disease that is most commonly drug induced. The exact pathogenesis of TEN is still unknown and many drugs, including prednisolone, cyclosporin and intravenous immunoglobulin (IVIG), have been used in an attempt to halt the disease process. The use of IVIG in particular is controversial. Recently, the US Food and Drug Administration (FDA) has made a labelling change to the drug information for carbamazepine. Owing to recent data implicating the HLA allele B*1502 as a marker for carbamazepine induced Stevens-Johnson syndrome and TEN in Han Chinese, the FDA recommends genotyping all Asians for the allele. We present an interesting case of carbamazepine induced TEN which was confused with oral thrush, had no skin lesions on presentation, and had an excellent response to a 5 day course of methylprednisolone and high dose IVIG in combination.