Abstract
Several case reports have described hypopituitarism following orthohantavirus infection, mostly following Puumala virus. The pathogenesis of this seemingly rare complication of orthohantavirus infection remains unknown. This review explores the possible pathophysiological mechanisms of pituitary damage due to orthohantavirus infection. In only three out of the 28 reported cases, hypopituitarism was detected during active infection. In the remaining cases, detection of pituitary damage was delayed, varying from two months up to thirteen months post-infection. In these cases, hypopituitarism remained undetected during the acute phase of infection or only occurred weeks to months post infection. Both ischemic and hemorrhagic damage of the pituitary gland have been detected in radiographic imaging and post-mortem studies in the studied case reports series. Ischemic damage could be caused by hypotension and/or vasospasms during the acute phase of hemorrhagic fever with renal syndrome (HFRS) while hemorrhage could be caused by thrombocytopenia, thrombopathy, and other known causes of coagulation disorders during orthohantavirus infection. Also, hypophysitis due to the presence of auto-antibodies have been suggested in the literature. In conclusion, a significant number of case reports and series describe hypopituitarism after orthohantavirus infection. In most cases hypopituitarism was diagnosed with a delay and therefore could very well be underreported. Clinicians should be aware of this potential endocrine complication, with substantial morbidity, and if unrecognized, significant mortality.
Highlights
Hemorrhagic fever with renal syndrome (HFRS) comprises a group of clinically similar rodent-borne infectious diseases caused by orthohantaviruses, including Hantaan (HTNV), Dobrava (DOBV), Seoul (SEOV), Saaremaa (SAAV), and Puumala virus (PUUV) [1]
One should keep in mind that a dysbalanced hormonal axis in these 30 patients was not necessary be the result of hypopituitarism
The exact pathophysiological mechanisms leading to hypopituitarism during or following orthohantavirus infection remains unknown
Summary
Hemorrhagic fever with renal syndrome (HFRS) comprises a group of clinically similar rodent-borne infectious diseases caused by orthohantaviruses, including Hantaan (HTNV), Dobrava (DOBV), Seoul (SEOV), Saaremaa (SAAV), and Puumala virus (PUUV) [1]. The clinical course of these infections is classically characterized by a triad of acute renal failure, fever, and hemorrhagic complications. Depending on which orthohantavirus species infects a patient, case fatality rates vary from. From the old world hantaviruses, DOBV infections are generally considered to result in the highest percentage of hemorrhagic complications (up to 15–30%), while PUUV is known to cause nephropathia epidemica (NE), a syndrome comparable to HFRS with a milder clinical course and mortality rates of. Several case reports have described hypopituitarism following orthohantavirus infection The pathogenesis of this complication remains unknown. Already in the 1950s, different post-mortem studies showed pituitary damage, e.g., foci of hemorrhage and necrosis, in 58–72% of patients with hemorrhagic fever, which are thought to be HFRS cases [6,7]. This review aims to explore the possible pathophysiological mechanisms for pituitary damage in orthohantavirus infections in literature and illustrates its clinical relevance
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