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Table of Contents    
Year : 2015  |  Volume : 63  |  Issue : 2  |  Page : 255-256

Pituitary cachexia after rabies encephalitis

Departments of Endocrinology, Neurology and Respiratory Medicine, Command Hospital, Chandimandir, Haryana, India

Date of Web Publication5-May-2015

Correspondence Address:
K. V. S. Hari Kumar
Departments of Endocrinology, Neurology and Respiratory Medicine, Command Hospital, Chandimandir, Haryana
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0028-3886.156295

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How to cite this article:
Kumar KH, Ahmad F, Dutta V. Pituitary cachexia after rabies encephalitis. Neurol India 2015;63:255-6

How to cite this URL:
Kumar KH, Ahmad F, Dutta V. Pituitary cachexia after rabies encephalitis. Neurol India [serial online] 2015 [cited 2020 Nov 25];63:255-6. Available from:


Rabies is a common zoonotic illness seen across the world and has the highest case fatality rate known for any infectious disease. The disease leads to about 60,000 deaths annually and there are only twelve survivors reported till date. [1]

In July 2014, a 16-year-old boy was referred to us in a severely cachectic state. History revealed that the boy had suffered an unprovoked bite from a street dog in March 2014 and had presented with a febrile encephalopathic illness after three weeks. He was initially managed with broad spectrum antibiotics, ventilatory support, steroids and other supportive therapy. Cerebro-spinal fluid (CSF) showed neutrophilic pleocytosis, hypoglycorrhachia and elevated proteins. The paired samples of serum and CSF showed high levels (>1:1,64,000) of rabies virus neutralizing antibodies. The nuchal skin biopsy stained positive for the presence of viral antigen confirming the diagnosis of rabies. MRI revealed lesions in bilateral thalami and in the cerebellum, sella and brainstem, including the upper cervical cord [Figure 1]a. He was further managed with rabies immunoglobulin, physiotherapy, nasogastric feeds and other supportive therapy. His neurological status, especially his sensorium, improved gradually over the next six weeks. However, he developed significant cachexia despite an intensive physiotherapy and a high caloric intake, prompting an endocrinological consultation. His anthropometric measures like body weight (27 kg) and body mass index (9.3 kg/m 2 ) suggested severe cachexia. His systemic examination revealed a dry skin, loss of pubic hair with no evidence of dehydration. His hormonal profile showed free triiodothyronine- 1.1 pmol/L (normal 3 - 6.2), free thyroxine - 0.4 ng/dL (normal 0.8 - 1.2), thyrotropin - 2.2 mIU/L (normal 0.3 - 4.6), prolactin- 4 ng/ml (normal 0 - 15), leutinising hormone (LH) - 0.6 IU/L (normal 0 - 8), follicle stimulating hormone (FSH) - 0.5 IU/L (normal 1 - 10), testosterone 126 ng/dL (normal 250 - 820) and IGF-1 of 86 IU/L (normal 145-540). His peak cortisol and growth hormone (GH) after hypoglycemia were 22.4 μg/dL and 1.16 ng/mL, respectively. His body composition analysis (BCA) by the dual energy X-ray absorptiometry (DEXA) showed complete absence of subcutaneous fat [Figure 1]b. He was diagnosed as a case of pituitary cachexia secondary to rabies encephalitis and was treated with levothyroxine, growth hormone, testosterone and vitamin supplements. During the last follow up, 3 months after the therapy, the body weight had improved by 4 kg and there is an appearance of subcutaneous fat at a few places as shown in the repeat BCA [Figure 1]C.
Figure 1: MRI image (a) showing the hyperintense pituitary along with diffuse cerebral atrophy and body composition analysis before (b) and after (c) therapy

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Pituitary cachexia or Simmonds' disease denotes the complete destruction of the anterior pituitary gland leading to a cachectic state. The disease is characterized by cutaneous changes like loss of secondary sexual characteristics, hypotension, muscle weakness, and premature senility. Our patient had developed most of these features fairly rapidly in a few weeks after the onset of rabies meningoencephalitis. Survival after rabies infection is reported in only a dozen patients till date and to the best of our knowledge, none of them have reported the features of pituitary cachexia. Simmonds' disease could be caused by infarction, bleeding, tumor, inflammation and occasionally infection. [2] Previous reports suggest hypersexuality and behavioral abnormalities during the acute phase of rabies infection.

Cachexia is also associated with the presence of a number of disease states like malignancy, HIV infection, chronic obstructive pulmonary disease and congestive cardiac failure. The loss of muscle and fat tissue is due to an altered endocrinal milieu coupled with increase in the proinflammatory cytokines. [3] Testosterone and insulin like growth factor-1 (IGF-1) play an important role in the maintenance of the muscle and fat tissue and our patient had deficiency of both these hormones leading to severe cachexia. To conclude, we report the case of a young boy, who survived the deadly rabies infection but had persistence of a cachectic state resulting from the loss of anterior pituitary hormones.

 » References Top

de Souza A, Madhusudana SN. Survival from rabies encephalitis. J Neurol Sci 2014 15;339:8-14.  Back to cited text no. 1
Escamilla RF, Lisser H. Simmonds' Disease (Hypophyseal Cachexia): Clinical report of several cases with discussion of diagnosis and treatment. Cal West Med 1938;48:343-8.  Back to cited text no. 2
Morley JE, Thomas DR, Wilson MM. Cachexia: Pathophysiology and clinical relevance. Am J Clin Nutr 2006;83:735-43.  Back to cited text no. 3


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