Journal of the association of physicians of india • vol 62 • november, 2014 55

Hypopituitarism and Autoimmune Thyroiditis Following Snake Bite : An Unusual Clinical ScenarioSahana Shetty*, Manesh S Abi**, Ravali Hickson***, Thambu David†, Simon Rajaratnam‡

AbstractSnake venom can cause local tissue damage and lead to coagulopathy, shock, neurotoxicity and acute kidney injury. Hypopituitarism is a rare complication following snake bite. It has been described following Russell’s viper bite from Burma and South India. Herein we describe a patient who presented with severe thyrotoxicosis and partial hypopituitarism following snake bite.

*Senior Registrar, Department of Endocrinology, Diabetes and

Metabolism, **Senior Registrar, ***Assistant Professor, †Professor

and Head, Department of Medicine, Unit-II, ‡Professor,

Department of Endocrinology, Diabetes and Metabolism, Christian Medical College,

Vellore – 632 004.Received: 01.03.2013;

Revised: 08.05.2013; Accepted: 14.05.2013

Case Report

A 19 year old lady was admitted with us in March 2012 a few hours following a snake bite on her right foot. The snake was not identified. She had severe pain

at the site of the bite with profuse bleeding. She started complaining of diplopia and subsequently developed bilateral ptosis. On examination she was drowsy; she had pallor, tachycardia (170/min) and low blood pressure (70 mmHg). Fang marks were visible on the right foot and there was no active bleeding.

Her investigations revealed features of disseminated intravascular coagulation (DIC), rhabdomyolysis and acute renal failure (Table 1). CT scan of the brain showed no structural abnormality and the sella appeared normal (Figure 1).

S h e wa s t r e a t e d w i t h polyvalent antisnake venom and was supported with blood products. She underwent dialysis. Her renal functions gradually recovered and she was asymptomatic at the time of discharge.

Three months later in June 2012, she presented to us with recurrent vomiting and weight loss of 13 kgs over one month. She did not resume her periods following the snake bite.

On examination she had mild pallor. Her pulse rate was 108 /min . Her b lood pressure was 100/60 mmHg. She has a fine tremor. There was no thyroid enlargement. H e r c a r d i o v a s c u l a r , respiratory and abdominal examination was normal. She

Table 1 : Investigations done at her 1st admission (March 2012)

Investigations Patients value Reference rangeHb 6.8 gm% 12- 14 gm%WBC count 9200/cumm 4000-11,000/cummPlatelet count 267000/cumm 1,50,000- 4,00,000/cummAPTT 54.4 secs 25-34.8 secsProthrombin time 15.5 secs 10-12.5 secsFibrinogen 110.9 mg/dl 200-400 mg/dlD- dimer 1146 ng/ml < 250 ng/mlCreatinine 5.17mg% 0.5-1.4 mg%CPK 8278 u/L 45-195 u/L

Fig. 1 : CT scan (20/3/2012) showing no structural abnormality, the sella appears normal

56 Journal of the association of physicians of india • vol 62 • november, 2014

had no neurological deficits. Her visual fields and optic fundi were normal.

Her biochemical evaluation revealed features of thyrotoxicosis with partial hypo-pituitarism (Table 2). Radioactive iodine uptake revealed negligible uptake over the thyroid; the uptake at 2 hours - 4% (normal 8-17%), at 6 hours - 3% (normal 13-25%) and at 24 hours - 1% (normal 23-40%). The Tc99m thyroid scan also showed no uptake over the thyroid (Figure 2). Her thyroid antibody levels were elevated confirming the diagnosis of underlying autoimmune thyroiditis.

She was started on both beta blockers for thyroiditis and steroid replacement for hypocortisolism. After one month her thyroid functions had normalised (T4 6.9 ug%, FTC 0.83 ug%). At her last follow up visit in March 2013 her weight had normalised and she was getting regular withdrawal bleeding with medication.

Table 2 : Investigations done during her 2nd admission (June 2012)

Investigations Patient’s values Reference rangesSodium 131 mmol/l 135-145 mmol/lPotassium 3.0 mmol/l 3.0-5.0 mmol/lBicarbonate 22 meq/l 22 -29 meq /lCreatinine 0.94 mg/dl 0.5 – 1.1 mg/dlT4 > 30.0 ug% 4.5 -12.5 ug%Free T4 5.3 ng% 0.8 -2.0 ng%TSH < 0.004 uIU/ml 0.3 – 4.5 uIU/mlAnti-thyroglobulin antibody 301 IU/mlAnti-microsomal antibody 11 IU/mlSerum cortisol (8 AM) 3.36 ug% 5.0 – 25.0 ug%Post synacthen cortisol 6.5 ug%FSH 0.758 iIU/ml 2.8 -11.3 mIU/mlLH 0.653 mIU/ml 1.1 -11.6 mIU/ml

Fig. 2 : Tc99m thyroid scan (16/6/2012) showing no uptake over the thyroid

Discussion

Viper venom causes neurotoxicity, myotoxicity, haemolysis and coagulopathy leading to shock and acute kidney injury. Hypopituitarism is a relatively uncommon complication following viper bite.

In our case, although the species of the snake were not identified, the association of DIC, acute renal failure and hypopituitarism make the possibility of a viperine bite more likely.

Hypopituitarism following Russell’s viper bite was first reported in 1976 by Eapen et al in 3 adults from Kerala.1 Russell’s vipers (Daboia russelii and Daboia siamensis) inhabit South and South East Asian countries and are the leading cause of fatal snake bite in India, Pakistan, Sri Lanka, Burma, Thailand and Indonesia.2

Russell’s viper venom is known to contain many toxins which include biologically active procoagulant enzymes which activate factors V, X and other steps in the coagulation cascade. This leads to DIC and consumptive coagulopathy.

R u s s e l l ’ s v i p e r v e n o m a l s o c o n t a i n s a metalloproteinase ‘haemorrhagina’ which damages the vascular endothelium and also contains other toxins which impair platelet function. This leads to thrombosis and spontaneous haemorrhage. Focal haemorrhage and micro vascular thrombin deposition in the pituitary may be responsible for the pathological finding of haemorrhagic infarction of the anterior pituitary leading to acute and chronic Hypopituitarism following snake bite.3

Our patient also had clinical and biochemical features of thyrotoxicosis. Transient thyrotoxicosis

Journal of the association of physicians of india • vol 62 • november, 2014 57

due to autoimmune destructive thyroiditis has been previously described in a patient with hypopituitarism following pituitary apoplexy.4 The development of autoimmune thyroid disease has also been reported following unilateral adrenalectomy for Cushing’s syndrome,5 following bilateral adrenalectomy for Carney’s complex and following the removal of ACTH producing pituitary adenomas in patients with Cushing’s disease.6 Hypocortisolaemia induced immunological alterations can lead to the development of autoimmune thyroiditis and exacerbate underlying autoimmune thyroid disease.

Our pat ient developed severe autoimmune thyroiditis and partial hypopituitarism following snake bite. Severe hypocortisolaemia secondary to hypopituitarism might have precipitated the autoimmune thyroiditis in this individual.

Following recovery from acute snake envenomation, if the patient subsequently presents with a chronic illness it should alert the physician to the possibility of underlying hypopituitarism. When there is severe weight loss in addition, the possibility of associated autoimmune thyroiditis should be considered.

References1. Eapen CK, Chandy N, Kochuovarkey KL, et al. Unusual complication

of snake bite: hypopituitarism after viper bites. In: Ohsaka A, Hayashi K, Sawai Y, eds. Animal, plant and microbial toxins. Vol 2. New York, NY, Plenum Press, 1976;( 2):467–73.

2. Warrell DA. Snake venoms in science and clinical medicine. Russell’s viper: biology, venom and treatment of bites. Trans R Soc Trop Med Hyg 1989;83:732–40.

3. Antonypillai CN, Wass JAH, Warrell DA, Rajaratnam HN. Hypopituitarism following envenoming by Russell’s Vipers (Daboia siamensis and D. russelii) resembling Sheehan’s syndrome: first case report from Sri Lanka, a review of the literature and recommendations for endocrine management. QJ Med 2011;104:97–108.

4. Sasaki H, Ohnishi O, Okudera T, Okumura M. Simultaneous occurrence of transient resolving thyrotoxicosis due to painless thyroiditis, hypopituitarism and diabetes insipidus following pituitary apoplexy. Postgraduate Medical Journal 1991;67:75-77.

5. Takasu N, Komiya I, Nagasawa Y, Asawa T, Yamada T. Exacerbation of autoimmune thyroid dysfunction after unilateral adrenalectomy in patients with Cushing’s syndrome due to an adrenocortical adenoma. The New England Journal of Medicine 1990;322:1708–1712.

6. Takasu N, Ohara N, Yamada T, Komiya I. Development of autoimmune thyroid dysfunction after bilateral adrenalectomy in a patient with Carney’s complex and after removal of ACTH-producing pituitary adenoma in a patient with Cushing’s disease. Journal of Endocrinological Investigation 1993;16:697–702.

Neurological Manifestations in a Patient of Kikuchi’s DiseaseMarina Vaz*, Carmen M Pereira**, Sindhoora Kotha***, Jamina Oliveira***

AbstractKikuchi’s disease is a rare condition that mainly presents in young females along with lymphadenitis. Involvement of the nervous system is rare. We report a young female who presented with fever, headache, vomiting, lymphadenopathy and neurological manifestations in the form of aseptic meningitis, ataxia and paraparesis. Since the disease can be mistaken clinically and histologically for SLE, lymphoma and tuberculosis it is important to differentiate it from these conditions. Also our case emphasizes the importance of recognising this disorder in diagnosing patients with meningitis.

*Lecturer, **Associate Professor, ***Jr. Resident, Dept of Medicine,

Goa Medical College, GoaReceived: 08.02.2013;

Revised: 09.04.2013; Accepted: 25.05.2013

Introduction

Kikuchi-Fujumoto disease was first described by Kikuchi in 1972 in Japan. Fujimoto and colleagues independently described it in the same year. Also known as

histiocytic necrotising lymphadenitis, it is an uncommon, idiopathic, generally self-limiting cause of lymphadenitis.1

No specific cause of Kikuchi’s disease has been found. Some kind of viral or post viral aetiology has been proposed. It has also been linked to SLE.1 The course is