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Insulinomas are rare pancreatic neuroendocrine tumours and the commonest cause for endogenous hyperinsulinaemic hypoglycemia. Small tumours are not easily detected by conventional cross-sectional imaging making localization prior to surgical removal a challenge. Selective arterial calcium stimulation is an invaluable adjunct to localization in such circumstances. This is further supplemented by intraoperative ultrasonography. A 39-year-old male was referred with features of Whipple’s triad of 10 months duration. Clinical and biochemical evaluation including C-peptide and serum insulin levels during supervised hypoglycemia concluded endogenous hyperinsulinaemia as the underlying aetiology. Contrast CT and MRI of the abdomen failed to localize the tumour. Selective arterial calcium stimulation localized the lesion in distal pancreas. During the surgery, tumour was further localized to the tail of the pancreas using intraoperative ultrasonography and enucleated. Histology confirmed an insulinoma and patient made an unremarkable recovery and was well more than a year after the surgery.

Diabetes prevalence shows a continuous increasing trend in South Asia. Although well-established treatment modalities exist for type 2 diabetes mellitus (T2DM) management, they are limited by their side effect profile. Sodium–glucose co-transporter 2 inhibitors (SGLT2i) with their novel insulin-independent renal action provide improved glycemic control, supplemented by reduction in weight and blood pressure, and cardiovascular safety. Based on the clinical outcomes with SGLT2i in patients with T2DM, treatment strategies that make a “good clinical sense” are desirable. Considering the peculiar lifestyle, body types, dietary patterns (long duration religious fasts), and the hot climate of the South Asian population, a unanimous decision was taken to design specific, customized guidelines for T2DM treatment strategies in these regions. The panel met for a discussion three times so as to get a consensus for the guidelines, and only unanimous consensus was included. After careful consideration of the quality and strength of the available evidence, the executive summary of this consensus statement was developed based on the American Association of Clinical Endocrinologists/American College of Endocrinology protocol.

Obesity and its complications have become a major public health problem. Health risk conferred by obesity can be reduced by sustained weight loss but this is difficult in a majority. Bariatric surgery (BS) has proven to provide an excellent answer to this problem but there is minimal data in South Asians and especially in Sri Lankans. In this study we aimed to find the effect of BS on improving obesity in Sri Lankans. We did a retrospective analysis of medical records of 170 obese patients who underwent BS at the Colombo South Teaching Hospital, Sri Lanka. Overall 74.1% were females. Laparoscopic sleeve gastrectomy (LSG) was the commonest BS (69.5%) performed, followed by laparoscopic mini gastric bypass (LMGB) (24.1%) and laparoscopic Roux-en-Y gastric bypass (4.9%). Mean age was 38.1 ± 10.4 years. Mean pre-operative body weight and body mass index were 115.0 ± 23.0 kg and 45.1 ± 6.8 kg/m2 respectively. The baseline waist circumference (WC) and body fat percentage (BFP) in females and males were 119.0 ± 11.0 cm vs 129.0 ± 14.9 cm, p

Background Hypokalaemic paralysis is a rare group of disorders with concomitant muscle weakness and hypokalaemia. Thyrotoxicosis is a recognized and a common cause for hypokalaemic paralysis among Asians, in which intracellular shift of potassium is enhanced. Gitelman syndrome, an autosomal recessive renal salt loosing condition is characterized by hypokalaemia, hypocalciuria and hypomagnesaemia. Concurrence of these two conditions is very rarely reported.Case Presentation We report two genetically unrelated Sri Lankan patients who presented with concurrent thyrotoxicosis and Gitelman syndrome. Both of them presented with symptomatic hypokalaemia and detected to have thyrotoxicosis. One had Grave’s disease, while the other patient had toxic multinodular goiter. They were initially managed symptomatically for thyrotoxic hypokalaemic paralysis. Despite rendering euthyroidism with medical management, they persisted to have symtomatic hypokalaemia. On evaluation for a second pathology, we detected them to have Gitelman syndrome, which is a rare concurrence.Conclusion Elevated thyroid hormone levels can precipitate a paralytic episode in a patient with subclinical chronic hypokalaemia due to an additional underlying disease. Gitelman syndrome is such a disease which should be considered and actively looked for in a patient with persistent hypokalaemia following rendering euthyroidism.

Background. Primary hyperaldosteronism is a known cause for secondary hypertension. In addition to its effect on blood pressure, aldosterone exhibits proinflammatory actions and plays a role in immunomodulation/development of autoimmunity. Recent researches also suggest significant thyroid dysfunction among patients with hyperaldosteronism, but exact causal relationship is not established. Autoimmune hyperthyroidism (Graves’ disease) and primary hyperaldosteronism rarely coexist but underlying mechanisms associating the two are still unclear.Case Presentation. A 32-year-old Sri Lankan female was evaluated for new onset hypertension in association with hypokalemia. She also had features of hyperthyroidism together with high TSH receptor antibodies suggestive of Graves’ disease. On evaluation of persistent hypokalemia and hypertension, primary hyperaldosteronism due to right-sided adrenal adenoma was diagnosed. She was rendered euthyroid with antithyroid drugs followed by right-sided adrenalectomy. Antithyroid drugs were continued up to 12 months, after which the patient entered remission of Graves’ disease.Conclusion. Autoimmune hyperthyroidism and primary hyperaldosteronism rarely coexist and this case report adds to the limited number of cases documented in the literature. Underlying mechanism associating the two is still unclear but possibilities of autoimmune mechanisms and autoantibodies warrant further evaluation and research.

Myxedema crisis is a life-threatening extreme form of hypothyroidism with a high mortality rate if left untreated. Myxedema crisis is commonly seen in older patients, especially in women, and is associated with signs of hypothyroidism, hypothermia, hyponatraemia, hypercarbia, and hypoxemia. Patients might present with different organ specific symptoms. Seizures are a recognized but rare manifestation of myxedema with a very high mortality rate. Prompt diagnosis and appropriate management may improve the prognosis. Many contributory factors may involve development of seizures in a patient with myxedema. Hyponatraemia is one such cause, which is seen in moderate-severe form in the background of myxedema. We report an elderly male who presented with generalized tonic clonic seizure preceded by memory impairment and drowsiness. He had moderate hyponatraemia and very high thyroid stimulatory hormone levels in association with low free thyroxin levels. Diagnosis of myxedema crisis was made and patient was successfully treated with sodium correction and thyroid hormone replacement.

Background Guillain–Barré syndrome is an immune mediated acute inflammatory polyradiculo-neuropathy involving the peripheral nervous system. Commonest presentation is acute or subacute flaccid ascending paralysis of limbs. Rarely autonomic dysfunction can be the presenting feature of Guillain–Barré syndrome. Raynaud’s phenomenon, although had been described in relation to many disease conditions, has not been described in association with Guillain–Barré syndrome up to date. Case presentation We report the first case of Guillain–Barré syndrome presenting with Raynaud’s phenomenon in a 21-year-old previously well boy. New onset Raynaud’s phenomenon was experienced followed by acute ascending flaccid paralysis of lower limbs and upper limbs together with palpitations and postural giddiness. Nerve conduction studies showed acute inflammatory demyelinating polyneuropathy with cerebrospinal fluid cyto-protein dissociation. He was treated with intravenous immunoglobulin and showed a satisfactory clinical recovery of muscle weakness, Raynaud’s phenomenon and autonomic disturbances. Conclusion Guillain–Barré syndrome presenting with Raynaud’s phenomenon is not being reported in literature previously. Although the underlying mechanism is not fully understood, Raynaud’s phenomenon should prompt the physician to consider Guillain–Barré syndrome with a complimentary clinical picture.

Background Lemierre's syndrome is a rare condition characterized by thrombophlebitis of internal jugular vein, septicemia and septic metastatic infection of different organs. It is preceded by an oropharyngeal infection by anaerobic organisms. Community-acquired methicillin-resistant Staphylococcus aureus is now emerging as a causative organism in Lemierre's syndrome. Clinical manifestations vary depending on the organ system affected by the infection. Although rare, patients may present with life-threatening conditions such as cardiac tamponade. Case presentation We report the first case, to our knowledge, of Lemierre's syndrome presenting with cardiac tamponade secondary to community-acquired methicillin-resistant S. aureus in a previously well 45-year-old Sri Lankan lady. Fever, sore throat and left-sided neck pain complicated with facial and left upper limb swelling were followed by severe shortness of breath for 24 h. There was tachycardia with pulsus paradoxus, low blood pressure and soft heart sounds. Pericardial effusion with cardiac tamponade was detected on echocardiogram and methicillin-resistant S. aureus species were isolated in both blood and pericardial fluid cultures. Venous duplex of neck veins and computed tomography scan of the neck showed thrombosis of left-sided internal jugular, external jugular, subclavian and axillary veins. Diagnosis of Lemierre's syndrome was made, and patient had a satisfactory recovery following emergency pericardiocentesis and a prolonged course of antibiotics. Conclusions Although uncommon, Lemierre's syndrome is a life-threatening condition. Patients may present with cardiac tamponade secondary to purulent pericarditis in Lemierre's syndrome, where emergency pericardiocentesis is lifesaving. Community-acquired methicillin-resistant S. aureus is emerging as a causative agent in Lemierre's syndrome, and awareness is required amongst physicians for prompt diagnosis and appropriate empirical treatment to prevent mortality and morbidity associated with the disease.

Background Guillain-Barré syndrome is an acquired polyradiculo-neuropathy, often preceded by an antecedent event. It is a monophasic disease but a recurrence rate of 1–6 % is documented in a subset group of patients. Patients with Guillain-Barré syndrome show cerebrospinal fluid albuminocytologic dissociation. Normal cerebrospinal fluid protein levels during both initial and recurrent episodes of Guillain-Barré syndrome is a rare occurrence and has not been described earlier in the literature. Case presentation Twenty-five-year-old Sri Lankan female with past history of complete recovery following an acute inflammatory demyelinating polyneuropathy (AIDP) variant of Guillain-Barré syndrome 12 years back presented with acute, ascending symmetrical flaccid quadriparasis extending to bulbar muscles, bilateral VII cranial nerves and respiratory compromise needing mechanical ventilation. Nerve conduction study revealed AIDP variant of Guillain-Barré syndrome. Cerebrospinal fluid analysis done after 2 weeks were normal during both episodes without albuminocytologic dissociation. She was treated with intravenous immunoglobulin resulting in a remarkable recovery. Both episodes had a complete clinical recovery in three and four months’ time respectively, rather a faster recovery than usually expected. Conclusion Recurrence of Guillain-Barré syndrome can occur in a subset of patients with Guillain-Barré syndrome even after many years of asymptomatic period. Normal cerebrospinal fluid profile does not exclude Guillain-Barré syndrome and may occur in subsequent recurrences of Guillain-Barré syndrome arising the need for further studies to identify the pathophysiology and the possibility of a different subtype of Guillain-Barré syndrome.

Background Acquired angioedema is a rare but recognized manifestation of lymphoproliferative disorders due to deficiency in C1 esterase inhibitor. Normal level of C1 esterase inhibitor proteins in association with angioedema due to lymphoproliferative disease is a rare and an uncommon finding caused by antibodies produced from the underlying disease. Antibodies cause inactivation of C1 esterase inhibitor, thus resulting in C1 esterase inhibitor dysfunction despite of normal quantity of C1 esterase inhibitor. Case presentation A 50-year-old Sri Lankan male presented with first episode of angioedema without any family history. Physical examination revealed mild pallor with swelling of tongue, lips and perioral region. On investigations, erythrocyte sedimentation rate was persistently high and bone marrow with immunohistochemistry revealed infiltration with B-cell type low grade non-Hodgkin lymphoma. Computed tomography scan of the chest and abdomen showed paratracheal and subcarinal lymphadenopathy and splenomegaly, with the findings being compatible with lymphoma. He had normal C1 esterase inhibitor protein level with reduced activity and low C1q, C4 levels indicating antibodies against C1 esterase inhibitor causing dysfunctional C1 esterase inhibitor. Conclusion Adult onset angioedema should prompt physicians to suspect underlying lymphoproliferative disorder despite of C1 esterase inhibitor protein level being normal. Though uncommon, presence of antibodies against C1 esterase inhibitor secondary to lymphoproliferative disorder should be considered in the presence of normal C1 esterase inhibitor protein levels with low functional capacity in the background of acquired angioedema.