Journal of Clinical and Diagnostic Research, ISSN - 0973 - 709X

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On Sep 2018




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Lucknow
On Sep 2018




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Calcutta National Medical College & Hospital , Kolkata




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Dr. Arundhathi. S
MBBS, MD (Pathology),
Sanjay Gandhi institute of trauma and orthopedics,
Bengaluru.
On Aug 2018




Dr. Mamta Gupta,
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My best wishes to Dr. Hemant Jain and all the editorial staff of JCDR for their untiring efforts to bring out this journal. I strongly recommend medical fraternity to publish their valuable research work in this esteemed journal, JCDR".



Dr. Mamta Gupta
Consultant
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Aug 2018




Dr. Rajendra Kumar Ghritlaharey

"I wish to thank Dr. Hemant Jain, Editor-in-Chief Journal of Clinical and Diagnostic Research (JCDR), for asking me to write up few words.
Writing is the representation of language in a textual medium i e; into the words and sentences on paper. Quality medical manuscript writing in particular, demands not only a high-quality research, but also requires accurate and concise communication of findings and conclusions, with adherence to particular journal guidelines. In medical field whether working in teaching, private, or in corporate institution, everyone wants to excel in his / her own field and get recognised by making manuscripts publication.


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Salient features of the JCDR: It is a biomedical, multidisciplinary (including all medical and dental specialities), e-journal, with wide scope and extensive author support. At the same time, a free text of manuscript is available in HTML and PDF format. There is fast growing authorship and readership with JCDR as this can be judged by the number of articles published in it i e; in Feb 2007 of its first issue, it contained 5 articles only, and now in its recent volume published in April 2011, it contained 67 manuscripts. This e-journal is fulfilling the commitments and objectives sincerely, (as stated by Editor-in-chief in his preface to first edition) i e; to encourage physicians through the internet, especially from the developing countries who witness a spectrum of disease and acquire a wealth of knowledge to publish their experiences to benefit the medical community in patients care. I also feel that many of us have work of substance, newer ideas, adequate clinical materials but poor in medical writing and hesitation to submit the work and need help. JCDR provides authors help in this regards.
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Thanking you
With sincere regards
Dr. Rajendra Kumar Ghritlaharey, M.S., M. Ch., FAIS
Associate Professor,
Department of Paediatric Surgery, Gandhi Medical College & Associated
Kamla Nehru & Hamidia Hospitals Bhopal, Madhya Pradesh 462 001 (India)
E-mail: drrajendrak1@rediffmail.com
On May 11,2011




Dr. Shankar P.R.

"On looking back through my Gmail archives after being requested by the journal to write a short editorial about my experiences of publishing with the Journal of Clinical and Diagnostic Research (JCDR), I came across an e-mail from Dr. Hemant Jain, Editor, in March 2007, which introduced the new electronic journal. The main features of the journal which were outlined in the e-mail were extensive author support, cash rewards, the peer review process, and other salient features of the journal.
Over a span of over four years, we (I and my colleagues) have published around 25 articles in the journal. In this editorial, I plan to briefly discuss my experiences of publishing with JCDR and the strengths of the journal and to finally address the areas for improvement.
My experiences of publishing with JCDR: Overall, my experiences of publishing withJCDR have been positive. The best point about the journal is that it responds to queries from the author. This may seem to be simple and not too much to ask for, but unfortunately, many journals in the subcontinent and from many developing countries do not respond or they respond with a long delay to the queries from the authors 1. The reasons could be many, including lack of optimal secretarial and other support. Another problem with many journals is the slowness of the review process. Editorial processing and peer review can take anywhere between a year to two years with some journals. Also, some journals do not keep the contributors informed about the progress of the review process. Due to the long review process, the articles can lose their relevance and topicality. A major benefit with JCDR is the timeliness and promptness of its response. In Dr Jain's e-mail which was sent to me in 2007, before the introduction of the Pre-publishing system, he had stated that he had received my submission and that he would get back to me within seven days and he did!
Most of the manuscripts are published within 3 to 4 months of their submission if they are found to be suitable after the review process. JCDR is published bimonthly and the accepted articles were usually published in the next issue. Recently, due to the increased volume of the submissions, the review process has become slower and it ?? Section can take from 4 to 6 months for the articles to be reviewed. The journal has an extensive author support system and it has recently introduced a paid expedited review process. The journal also mentions the average time for processing the manuscript under different submission systems - regular submission and expedited review.
Strengths of the journal: The journal has an online first facility in which the accepted manuscripts may be published on the website before being included in a regular issue of the journal. This cuts down the time between their acceptance and the publication. The journal is indexed in many databases, though not in PubMed. The editorial board should now take steps to index the journal in PubMed. The journal has a system of notifying readers through e-mail when a new issue is released. Also, the articles are available in both the HTML and the PDF formats. I especially like the new and colorful page format of the journal. Also, the access statistics of the articles are available. The prepublication and the manuscript tracking system are also helpful for the authors.
Areas for improvement: In certain cases, I felt that the peer review process of the manuscripts was not up to international standards and that it should be strengthened. Also, the number of manuscripts in an issue is high and it may be difficult for readers to go through all of them. The journal can consider tightening of the peer review process and increasing the quality standards for the acceptance of the manuscripts. I faced occasional problems with the online manuscript submission (Pre-publishing) system, which have to be addressed.
Overall, the publishing process with JCDR has been smooth, quick and relatively hassle free and I can recommend other authors to consider the journal as an outlet for their work."



Dr. P. Ravi Shankar
KIST Medical College, P.O. Box 14142, Kathmandu, Nepal.
E-mail: ravi.dr.shankar@gmail.com
On April 2011

Important Notice

Case report
Year : 2010 | Month : October | Volume : 4 | Issue : 5 | Page : 3233 - 3235

Persistent Hyperinsulinemic Hypoglycemia Of Infancy: A Case Report

BHAKHRI B K, ARYA S, DEBATA P K, CHELLANI H

Department of Pediatrics, VMMC and Safdarjung Hospital, New Delhi, New India.

Correspondence Address :
Dr Sugandha Arya
Specialist Pediatrician
Department of Pediatrics, VMMC and Safdarjung Hospital, New Delhi- 29
Phone: +919868102166
Email: sugandha_arya@hotmail.com

Abstract

Hypoglycaemia in newborns is usually a transient metabolic event. Hyperinsulinaemic hypoglycaemia is an important cause of nonketotic hypoglycaemia and it is characterized by macrosomia and hypoglycaemia with potential short and long term complications, if not properly managed with available medical and surgical options. We are presenting a neonate with this condition, who was managed in our unit and who underwent pancreactomy to control hypoglycaemia.

Keywords

Hypoglycaemia, Infant, insulin

Introduction
Hypoglycaemia in newborns is usually a transient metabolic event. It is considered to be persistent when >6-8 mg/kg/min of dextrose infusion is required for more than 7 days of life to keep the blood sugar level above 40-50 mg%(1). Various disorders at different steps of glucose metabolism can give rise to this condition. Hyperinsulinaemic hypoglycaemia is an important cause of nonketotic hypoglycaemia and it is characterized by macrosomia and hypoglycaemia with potential short and long term complications, if not properly managed with available medical and surgical options. We are presenting a neonate with this condition, who was managed in our unit and who underwent pancreactomy to control hypoglycaemia.

Case Report

This term neonate was male baby who was born to nondiabetic nonconsanguinously related parents, with one live issue and one first trimester spontaneous abortion. The baby was delivered by LSCS in view of the large size of the baby, with out any evidence of perinatal asphyxia. At birth, the baby was haemodynamically stable and had weight of 6.26 kgs (>97th centile), length of 62 cm (>97th centile) and a head circumference of 39 cm (>97th centile). There was no organomegaly, dysmorphism or gross malformation (Table/Fig 1).

The baby started having tachypnoea at 6 hrs of life, with documented hypoglycaemia while on entral feeds and was therefore started on parenteral dextrose therapy. Starting from glucose infusion rate (GIR) of 6 mg/kg/min and on regular blood sugar monitoring. His glucose requirement went on increasing for the first 2 weeks of life, reaching a maximum of upto 14 mg/kg/min (Table/Fig 2). He was intermittently symptomatic, including one episode of multifocal seizure at the time of documented hypoglycaemia.

His investigations revealed haemoglobin- 17 g%, PCV~ 50% and TLC- 9000/cmm. His serum electrolytes were normal, with normal renal functions. His serum calcium was 10.8 mg% and serum magnesium was 2 meq/l. His blood lactate was 1.2 mmol/l (normal range - 0.5-1.3 mmol/l). There were no reducing substances or ketones in the urine examination. His serum insulin was 64.6 µl/ml (normal<8 µl/ml) at the time of documented hypoglycaemia and his serum basal cortisol was 40.1 µgm/ml. Imaging did not reveal any focal lesion in pancrease. In the view of persistent hypoglycaemia in spite of a GIR of 14 mg/kg/min, he was started on hydrocortisone 10 mg/kg/24 hrs, but with no desirable effects on blood sugar levels over 24 hours. On administering octreotide (20g/kg/24 hrs), the blood sugar levels rose and remained above 40 mg%, allowing a reduction in GIR to 8 mg/kg/min. However, there were downward fluctuations in blood sugar levels again, thus requiring the GIR to be increased upto 10mg/kg/min. In view of the clinical course and laboratory findings, the patient was diagnosed as a case of persistent hyperinsulinaemic hypoglycaemia and was advised subtotal pancreatectmy, that he underwent during the third week of life. The diagnosis was confirmed by gross and histopathology (Table/Fig 3) with tiny nodules of abnormal  cells scattered throughout the pancrease. Supplemental insulin was given for the first 3 postoperative days; subsequently, the baby was euglycaemic on feeds. At 3 months of age, the baby was well on feeds and anthropometric measures, though above normal, were found to be approaching normalcy.

Discussion

Persistent hyperinsulinaemic hypoglycaemia of infancy (PHHI) is a major cause of persistent nonketotic hypoglycaemia in the neonatal period. The incidence of the disease ranges from 1 in 50,000 live births in sporadic cases to 1 in 2,500 live births(2) in certain communities with familial predisposition.

This genetic defect is identifiable in up to half of the patients and is a functional defect in the SUR1 and the Kir6.2 genes which are located on the 11p chromosome, resulting in insulin hypersecretion (3). On histopathological examination, the abnormal  cells were found to be present in the pancreas, either locally or in the diffuse form. Other rare disorders with hyperinsulinism are the Beckwith Wiedman syndrome and insulinoma.

About 2/3rd of the affected patients present in the neonatal period with relatively poor response to conservative therapy. The clinical features are in the form of macrosomia, jitteriness, seizures, coma and documented hypoglycaemia, requiring a dextrose infusion rate persistently above 10 mg/kg/min to maintain the blood sugar level at 40-50 mg%.

Investigations show that there were high insulin levels (>10 μg/dl with increased C- peptide secretion) during episode of documented hypoglycaemia. Plasma free fatty acids were decreased and there was an inappropriate (>40 mg %) glycaemic response to glucagon. The list of intermediary metabolites and hormones to be measured at the point of hypoglycaemia is given in (Table/Fig 4). Imaging has a negligible role in the diffuse disease. Apart from high parenteral dextrose infusion, other options in the therapeutic armamentarium (Table/Fig 5) are oral drugs – diazoxide, nifedipine, and chlorthiazide and parenteral drugs such as octreotide and glucagon, with responses varying from 30-60% in various studies (1). Surgical therapy i.e. total and subtotal pancreatectomy is indicated in those with focal disease in imaging, or in those with high dose dextrose infusion dependency, despite taking maximum doses of drugs available. Post operatively, euglycaemia is achieved in approximately 27% of the patients and IDDM is seen in 27% of the patients after a mean follow up of 11 years, the other concern being exocrine pancreatic deficiencies (4). Overall, about half of the patients develop long-term neurological morbidities with mental retardation in 44% of the patients and epilepsy in 25% of the patients and hence require a close follow up for physical and psychomotor development (5),(6).

(Table/Fig 4): Intermediary metabolites and hormones to be measured at the point of hypoglycemia

(Table/Fig 5): Drugs used in the medical management of hyperinsulinism.

References

1.
A Aynsley, K Hussain, J Hall, J M Saudubray. Practical management of hyperinsulinism in infancy. Arch Dis Child Fetal Neonatal Ed 2000;82: F98-F107.
2.
Ruth M Shepherd, Karen E Cosgrove, Rachel E O’Brian, Phillipa D Barnes. Hyperinsulinism of infancy : Towards an understanding of unregulated insulin release. Arch Dis Child Fetal Neonatal Ed 2000;82: F87-F97.
3.
C Sempoux, Yues Guiot, Karin Dahan, Pierre Moulin. The focal form of PHHI. Diabetes 2003; 52: 784-94.
4.
G Leibowitz, B Glaser, A A Higazi, M Salameh. PHHI in clinical remission: High incidence of beta cell dysfunction at long term follow up. J Clin Endo Metab 1995; 80(2): 386-391.
5.
T Meissner, U Wendel, Peter Burgard, S Schaetzle. Long term follow up of 114 patients with congenital hyperinsulinism. Eu J Endo 2003; 149: 43-51.
6.
F Menni, P Lonlay, C Sevin, G Touati. Neurologic outcomes of 90 neonates and infants with PHHI. Paediatrics 2001;107(3):476-79.

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