Parel, India
Parel, India

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News Article | December 15, 2016

Last year I was visiting a rural hospital in Chhattisgarh, one of the poorest and hungriest states in India. The patients waiting in the corridors were thin and bony, with dangerously low blood counts and anemia. So I was shocked when I watched the doctors at Jan Swasthya Sahyog clinic treat patient after patient for diabetes and heart disease. The public perception of type II diabetes is that it's a disease of excess—the result of too much sugar in our diets and a sedentary lifestyle. But a documentary by executive producer Elliot Kirschner, director Adam Bolt, producer Jessica Harrop, and editor Regina Sobel, published here on Motherboard, builds on the idea that this is only one part of the picture when dealing with a misunderstood disease. Diabetes can burden people without enough food and nutrients, just as it does those who eat too much. In India, where people's average weight and body mass index (BMI) is far lower than in the US, 62 million adults have diabetes, the largest diabetic population in the world. I remember watching pregnant women stand on weighing scales as the doctors went on village visits—many were just 75 pounds while seven months pregnant. Even so, experts have been attributing the uptick in diabetes to the sudden economic growth in the country—and the lifestyle and diet changes that followed. More junk food on the shelves, more access to carbohydrates and sugar, they thought, might be the culprit. But that couldn't account for the largely poor population in rural areas. Dr. Yajnik, a researcher and physician at Pune's KEM Hospital Research Center, has been focused on this mystery for decades. He and his team conducted a longitudinal study in villages outside of Pune, where families still rely on farming as their main livelihood. His team tracked pregnant mothers and how their nutrition impacted their children—mothers who would spend their days plowing the land or weeding until just days before their delivery. He found that the lack of one particular vitamin—B12—led to babies growing up with more visceral fat, despite their low weight in both their childhood and adult life. This then correlated to insulin resistance, the body's inability to properly break down sugar, and a precursor to diabetes. "Chemicals like vitamin B12 can influence the genetic structure. The code remains the same but changes the way the gene expresses itself," Yajnik said. This finding aligns with the concept of epigenetics—the idea that the environment can influence genes. It's a big shift in our genetic thought, but it has been tested before, most famously on the agouti mice named after the agouti gene, according to one such study from Duke University. In a series of experiments, identical mice were exposed to different chemicals like BPA, found in plastics, and various diets. When the mother mouse was fed a methylated diet with nutrients like vitamin B12 and folate, her babies had a lower disease risk and a brown coat. When she was fed a diet deficient in these nutrients, the mice were more susceptible to disease and had a yellow coat. While most of the medical community treats type II diabetes as something to be prevented through exercise and healthy food, the rapid rate of the disease in developing countries calls for a more thorough approach and an understanding of epigenetics. Doctors can no longer focus on body weight as a measure of disease risk. And researchers will have to continue to probe how nutrition and the environment, starting in a mother's womb, can influence a child's genetic expression. "This was non-communicable disease, but now we're saying they can be communicated from mother to children," Yajnik said.

OBJECT: Understanding that atlantoaxial instability is the cause of Chiari malformation (CM), the author treated 65 patients using atlantoaxial stabilization. The results are analyzed. METHODS: Cases of CM treated using atlantoaxial fixation during the period from January 2010 to November 2013 were reviewed and analyzed. Surgery was aimed at segmental arthrodesis. RESULTS: The author treated 65 patients with CM in the defined study period. Fifty-five patients had associated syringomyelia. Forty-six patients had associated basilar invagination. Thirty-seven patients had both basilar invagination and syringomyelia. Three patients had been treated earlier using foramen magnum decompression and duraplasty. According to the extent of their functional capabilities, patients were divided into 5 clinical grades. On the basis of the type of facetal alignment and atlantoaxial instability, the patients were divided into 3 groups. Type I dislocation (17 patients) was anterior atlantoaxial instability wherein the facet of the atlas was dislocated anterior to the facet of the axis. Type II dislocation (31 patients) was posterior atlantoaxial instability wherein the facet of the atlas was dislocated posterior to the facet of the axis. Type III dislocation (17 patients) was the absence of demonstrable facetal malalignment and was labeled as "central" atlantoaxial dislocation. In 18 patients, dynamic images showed vertical, mobile and at-least partially reducible atlantoaxial dislocation. All patients were treated with atlantoaxial plate and screw fixation using techniques described in 1994 and 2004. Foramen magnum decompression or syrinx manipulation was not performed in any patient. Occipital bone and subaxial spinal elements were not included in the fixation construct. One patient died, and death occurred in the immediate postoperative phase and was related to a vertebral artery injury incurred during the operation. One patient had persistent symptoms. In the rest of the patients there was gratifying clinical improvement. More remarkably, in 7 patients, the symptoms of lower cranial nerve paresis improved. No patient worsened in their neurological function after surgery. Reductions in the size of the syrinx and regression of the CM were observed in 6 of 11 cases in which postoperative MRI was possible. During the follow-up period, there was no delayed worsening of neurological function or symptoms in any patient. Sixty-three patients improved after surgery, and the improvement was sustained during the average follow-up period of 18 months. CONCLUSIONS: On the basis of outcomes in this study, it appears that the pathogenesis of CM with or without associated basilar invagination and/or syringomyelia is primarily related to atlantoaxial instability. The data suggest that the surgical treatment in these cases should be directed toward atlantoaxial stabilization and segmental arthrodesis. Except in cases in which there is assimilation of the atlas, inclusion of the occipital bone is neither indicated nor provides optimum stability. Foramen magnum decompression is not necessary and may be counter-effective in the long run. ©AANS, 2015.

Chaudhari S.,KEM Hospital
Indian Pediatrics | Year: 2011

There has been a marked increase in the survival of extremely low birth weight (ELBW) infants, but these babies have a long stay in the NICU. Strategies to decrease their neurodevelopmental impairment become very important. The maximum development of the brain occurs between 29-41 weeks. From the warm, dark, acquatic econiche, where the baby hears pleasant sounds like the mother's heart beat, the baby suddenly finds itself in the dry, cold, excessively bright, noisy, environment of the NICU. Noise, bright light, painful procedures, and ill-timed caregiving activities, adversely affect the infant's development. Excessive radiation from X-rays of babies on the ventilator and CT scans also affect the brain. Medications like steroids for chronic lung disease also cause damage to the brain. Aminoglycides and frusemide are known to cause hearing impairment. Hence a developmentally supportive, humanized care will go a long way in enhancing the developmental outcome of these babies.

Shetty S.,KEM Hospital | Ghosh K.,KEM Hospital
Thrombosis Research | Year: 2011

Budd chiari syndrome (BCS) is characterized by venous outflow obstruction either at hepatic veins or inferior vena cava, while portal vein thrombosis (PVT) is the consequence of thrombotic occlusion in the extrahepatic venous system. The aetiology of both these disorders is complicated wherein genetic, acquired and local factors interact in the pathogenesis. Among the inherited thrombophilia, factor V Leiden mutation has shown stronger association with BCS than PVT while the converse is true for prothrombin G20210A mutation. Very few studies are available on the role of fibrinolytic potential or the single nucleotide polymorphisms (SNPs) of fibrinolysis proteins, in both BCS and PVT. Among the acquired thrombophilia, myeloproliferative disorders (MPD) are the most frequent cause, while antiphospholipid antibodies (APA) and hyperhomocysteinemia have not shown very strong association with BCS and PVT. Oral contraceptives, infection, chronic inflammatory diseases like Behcets syndrome, inflammatory bowel disease, tumors, paroxysmal nocturnal hemoglobinuria (PNH), pregnancy, puerperium, poor nutrition are some of the other acquired and local risk factors associated with both these disorders. There exists a clear geographical variation both in the clinical manifestation and the underlying aetiology. Almost all the studies have proved that a multifactorial aetiology is the requisite for the manifestation. Evaluation of an extensive thrombophilia profile is essential for optimal management of patients which is further justified with the availability of specific treatment options for at least some thrombophilia markers. © 2010 Elsevier Ltd. All rights reserved.

Inherited macrothrombocytopenia is one of the subgroup of inherited thrombocytopenias with variable bleeding tendencies presenting with low platelet count and giant platelets and different gene mutations are involved in its molecular pathophysiology and affect various cell functions. Herein, we describe a family with an isolated giant platelet disorder with variable bleeding diathesis with autosomal mode of inheritance. Copyright © 2016 YEAR Wolters Kluwer Health, Inc. All rights reserved.

Shetty S.,KEM Hospital | Ghosh K.,KEM Hospital
Haemophilia | Year: 2015

Summary: The major therapy for haemophilia is plasma derived or recombinant clotting factors which are evolving steadily to increase potency, stability and half-life. Research in the area of haemophilia therapeutics, however, is not restricted only to modifications in the recombinant products, but alternate therapeutic strategies are being developed which are in different phases of experimental and clinical trials. This chapter reviews the diverse molecular innovations which are being developed for alternate therapeutic approaches in haemophilia. The data is mainly extracted from the literature and the Conference abstracts. Some of the novel therapeutic approaches include inhibition of anticoagulant pathway factors (activated protein C, antithrombin, tissue factor pathway inhibitor) by monoclonal antibodies, peptide inhibitors, DNA or RNA aptamers, use of variant coagulation factors (factor Xa, factor Va) which are more resistant to inactivation or enzymatically more active and antibody-mediated therapy including a humanized anti-factor IXa/X bispecific antibody mimicking factor VIII. Other approaches include nonsense mutation suppression, induction of prothrombotic microparticles by P-selectin-immunoglobulin chimeras, suppression of fibrinolytic potential either by antifibrinolytics or by the use of mutant molecules of fibrinolytic inhibitors. Few products are proposed as 'stand alone' treatment for haemophilia, while a few can be used as adjuvant therapies to recombinant factors with an aim to reduce the amount of factor intake. All efforts are underway to produce an alternate, novel drug for haemophilia which will have an increased half-life, subcutaneously injectable, non-immunogenic and effective both in the presence and absence of inhibitors. © 2014 John Wiley & Sons Ltd.

Goel A.,Kem Hospital | Shah A.,Kem Hospital
Journal of Neurosurgery: Spine | Year: 2011

The authors report their experience with 14 children in whom acute torticollis or a fixed flexion neck deformity developed. Other than neck deformity, there was no other significant functional or neurological symptom. Although several possible pathogenetic factors have been speculated, the exact cause remains unknown. Conservative observation and/or attempts at closed reduction failed to effect deformity resolution. Investigations revealed "locking" of facets that resulted in rotatory or translatory atlantoaxial dislocation depending on the nature of facet dislocation. The management issues in such cases are evaluated. The authors discuss the validity of atlantoaxial facet distraction and manipulation/reduction and fixation under direct visualization. In all cases recovery from neck deformity was significant immediately after surgery. The deformity resolution was sustained during a mean follow-up period of 23 months (range 3-52 months), although the range of neck movements remained marginally restricted. The craniovertebral realignment is demonstrated by images and clinical photographs.

The authors discuss their successful preliminary experience with 36 cases of cervical spondylotic disease by performing facetal distraction using specially designed Goel cervical facet spacers. The clinical and radiological results of treatment are analyzed. The mechanism of action of the proposed spacers and the rationale for their use are evaluated. Between 2006 and February 2010, 36 patients were treated using the proposed technique. Of these patients, 18 had multilevel and 18 had single-level cervical spondylotic radiculopathy and/or myelopathy. The average follow-up period was 17 months with a minimum of 6 months. The Japanese Orthopaedic Association classification system, visual analog scale (neck pain and radiculopathy), and Odom criteria were used to monitor the clinical status of the patient. The patients were prospectively analyzed. The technique of surgery involved wide opening of the facet joints, denuding of articular cartilage, distraction of facets, and forced impaction of Goel cervical facet spacers into the articular cavity. Additionally, the interspinous process ligaments were resected, and corticocancellous bone graft from the iliac crest was placed and was stabilized over the adjoining laminae and facets after adequately preparing the host bone. Eighteen patients underwent single-level, 6 patients underwent 2-level, and 12 patients underwent 3-level treatment. The alterations in the physical architecture of spine and canal dimensions were evaluated before and after the placement of intrafacet joint spacers and after at least 6 months of follow-up. All patients had varying degrees of relief from symptoms of pain, radiculopathy, and myelopathy. Analysis of radiological features suggested that the distraction of facets with the spacers resulted in an increase in the intervertebral foraminal dimension (mean 2.2 mm), an increase in the height of the intervertebral disc space (range 0.4-1.2 mm), and an increase in the interspinous distance (mean 2.2 mm). The circumferential distraction resulted in reduction in the buckling of the posterior longitudinal ligament and ligamentum flavum. The procedure ultimately resulted in segmental bone fusion. No patient worsened after treatment. There was no noticeable implant malfunction. During the follow-up period, all patients had evidence of segmental bone fusion. No patient underwent reexploration or further surgery of the neck. Distraction of the facets of the cervical vertebra can lead to remarkable and immediate stabilization-fixation of the spinal segment and increase in space for the spinal cord and roots. The procedure results in reversal of several pathological events related to spondylotic disease. The safe, firm, and secure stabilization at the fulcrum of cervical spinal movements provided a ground for segmental spinal arthrodesis. The immediate postoperative improvement and lasting recovery from symptoms suggest the validity of the procedure.

Aim: Quantitative anatomy of the facets of the sub-axial cervical spine was performed. The purpose of the evaluation was to determine the feasibility of insertion of Goel inter-facetal articular spacers in the sub-axial cervical spine. Only few studies detailing the morphometry of the facets are available in the literature. Materials and Methods: Ten cervical vertebrae from C3 to C7 with a total of 20 facets were evaluated by the author. The anatomic parameters studied were the height, width, thickness, shape, orientation, and inclination of each of the superior and inferior facets. The alterations in a number of intervertebral segmental distances were measured before and after spacer insertion. The distance of the inferior facet from the foramen tranversarium, spinal canal, and neural foramina was measured to assess safety of spacer insertion with respect to the vertebral artery and neural structures. Results: The height, width and thickness of the superior facets from C3 to C7 ranged from 6 to 12 mm, 8 to 12 mm, and 2.5 to 6 mm, respectively. The inferior facets had an average height of 10.5 mm, average width of 11.2 mm and average thickness of 3.5 mm. The inclination of the superior facets with respect to the transverse plane ranged from 22° to 45° and that of the inferior facets ranged from 29° to 53°. The distance of the anterior margin of the inferior facet from the posterior border of the foramen transversium ranged from 5 to 7 mm. This distance was maximum at C3 level, then decreased at C4 and remained constant from C5 to C7. Conclusion: This anatomic evaluation aided in understanding the morphology of the cervical facets and the suitability of the cervical facetal articular cavity for insertion of spacers.

Rajadhyaksha A.,KEM Hospital | Mehra S.,KEM Hospital
Lupus | Year: 2012

Dengue viremia may be the trigger for immune complex formation in patients who are predisposed to developing autoimmune disease. We report a rare case of dengue virus infection evolving into systemic lupus erythematosus (SLE) and lupus nephritis. To the best of our knowledge this is the first case of dengue fever evolving into lupus nephritis.A 22 year old female presented with having had high grade fever, skin rash, breathlessness, retro-orbital pain, abdominal pain, arthralgias and myalgias for 10 days. She tested positive for dengue immunoglobulin M (IgM). She was given supportive treatment and was subsequently discharged. Four weeks later she developed recurrent fever, arthralgia, rash and anasarca. She was suspected as having SLE with active lupus nephritis. Antinuclear antibody (ANA), and anti double stranded deoxyribonucleic acid (anti dsDNA) titers were positive and complements were low. Renal biopsy showed diffuse proliferative glomerulonephritis grade IV. She was treated with steroids and immunosuppressants to which she responded. Dengue viremia incites antibody production, which if excessive causes deposition of viral antigen-antibody immune complexes. This could possibly lead to renal tubular damage and glomerulonephritis in susceptible individuals. Dengue fever leading to development of glomerulonephritis is rarely seen. Our patient developed dengue fever and after a month presented with manifestations of SLE and lupus nephritis. Both dengue fever and SLE have common manifestations of fever, arthralgia, rash, leucopenia with thrombocytopenia and serositis. Bacterial and viral infections may act as a 'trigger' for starting or relapsing lupus activity in genetically predetermined individuals. In our case it may be possible that dengue virus could have triggered a dysfunctional immune response, resulting in the developing of autoimmunity and SLE with lupus nephritis. © The Author(s), 2012. Reprints and permissions.

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