Background:Hypertension is the most prevalent non-communicable disease causing significant morbidity/mortality through cardiovascular, cerebrovascular, and renal complications.Objectives:This community-based study tested the efficacy of non-pharmacological interventions in preventing/controlling hypertension.Materials and Methods:This is a cross-over randomized controlled trial (RCT) of the earlier RCT (2007) of non-pharmacological interventions in hypertension, conducted in the urban service area of our Institute. The subjects, prehypertensive and hypertensive young adults (98 subjects: 25, 23, 25, 25 in four groups) were randomly allotted into a group that he/she had not belonged to in the earlier RCT: Control (New Group I), Physical Exercise (NG II)-brisk walking for 50 to 60 minutes, three to four days/week, Salt Intake Reduction (NG III) to at least half of their previous intake, Yoga (NG IV) for 30 to 45 minutes/day, five days/week. Blood pressure was measured before and after eight weeks of intervention. Analysis was by ANOVA with a Games-Howell post hoc test.Results:Ninety-four participants (25, 23, 21, 25) completed the study. All three intervention groups showed significant reduction in BP (SBP/DBP mmHg: 5.3/6.0 in NG II, 2.5/2.0 in NG III, and 2.3/2.4 in NG IV, respectively), while the Control Group showed no significant difference. Persistence of significant reduction in BP in the three intervention groups after cross-over confirmed the biological plausibility of these non-pharmacological interventions. This study reconfirmed that physical exercise was more effective than Salt Reduction or Yoga. Salt Reduction, and Yoga were equally effective.Conclusion:Physical exercise, salt intake reduction, and yoga are effective non-pharmacological methods for reducing blood pressure in young pre-hypertensive and hypertensive adults.
The determined objective values, after testing on diagnostic rectal biopsies, may serve to formulate a diagnostic algorithm along with immunostaining for diagnosis of HSCR in colorectal specimens.
Introduction: Inherited factor V deficiency / Owren's disease has varied clinical manifestations ranging from asymptomatic laboratory abnormalities to massive hemorrhage. The acquired form due to inhibitors following antibiotic therapy, infection, or surgery is less common, and spontaneous development of inhibitors is not known. Case Report: An 18-year-old boy presented with bleeding axillary and groin ulcers. At the age of 15, due to recurrent epistaxis and gum bleed, he was diagnosed with acquired factor V deficiency with positive inhibitor screen and treated with fresh frozen plasma (FFP) transfusion and temporary azathioprine. Coagulation workup at his current presentation also revealed acquired factor V deficiency with presence of inhibitors. The tests were repeated after 6 weeks of intermittent FFP transfusion, and the differences observed included negative inhibitor screen and complete correction on mixing studies, but factor V level was 2%. Discussion: Evidence of inhibitors at presentation favored acquired disease. However, younger age of onset, detection of inhibitors 1 year after first episode of self-regressing bleed, lack of identifiable triggers, and persistent bleeding with reduced factor levels after disappearance of inhibitors favored inherited factor V deficiency. Conclusion: In this case report, we have described an interesting case of severe inherited factor V deficiency with spontaneous appearance and disappearance of inhibitors exhibiting nonspecific factor inhibitory activity.
Calcium pyrophosphate dihydrate (CPPD) deposition disease is a metabolic arthropathy which results from deposition of calcium pyrophosphate crystals in and around joints especially the hyaline cartilage and disc material. This metabolic disease in uncommon in the smaller joints and multiple diagnostic modalities along with biochemical investigations would be necessary for definite diagnosis. We highlight the case of a 48 year old male who presented with a painful mass at the base of left thumb and was clinic-radiologically suspected as malignancy. Cytological examination (fine needle aspiration cytology [FNAC]) showed numerous extracellular rods shaped and rhomboid blunt-ended crystals along with foreign body type of giant cells. The main emphasis here is on the pivotal role played by FNAC in accurately diagnosing the disease where other modalities like radiology and histopathology failed to do so. The exact categorization of crystals is important from treatment point of view to avoid any major deformities in the joints/systemic manifestation.
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We present the case of a 29-year-old female arriving with an antalgic gait, who presented with complaints of generalized diffuse bone pain and walking difficulty for six months duration. She had no prior history of fall or trauma and her dietary milk intake was adequate. Her childhood was uneventful with normal developmental milestones. She was taking over-the-counter painkillers for the same.Biochemical paramaters showed serum calcium of 8.1 mg/dl (Normal Range (NR), 9-11), phosphate of 1.3 mg/dl (NR, 2.5-4.5), albumin of 4.5 g/dl (NR, 3.5-5.5), alkaline phosphatase of 528 IU/l (NR, 40-150), creatinine of 0.9 mg/dl (NR, 0.7-1.2), intact parathormone of 52.9 pg/ml (NR, 9-52) and 25-hydroxyvitamin D 22.91 ng/ml (NR, 30-100 ng/ml). Baseline investigations revealed hypophosphatemia along with mild hypocalcaemia and high normal parathormone levels. These findings, in addition to the Looser's zone seen on right fibular xeroradiography [Table/ Fig-1] pointed to the diagnosis of hypophosphatemic/phosphopenic osteomalacia. Her Tubular Reabsorption of Phosphate (TRP) was 73.4% (NR, 85-95%) and ratio of maximum rate of renal tubular reabsorption of phosphate to glomerular filtration rate (TmPO4/GFR) was 1.0 (NR, 2.7-4.4). Thus renal wasting of phosphate was confirmed by low TRP and TmPO4/ GFR. Absent urinary sugars and protein ruled out the possibility of renal Fanconi syndrome being the cause of phosphaturia. Her serum C-terminal FGF-23 level was 257 RU/ml (NR, 0-150). An elevated serum FGF-23 level confirmed its role in renal phosphate wasting in this case. Absence of similar complaints among her family members negated the possibility of the heritable forms of phosphopenic osteomalacia, namely Autosomal Recessive Hypophosphatemic Rickets (ARHPR), Autosomal Dominant Hypophosphatemic Rickets (ADHPR) and X-Linked Dominant Hypophosphatemic Rickets (XLHPR). Hence, the suspicion of a tumour producing FGF-23 arose, warranting extensive anatomical and functional radioimaging of the body in order to localise the offending lesion.Bone scan revealed multiple old healed fractures. Magnetic Resonance Imaging (MRI) thigh showed a well-defined T1 hypointense, T2 hyperintense lesion in the subcutaneous plane of left posterior thigh [Table/ Fig-2], which corresponded spatially with the octreotide receptor scintigraphy scan featuring increased uptake in the thigh lesion [Table/ Fig-3]. It was subcentimetric in size. Lesion was excised by ultrasonographic aid. Histopathological sections from the specimen revealed two tiny circumscribed unencapsulated spindle cell lesions separated by fibroadipose tissue and each measuring 0.7 cm in greatest dimension. The bland appearing streaming, spindle cells were arranged with vessels in a haemangiopericytomatous pattern, amidst which were foci of speckled grungy/blotchy calcification Keywords: Fibroblast growth factor-23, Phosphaturic mesenchymal tumour, Scintigraphy [table/ Fig-1]: Looser's zone seen on right fibular xeroradiography.[table/ Fig-2]: MRI thigh showed a well-defined T1 hypointense, T2 ...
The authors form a quiz around an uncommon nodal infection which can easily be diagnosed by the alert mind because of the negative images in the background and inside the foamy macrophages.
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