Adrenal incidentaloma does it require surgical treatment? Case report and review of literature

AbstractINTRODUCTIONAdrenal incidentalomas have a prevalence of at least 5% in the general population. Among these adrenal myelolipoma are rare nonfunctioning tumors of adrenal with an incidence of 0.1–0.2% as documented in CT and autopsy series. We report such a rare case of adrenal myelolipoma incidentally detected while evaluating a case of chronic nonspecific flank pain.PRESENTATION OF CASE38-year-old obese female patient, known hypertensive on treatment presented with nonspecific right flank pain since 1 year. Ultrasonography and Computed tomography of the abdomen showed right adrenal gland mass with fat density measuring 6.3cm×6.2cm×5cm. Patient underwent right side adrenalectomy, post operatively patient had an uneventful recovery. Histopathological examination of the specimen revealed features of adrenal myelolipoma.DISCUSSIONMyelolipoma is an uncommon, benign; tumor like lesion composed of mature adipose tissue admixed with hematopoietic cells. Most myelolipomas appear as unilateral adrenal masses. Adrenal myelolipomas are usually small and asymptomatic. CT or MRI detects the areas of gross fat with in the lesion. These tumors can present as acute abdomen following tumor hemorrhage which is more likely in myelolipomas greater than 4cm in size, hence warrants adrenalectomy.CONCLUSIONadrenal myelolipoma are rare benign tumors, incidentally detected on CT. CT or MRI is diagnostic. Large myelolipoma warrants surgery due to the risk of hemorrhage

The Biochemical and Cellular Basis for Nutraceutical Strategies to Attenuate Neurodegeneration in Parkinson’s Disease

Future therapeutic intervention that could effectively decelerate the rate of degeneration within the substantia nigra pars compacta (SNc) could add years of mobility and reduce morbidity associated with Parkinson’s disease (PD). Neurodegenerative decline associated with PD is distinguished by extensive damage to SNc dopaminergic (DAergic) neurons and decay of the striatal tract. While genetic mutations or environmental toxins can precipitate pathology, progressive degenerative succession involves a gradual decline in DA neurotransmission/synaptic uptake, impaired oxidative glucose consumption, a rise in striatal lactate and chronic inflammation. Nutraceuticals play a fundamental role in energy metabolism and signaling transduction pathways that control neurotransmission and inflammation. However, the use of nutritional supplements to slow the progression of PD has met with considerable challenge and has thus far proven unsuccessful. This review re-examines precipitating factors and insults involved in PD and how nutraceuticals can affect each of these biological targets. Discussed are disease dynamics (Sections 1 and 2) and natural substances, vitamins and minerals that could impact disease processes (Section 3). Topics include nutritional influences on α-synuclein aggregation, ubiquitin proteasome function, mTOR signaling/lysosomal-autophagy, energy failure, faulty catecholamine trafficking, DA oxidation, synthesis of toxic DA-quinones, o-semiquinones, benzothiazolines, hyperhomocyseinemia, methylation, inflammation and irreversible oxidation of neuromelanin. In summary, it is clear that future research will be required to consider the multi-faceted nature of this disease and re-examine how and why the use of nutritional multi-vitamin-mineral and plant-based combinations could be used to slow the progression of PD, if possible

Prophylactic crystalloids or prophylactic crystalloids with ephedrine: Comparison of hemodynamic effects during caesarean section under spinal anaesthesia using 0.5% bupivacaine

Background: Spinal anaesthesia is usually chosen for caesarean section not only because of its faster onset and reliability but also because general anaesthesia is associated with more complications. However, hypotension is one of the most common complications of spinal anaesthesia in obstetric patients. Several measures have been devised to prevent hypotension, which include left uterine displacement, infusion of crystalloids before giving spinal anaesthesia (preloading) and administration of a prophylactic vasopressor. This study compared the hemodynamic effects of preloading crystalloids or crystalloids with ephedrine for caesarean section under spinal anaesthesia using 0.5% bupivacaine. Materials and Method: In this randomized, single blind, comparative clinical study, 80 parturients (American Society of Anesthesiologists grade 1) presenting for elective caesarean section under spinal anaesthesia were allocated to one of the two groups; group I received crystalloid preload and group II received crystalloid with ephedrine before spinal block. After institution of spinal anaesthesia in the lateral position with 2.0 ml (10 mg) of bupivacaine, 0.5% (heavy) using 25 G Quincke type spinal needle, parturients were made to assume a supine position with left lateral tilt. Heart rate, systolic blood pressure and diastolic blood pressure were monitored intraoperatively every 2 minutes till delivery and every 5 minutes after delivery. The amount of ephedrine used intraoperatively was also noted and compared among different groups. Results: Incidence of hypotension was 70% in the crystalloid group and 5% in the crystalloid with ephedrine group. This difference between the two groups was statistically significant (P < 0.001). The number of patients receiving rescue bolus of ephedrine was higher in the crystalloid group (40% before delivery and 30% after delivery) compared to crystalloid with ephedrine group (5% before delivery and none after delivery); the difference was statistically significant (P < 0.001). Sixteen patients (40%) in the crystalloid group experienced nausea compared to 6 patients (15%) in the crystalloid with ephedrine group; the difference was statistically significant with a P value of 0.012. Conclusion: This study demonstrates that prophylactic ephedrine given by infusion along with crystalloids is not only a simple and effective method for prevention of hypotension during spinal anaesthesia during elective caesarean section in ASA Grade I patients but also contributes to less incidence of intraoperative nausea and vomiting

Schematic representation of PLA2G6 and location of mutations identified in present study.

<p>PLA2G6 consists of seven ankyrin repeats (diamond), a proline-rich motif (gridded box), a nucleotide binding motif (hexagon), a lipase motif (oval) and a binding site for calmodulin (circle). Numbers shown below are the amino acid positions. Five novel mutations are shown in bold.</p

Muscle nerve pathology of affected individual II-1 from family 7.

<p>(A) Muscle biopsy reveals marked axonal distension of intramuscular nerve twig (arrow), using Masson's trichrome staining. (B) The intraaxonal contents in the distended axon contain NADH-TR (arrow). (C) Phosphorylated neurofilament staining (arrow). (D) Ubiquitin staining (arrow). Magnifications: (A) 200X; (B) 200X; (C) 400X; and, (D) 200X.</p

Genetic Analysis of <i>PLA2G6</i> in 22 Indian Families with Infantile Neuroaxonal Dystrophy, Atypical Late-Onset Neuroaxonal Dystrophy and Dystonia Parkinsonism Complex

<div><p>Mutations in <i>PLA2G6</i> were identified in patients with a spectrum of neurodegenerative conditions, such as infantile neuroaxonal dystrophy (INAD), atypical late-onset neuroaxonal dystrophy (ANAD) and dystonia parkinsonism complex (DPC). However, there is no report on the genetic analysis of families with members affected with INAD, ANAD and DPC from India. Therefore, the main aim of this study was to perform genetic analysis of 22 Indian families with INAD, ANAD and DPC. DNA sequence analysis of the entire coding region of <i>PLA2G6</i> identified 13 different mutations, including five novel ones (p.Leu224Pro, p.Asp283Asn, p.Arg329Cys, p.Leu491Phe, and p.Arg649His), in 12/22 (54.55%) families with INAD and ANAD. Interestingly, one patient with INAD was homozygous for two different mutations, p.Leu491Phe and p.Ala516Val, and thus harboured four mutant alleles. With these mutations, the total number of mutations in this gene reaches 129. The absence of mutations in 10/22 (45.45%) families suggests that the mutations could be in deep intronic or promoter regions of this gene or these families could have mutations in a yet to be identified gene. The present study increases the mutation landscape of <i>PLA2G6</i>. The present finding will be useful for genetic diagnosis, carrier detection and genetic counselling to families included in this study and other families with similar disease condition.</p></div

Clinical features of the affected individuals from 22 Indian families with INAD, ANAD and DPC.

<p>Clinical features of the affected individuals from 22 Indian families with INAD, ANAD and DPC.</p