Disturbances in calcium metabolism and cardiomyocyte necrosis: the role of calcitropic hormones

A synchronized dyshomeostasis of extra- and intracellular Ca(2+), expressed as plasma ionized hypocalcemia and excessive intracellular Ca(2+) accumulation, respectively, represents a common pathophysiologic scenario that accompanies several diverse disorders. These include low-renin and salt-sensitive hypertension, primary aldosteronism and hyperparathyroidism, congestive heart failure, acute and chronic hyperadrenergic stressor states, high dietary Na(+), and low dietary Ca(2+) with hypovitaminosis D. Homeostatic responses are invoked to restore normal extracellular [Ca(2+)](o), including increased plasma levels of parathyroid hormone and 1,25(OH)(2)D(3). However, in cardiomyocytes these calcitropic hormones concurrently promote cytosolic free [Ca(2+)](i) and mitochondrial [Ca(2+)](m) overloading. The latter sets into motion organellar-based oxidative stress, in which the rate of reactive oxygen species generation overwhelms their detoxification by endogenous antioxidant defenses, including those related to intrinsically coupled increments in intracellular Zn(2+). In turn, the opening potential of the mitochondrial permeability transition pore increases, allowing for osmotic swelling and ensuing organellar degeneration. Collectively, these pathophysiologic events represent the major components to a mitochondriocentric signal-transducer-effector pathway to cardiomyocyte necrosis. From necrotic cells, there follows a spillage of intracellular contents, including troponins, and a subsequent wound healing response with reparative fibrosis or scarring. Taken together, the loss of terminally differentiated cardiomyocytes from this postmitotic organ and the ensuing replacement fibrosis each contribute to the adverse structural remodeling of myocardium and progressive nature of heart failure. In conclusion, hormone-induced ionized hypocalcemia and intracellular Ca(2+) overloading comprise a pathophysiologic cascade common to diverse disorders and that initiates a mitochondriocentric pathway to nonischemic cardiomyocyte necrosis.     

Pulsatile Scalp Swelling

Metastasis from follicular carcinoma is usually blood-borne. Here, we present a case of skull metastasis with intracranial extension presenting as a pulsatile scalp swelling from the follicular thyroid carcinoma.     

Risk factors for maternal mortality in Delhi slums: a community-based case-control study

BACKGROUND: In order to develop, implement and evaluate policy for reducing maternal mortality, it is essential to study the risk factors associated with maternal deaths. AIMS: The study aims to determine the epidemiological risk factors and its related causes associated with maternal deaths in Delhi slums. MATERIALS AND METHODS: A community-based case-control study was designed, wherein snowball-sampling method was used to identify the maternal deaths (cases) in the community and circular systematic random sampling procedure was used to select the controls from the same area where a maternal death was found. STATISTICAL ANALYSIS: Data on 70 cases and 384 controls that had live births as the outcome of the pregnancy were analyzed. Logistic regression was applied to identify the risk factors. RESULTS: In the study population, most of the deliveries were conducted at home by untrained 'dais.' Cases were mostly illiterate, young, having high parity and no antenatal care taken during pregnancy (P CONCLUSIONS: The study findings suggest that women should be educated about the importance of antenatal registration and regular checkups. Untrained 'dais' should be trained to recognize the obstetric complications at an early stage and refer high-risk cases for adequate management. These preventive measures could help in reducing maternal mortality at the community level.     

Disseminated nodular granulomatous perifolliculitis

Nodular granulomatous perifolliculitis is a well-recognized infection of the dermal and subcutaneous tissue caused by dermatophytes, which normally do not invade beyond the epidermis. We report here one such case that occurred in an immunosuppressed individual. The patient was a 35-year-old farmer who presented with small pruritic eruption that had initially appeared on the lower leg and then had gradually spread to hair-bearing areas of the body, finally producing nodular and pustular inflammatory lesions with exacerbations and remissions. Fungal examination by direct potassium hydroxide mount and culture revealed Trichophyton rubrum. Granulomatous changes were seen on histopathological examination. The patient completely responded to systemic antifungal therapy.