Extension of P1 is very inefficient with this 6-month regimen. Operational research should define appropriate algorithms allowing an earlier switch to the next higher regimen for those in need, using follow-up smears for screening.
No abstract
A 61-year-old female with past medical history of depression, hypoparathyroidism (hypoPtH), and hypothyroidism had disappeared from her home and was found wandering a few hours away with persecutory delusions, visual and auditory hallucinations. Serum calcium (Ca) was 6.3 mg/dL (range 8.6–10.2), albumin 3.7 g/dL (range 3.5–5.2) and ionized Ca 0.89 mmol/L (range 1.12–1.30). She was admitted and treated with Ca and calcitriol. Work-up for altered mental status was negative except for hypocalcemia (hypoCa) and scattered bilateral basal ganglia calcifications (BGC) with cortical and subcortical frontal lobe calcifications on CT. Psychiatry diagnosed delirium due to hypoCa. Acute psychosis resolved once Ca levels improved. Diagnosis of idiopathic hypoPtH was in 1997. Her regimen included Ca citrate 1500mg daily and 10 mcg of Forteo twice daily. She had skipped her medications for at least 2 days prior to presentation. Her medical records revealed that she was seen for severe depression, progressive gait abnormalities, slowed movements, and imbalance, in 2015. CT scan and MRI brain showed BGC. Her son gave a history of multiple admissions for psychosis, violence, delusions with agitation, and wandering at times when the patient was hypoCa, which was diagnosed as schizophrenia. Neuropsychiatric disturbances are commonly associated with hypercalcemia. Review of literature found a few case reports of psychosis and hypoPtH 1,2 BGC is common in hypoPtH. Psychotic symptoms due to BGC include auditory hallucinations, delusions of influence, paranoid states, and complex perceptual distortions.3,5 HypoCa is associated with cognitive impairment. Neurological manifestations tend to improve with Ca correction, but psychiatric symptoms do not improve substantially.4,5 Further studies are needed in hypoPtH with BGC to appropriately diagnose organic psychosis. This is important in management of the vicious cycle of psychiatric illness leading to noncompliance resulting in psychosis. Prevention of BGC will play a key role. References: 1. Finan M, Axelband J. This is your brain on calcium: psychosis as the presentation of isolated hypoparathyroidism. Am J Emerg Med. 2014;32:945.e1-4. 2. Ang AW, Ko SM, Tan CH. Calcium, magnesium, and psychotic symptoms in a girl with idiopathic hypoparathyroidism. Psychosom Med. 1995;57:299–302. 3. Burns K, Brodaty H. Fahr’s disease and psychosis. In: Sachdev PS, Keshavan MS, editors. Secondary schizophrenia. Cambridge: Cambridge University; 2010. p. 358–66. 4. Maiti A, Chatterjee S. Neuropsychiatric manifestations and their outcomes in chronic hypocalcaemia. J Indian Med Assoc. 2013;111:174–7. 5. Amara A, Novais C, Coelho M, Silva A, Curral R, Brandao I, Torres A. Organic psychosis due to hypoparathyroidism in an older adult: a case report. Braz. J. Psychiatry; 2016; 38(4)
Context:Microalbuminuria is a known indicator of atherosclerosis and its association with ischemic heart disease (IHD) has been extensively studied in the diabetic population. The significance of urine microalbumin in non-diabetics, however, is yet to be elucidated.Aim:To determine whether an independent association exists between microalbuminuria and IHD in non-diabetic Asian-Indians, and the level of microalbuminuria predictive of concomitant IHD.Materials and Methods:A cross-sectional case-control study was conducted between July 2009 and June 2011. Non-diabetic patients undergoing evaluation for IHD were divided into cases and controls, based on the presence or absence of IHD, respectively. Fifty cases and 50 controls were included, and matched by age, sex, smoking habit, hypertension and body-mass index (BMI). Fasting blood glucose (FBG), fasting lipid profile, and urine microalbumin were recorded for all patients.Results:Mean fasting glucose, mean low density lipoprotein (LDL)-cholesterol and mean urine microalbumin were all significantly higher in cases compared to controls. Urine microalbumin was independently associated with IHD, and microalbumin greater than 12.6 mg/g was predictive of IHD (OR: 13.5; 95% CI, 4.6–39.9; P < 0.001).Conclusion:Urine microalbumin is independently associated with IHD in non-diabetics and levels greater than 12.6 mg/g are predictive of IHD.
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