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1.  Expanded dengue syndrome: subacute thyroiditis and intracerebral hemorrhage 
BMC Infectious Diseases  2012;12:240.
Background
Although most symptomatic dengue infections follow an uncomplicated course, complications and unusual manifestations are increasingly being reported due to rising disease burden. Expanded dengue syndrome is a new entity added into World Health Organization (WHO) classification system to incorporate this wide spectrum of unusual manifestations. We report a case of expanded dengue syndrome with subacute thyroiditis and intracerebral hemorrhage. This is the first case report of thyroiditis in dengue infection.
Case presentation
A 20 years old man presented with fever, myalgias, arthralgias, retro-orbital pain, vomiting and gum bleeding during a large dengue outbreak in Lahore, Pakistan. On 7th day of illness patient became afebrile, but he developed severe headaches, unconsciousness followed by altered behavior. On 9th day of illness patient developed painful neck swelling accompanied by fever, tremors, palpitations, hoarseness of voice and odynophagia. Examination revealed acutely swollen, tender thyroid gland along with features of hyperthyroidism. Laboratory evaluation revealed stable hematocrit, thrombocytopenia and leukopenia. Patient had seroconverted for anti-dengue IgM antibodies on the 10th day of illness. A non-contrast Computed Tomogram (CT) of the brain showed right frontal lobe hematoma. Thyroid profile showed increased free T3 and T4 and low TSH. Technetium thyroid scan showed reduced tracer uptake. He was diagnosed as having subacute thyroiditis and treated with oral prednisolone and propranolol. Follow up CT brain showed resolving hematoma. Patient’s recovery was uneventful.
Conclusion
Subacute thyroiditis may develop during the course of dengue fever and should be included as a manifestation of expanded dengue syndrome. It should be suspected in patients with dengue fever who develop painful thyroid swelling and clinical features of hyperthyroidism.
doi:10.1186/1471-2334-12-240
PMCID: PMC3482561  PMID: 23033818
Dengue fever; Expanded dengue syndrome; Thyroiditis; Intracerebral Hemorrhage
2.  Gitelman syndrome manifesting in early childhood and leading to delayed puberty: a case report 
Introduction
Gitelman syndrome is an inherited autosomal recessive renal salt-wasting disorder. It presents with variable clinical symptoms including muscle weakness and fatigue, and the diagnosis is based on metabolic alkalosis, hypokalemia, hypomagnesemia and hypocalciuria. It is usually diagnosed incidentally in early adulthood. There are rare cases of Gitelman syndrome presenting in early childhood; however, to the best of our knowledge it has not previously been associated with delayed puberty.
Case presentation
A 17-year-old South Asian man with recurrent episodes of generalized muscle weakness, fatigue and cramps from the age of two years was admitted for further workup. Before the age of 12 years, the episodes had been mild, but they then got progressively worse. Other symptoms include polyuria, polydipsia, nocturia, paresthesia and occasional watery diarrhea. He also had a history of short stature, poor weight gain and delayed developmental landmarks. His family history was unremarkable except for the consanguineous marriage of his parents. An examination revealed a thin and lean man with blood pressure of 95/60mmHg. His height and weight were below the third percentile and his sexual development was at Tanner Stage II. Laboratory work revealed serum sodium of 124mmol/L, potassium 2.4mmol/L, calcium 6.5mmol/L and magnesium of 1.2mg/dL. His testosterone level was low (0.85ng/mL, normal for his age 2.67 to 10.12ng/mL) with normal levels of luteinizing hormone and follicle-stimulating hormone. The sex hormone findings were attributed to delayed puberty. A 24-hour urinary analysis revealed decreased excretion of calcium (25.9mg/24 hours). Based on the findings of hypokalemic metabolic alkalosis without hypertension, severe hypomagnesemia and hypocalciuria, a diagnosis of Gitelman syndrome was made. Treatment was started with oral supplementation of potassium, magnesium and calcium along with spironolactone and liberal salt intake.
Conclusion
Diagnosis of Gitelman syndrome is usually made incidentally during adolescence or early adulthood based on clinical and biochemical findings. We report that Gitelman syndrome can present during the early childhood years. If undiagnosed and untreated, it can lead to growth retardation and delayed puberty.
doi:10.1186/1752-1947-6-331
PMCID: PMC3470992  PMID: 23031616
4.  Gestational diabetes mellitus is rare in primigravida Pakistani women 
Background:
Gestational diabetes mellitus is a metabolic disorder defined as glucose intolerance with onset or first recognition during pregnancy. Similar to other members of the Asian race, Pakistani women are also considered to be at a high risk for developing gestational diabetes.
Materials and Methods:
In order to better understand whether this heightened risk attributed to race really exists, we conducted a prospective study to assess the glycemic status of primigravida women presenting to our hospital.
Results:
The mean age of 135 subjects enrolled was 22 (16-31), with 21 (16%), 60 (44%), and 54 (40%) subjects in the first, second, and third trimesters of pregnancy, respectively. The mean fasting, 1-hour, and 2-hour plasma glucose levels were 69.9 mg/dL (3.9 mmol/L), 129 mg/dL (7.2 mmol/L), and 103.6 mg/dL (5.76 mmol/L), respectively. Of 135 women, 6 had a blood pressure reading ≥140/90 mm Hg and only one met the criteria for gestational diabetes mellitus. In our study, despite using the newly proposed International Association of Diabetes and Pregnancy Study (IADPS) cut-offs for diagnosis of gestational diabetes, the incidence rate of gestational diabetes mellitus in primigravida was still <1%.
Conclusion:
Larger trials are needed to truly assess the disease burden of gestational diabetes mellitus in Pakistani women.
doi:10.4103/2230-8210.83404
PMCID: PMC3156539  PMID: 21897896
Gestational diabetes mellitus; hyperglycemia; International Association of Diabetes and Pregnancy Study Groups; The Hyperglycemia and Adverse Pregnancy Outcome study
5.  Beta-blockers have a Beneficial Effect upon Endothelial Function and Microalbuminuria in African-American Subjects with Diabetes and Hypertension 
Background
Type-2 Diabetes Mellitus(T2DM) with microalbuminuria(MA) is associated with increased risk of cardiovascular events(CVE) that may be attenuated by Angiotensin-Converting-Enzyme Inhibitors(ACEIs), unless microalbuminuria persists(PMA). African-Americans(AA) have a higher prevalence of nephropathy with suboptimal response to ACEIs. We studied the effects of beta-blockers addition and comparative effects of carvedilol with metoprolol on 24-hour urinary-albumin excretion(UAE) and endothelial function(EF) in AA with PMA.
Methods
Thirty-four AA 30–70 years age with T2DM and PMA despite ACEI therapy were randomized to receive carvedilol or metoprolol in addition to ACEI and any other concurrent therapy. Carvedilol/metoprolol dose was titrated to achieve blood pressure(BP)<130/80mmHg. UAE and brachial-artery reactivity were studied at baseline and 12-weeks. We analyzed the effects of addition of beta-blockers and whether there was any difference in response between the two beta-blockers.
Results
Thirty-three subjects completed the study; BP decreased to <135/80mmHg. After 12-weeks, beta-blocker treatment resulted in significant increase in flow-mediated dilatation(FMD) from 3.5±1% to 8.5±1%(p=0.004) and significant reduction in mean log-transformed UAE from 2.655gm/gm Cr±0.087 to 2.533gm/gm Cr±0.093(p=0.028). FMD increased by 240%(p=0.033) with carvedilol and by 110%(p=0.096;NS) with metoprolol. UAE decreased with carvedilol by 0.35gm/gm Cr(p=0.023) and with metoprolol by 0.23gm/gm Cr(p=0.298;NS).
Conclusion
Our results clearly indicate that addition of beta-blockers to ACEI improves EF and reduces UAE in high risk AA T2DM patients with PMA. Carvedilol but not metoprolol improves EF and reduces UAE in AA with identical BP control. Larger trials are needed to further elucidate the differential effects of carvedilol/metoprolol on EF and UAE and its impact on CVE in such patients.
doi:10.1016/j.jdiacomp.2007.05.003
PMCID: PMC2590589  PMID: 18413195
Type 2 Diabetes Mellitus; Beta-Blockers; African American; Endothelial Function; Microalbuminuria

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