This not only mandated the WHO to prioritize strengthening the surgical and anesthesia care globally, but also led to governments of the member states recognizing the urgent need for increasing capacity in surgery and anesthesia. Additionally, the third edition of Disease Control Priorities (DCP3), published in 2015 by the World Bank, declared surgery as essential and featured an entire volume dedicated to building surgical capacity.Data from WHO and the World Bank indicate that scaling up infrastructure to enable access to surgical care in regions where it is currently limited or is non-existent is a low-cost measure relative to the significant morbidity and mortality caused by lack of surgical treatment. In fact, a systematic review found that the cost-effectiveness ratio – dollars spent per DALYs averted – for surgical interventions is on par or exceeds those of major public health interventions such as oral rehydration therapy, breastfeeding promotion, and even HIV/AIDS antiretroviral therapy. This finding challenged the common misconception that surgical care is financially prohibitive endeavor not worth pursuing in LMICs. A key policy framework that arose from this renewed global commitment towards surgical care worldwide is the National Surgical Obstetric and Anesthesia Plan (NSOAP). NSOAP focuses on policy-to-action capacity building for surgical care with tangible steps as follows: (1) analysis of baseline indicators, (2) partnership with local champions, (3) broad stakeholder engagement, (4) consensus building and synthesis of ideas, (5) language refinement, (6) costing, (7) dissemination, and (8) implementation.
Molybdenum deficiency refers to the clinical consequences of inadequate supplies of molybdenum in the diet. The amount of molybdenum required is relatively small, and molybdenum deficiency usually does not occur in natural settings. However, it can occur in individuals receiving parenteral nutrition. Signs and symptoms
Descriptions of human molybdenum deficiency are few. A patient receiving prolonged parenteral nutrition acquired a syndrome described as ‘acquired molybdenum deficiency.’ This syndrome, exacerbated by methionine administration, was characterized by high blood methionine, low blood uric acid, and low urinary uric acid and sulfate concentrations. The patient suffered mental disturbances that progressed to a coma. Pathological changes occurring in individuals with a genetic disease that results in a sulfite oxidase (a molybdoenzyme) deficiency include increased plasma and urine sulfite, sulfate, thiosulfate, S-sulfocysteine and taurine; seizures, and brain atrophy/lesions; dislocated lenses; and death at an early age.. Diagnosis
Treatment
300 mcg Ammonium Molybdate per day can bring about recovery of “acquired molybdenum deficiency” [3]

See also
Molybdenum cofactor deficiency

References
Further reading


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